Article

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

To the Editor:

Primary cutaneous B-cell lymphomas (pcBCLs) can clinically mimic basal cell carcinomas (BCCs); however, histopathologic examination typically demonstrates features of lymphoma without evidence of an epithelial tumor. We present the case of a patient who demonstrated histologic features of both pcBCL and BCC in the same lesion, which was discovered during Mohs micrographic surgery.

An 84-year-old man presented for Mohs surgery for a biopsy-proven nodular and infiltrative BCC on the right superior helix of the ear of 1 year’s duration. Physical examination of the ear revealed a 1.0×1.3–cm ulcerated indurated plaque with rolled borders and a central hyperkeratotic crust (Figure 1). Frozen sections from the first Mohs stage demonstrated residual superficial, infiltrative, and basosquamous BCC (Figure 2). In addition, there was a brisk inflammatory infiltrate throughout the deep margins. The second stage showed no residual BCC, but there still was a brisk atypical lymphocytic infiltrate, with some areas showing lymphocytes in a linear cordlike distribution (Figure 3). Permanent sections demonstrated infiltration of small to medium lymphoid cells. Immunohistochemistry stains were positive for CD20 and BCL2 and negative for CD5, CD10, BCL6, and CD43; a low Ki-67 proliferation fraction also was observed. B-cell clonality studies and polymerase chain reaction demonstrated rearrangements of the IgH and IgK genes, consistent with primary cutaneous marginal zone lymphoma (pcMZL). Positron emission tomography showed no spread of malignancy; therefore, medical oncology recommended observation and close monitoring.

Primary cutaneous B-cell lymphoma accounts for approximately 25% of all cutaneous lymphomas.¹ Three main cutaneous subtypes exist: pcMZL; primary cutaneous follicular center lymphoma; and primary cutaneous diffuse large B-cell lymphoma, leg type. The second most common type of cutaneous lymphoma, pcMZL, accounts for 25% of cases of pcBCL.¹ Primary cutaneous follicular center lymphoma makes up 60% of cutaneous lymphomas, and the remainder are primary cutaneous diffuse large B-cell lymphoma, leg type. All share a notable male predominance and onset most commonly in the sixth through eighth decades of life, although they also can occur in younger patients.¹

Histologically, pcMZL has 2 distinct subtypes: one resembling mucosal-associated lymphoid tissue lymphomas and a more clinically aggressive subtype with heavy chain class switching, although intermediate forms also exist. Both are characterized by diffuse and/or nodular infiltrates in the subcutis and dermis with sparing of the epidermis. Often, these infiltrates are more prominent in the deeper sections examined, and occasionally they may be accompanied by germinal center follicles. Immunohistochemical stains are key in determining the pcBCL subtype. Primary cutaneous marginal zone lymphoma will most commonly show a BCL2+, BCL6–, CD20+, and CD10– immunophenotype, as in our case. If a majority of cells have undergone plasmacytoid differentiation, loss of CD20 can occur, but retention of other B-cell markers, such as CD79a and CD19, will be seen. Proliferation fraction via Ki-67 commonly is low, reflecting the indolence of this subtype of lymphoma.¹

Monoclonal rearrangement of immunoglobulins also can occur, with IgH rearrangements detected in 60% to 80% of cases of pcMZL. Translocations are not a reliable method of diagnosis for pcMZL but can be present in a variable manner, with t(14;18), t(3;14), and t(11;18) reported in a subset of cases.² Leukemic infiltrates encountered on frozen sections should prompt the Mohs surgeon to consider the possibility of a concomitant leukemia or lymphoma. In one study, 36% (20/55) of patients with chronic lymphocytic leukemia (CLL) were found to have predominantly leukemic B-cell infiltrates on frozen sections.³ Numerous reports also exist of asymptomatic patients being diagnosed with CLL due to leukemic infiltrates identified during Mohs surgery.^4,5 Patients with systemic hematologic malignancies, including CLL and non-Hodgkin lymphoma, also are known to be at an increased risk for skin cancers, including keratinocyte cancers, melanoma, and Merkel cell carcinoma. This can be attributed partially to immunosuppression, a well-known risk factor for development of cutaneous malignancies.⁵ Padgett et al⁵ speculated that local immune suppression due to underlying pcBCL and reaction of lymphocytes to tumor antigens could have played a role in the development of BCC at this site. If a leukemic infiltrate is demonstrated, the surgeon should consider sending tissue for permanent section and immunostaining. This can be helpful to determine if it is a reactive or neoplastic process and aid in characterizing the leukemic infiltrate if it is suspected to be neoplastic in nature.

There are numerous reports of pcBCL imitating the cutaneous findings of BCC clinically, but this is quite uncommon on histopathology. As in our case, findings of sheets of dense, monomorphic lymphocytes; inability to clear inflammation on deeper Mohs sections; presence of primordial follicles; and atypical cytology, including predominance of blastic forms, plasmacytoid cells, or cleaved lymphocytes, should give the clinician pause to consider further evaluation through permanent sections as well as genetic and immunoglobulin studies by a dermatopathologist. This case highlights the importance of further evaluation when an atypical finding is encountered during Mohs surgery.

To the Editor:

Primary cutaneous B-cell lymphomas (pcBCLs) can clinically mimic basal cell carcinomas (BCCs); however, histopathologic examination typically demonstrates features of lymphoma without evidence of an epithelial tumor. We present the case of a patient who demonstrated histologic features of both pcBCL and BCC in the same lesion, which was discovered during Mohs micrographic surgery.

An 84-year-old man presented for Mohs surgery for a biopsy-proven nodular and infiltrative BCC on the right superior helix of the ear of 1 year’s duration. Physical examination of the ear revealed a 1.0×1.3–cm ulcerated indurated plaque with rolled borders and a central hyperkeratotic crust (Figure 1). Frozen sections from the first Mohs stage demonstrated residual superficial, infiltrative, and basosquamous BCC (Figure 2). In addition, there was a brisk inflammatory infiltrate throughout the deep margins. The second stage showed no residual BCC, but there still was a brisk atypical lymphocytic infiltrate, with some areas showing lymphocytes in a linear cordlike distribution (Figure 3). Permanent sections demonstrated infiltration of small to medium lymphoid cells. Immunohistochemistry stains were positive for CD20 and BCL2 and negative for CD5, CD10, BCL6, and CD43; a low Ki-67 proliferation fraction also was observed. B-cell clonality studies and polymerase chain reaction demonstrated rearrangements of the IgH and IgK genes, consistent with primary cutaneous marginal zone lymphoma (pcMZL). Positron emission tomography showed no spread of malignancy; therefore, medical oncology recommended observation and close monitoring.

Primary cutaneous B-cell lymphoma accounts for approximately 25% of all cutaneous lymphomas.¹ Three main cutaneous subtypes exist: pcMZL; primary cutaneous follicular center lymphoma; and primary cutaneous diffuse large B-cell lymphoma, leg type. The second most common type of cutaneous lymphoma, pcMZL, accounts for 25% of cases of pcBCL.¹ Primary cutaneous follicular center lymphoma makes up 60% of cutaneous lymphomas, and the remainder are primary cutaneous diffuse large B-cell lymphoma, leg type. All share a notable male predominance and onset most commonly in the sixth through eighth decades of life, although they also can occur in younger patients.¹

Histologically, pcMZL has 2 distinct subtypes: one resembling mucosal-associated lymphoid tissue lymphomas and a more clinically aggressive subtype with heavy chain class switching, although intermediate forms also exist. Both are characterized by diffuse and/or nodular infiltrates in the subcutis and dermis with sparing of the epidermis. Often, these infiltrates are more prominent in the deeper sections examined, and occasionally they may be accompanied by germinal center follicles. Immunohistochemical stains are key in determining the pcBCL subtype. Primary cutaneous marginal zone lymphoma will most commonly show a BCL2+, BCL6–, CD20+, and CD10– immunophenotype, as in our case. If a majority of cells have undergone plasmacytoid differentiation, loss of CD20 can occur, but retention of other B-cell markers, such as CD79a and CD19, will be seen. Proliferation fraction via Ki-67 commonly is low, reflecting the indolence of this subtype of lymphoma.¹

Monoclonal rearrangement of immunoglobulins also can occur, with IgH rearrangements detected in 60% to 80% of cases of pcMZL. Translocations are not a reliable method of diagnosis for pcMZL but can be present in a variable manner, with t(14;18), t(3;14), and t(11;18) reported in a subset of cases.² Leukemic infiltrates encountered on frozen sections should prompt the Mohs surgeon to consider the possibility of a concomitant leukemia or lymphoma. In one study, 36% (20/55) of patients with chronic lymphocytic leukemia (CLL) were found to have predominantly leukemic B-cell infiltrates on frozen sections.³ Numerous reports also exist of asymptomatic patients being diagnosed with CLL due to leukemic infiltrates identified during Mohs surgery.^4,5 Patients with systemic hematologic malignancies, including CLL and non-Hodgkin lymphoma, also are known to be at an increased risk for skin cancers, including keratinocyte cancers, melanoma, and Merkel cell carcinoma. This can be attributed partially to immunosuppression, a well-known risk factor for development of cutaneous malignancies.⁵ Padgett et al⁵ speculated that local immune suppression due to underlying pcBCL and reaction of lymphocytes to tumor antigens could have played a role in the development of BCC at this site. If a leukemic infiltrate is demonstrated, the surgeon should consider sending tissue for permanent section and immunostaining. This can be helpful to determine if it is a reactive or neoplastic process and aid in characterizing the leukemic infiltrate if it is suspected to be neoplastic in nature.

There are numerous reports of pcBCL imitating the cutaneous findings of BCC clinically, but this is quite uncommon on histopathology. As in our case, findings of sheets of dense, monomorphic lymphocytes; inability to clear inflammation on deeper Mohs sections; presence of primordial follicles; and atypical cytology, including predominance of blastic forms, plasmacytoid cells, or cleaved lymphocytes, should give the clinician pause to consider further evaluation through permanent sections as well as genetic and immunoglobulin studies by a dermatopathologist. This case highlights the importance of further evaluation when an atypical finding is encountered during Mohs surgery.

To the Editor:

Primary cutaneous B-cell lymphomas (pcBCLs) can clinically mimic basal cell carcinomas (BCCs); however, histopathologic examination typically demonstrates features of lymphoma without evidence of an epithelial tumor. We present the case of a patient who demonstrated histologic features of both pcBCL and BCC in the same lesion, which was discovered during Mohs micrographic surgery.

An 84-year-old man presented for Mohs surgery for a biopsy-proven nodular and infiltrative BCC on the right superior helix of the ear of 1 year’s duration. Physical examination of the ear revealed a 1.0×1.3–cm ulcerated indurated plaque with rolled borders and a central hyperkeratotic crust (Figure 1). Frozen sections from the first Mohs stage demonstrated residual superficial, infiltrative, and basosquamous BCC (Figure 2). In addition, there was a brisk inflammatory infiltrate throughout the deep margins. The second stage showed no residual BCC, but there still was a brisk atypical lymphocytic infiltrate, with some areas showing lymphocytes in a linear cordlike distribution (Figure 3). Permanent sections demonstrated infiltration of small to medium lymphoid cells. Immunohistochemistry stains were positive for CD20 and BCL2 and negative for CD5, CD10, BCL6, and CD43; a low Ki-67 proliferation fraction also was observed. B-cell clonality studies and polymerase chain reaction demonstrated rearrangements of the IgH and IgK genes, consistent with primary cutaneous marginal zone lymphoma (pcMZL). Positron emission tomography showed no spread of malignancy; therefore, medical oncology recommended observation and close monitoring.

Primary cutaneous B-cell lymphoma accounts for approximately 25% of all cutaneous lymphomas.¹ Three main cutaneous subtypes exist: pcMZL; primary cutaneous follicular center lymphoma; and primary cutaneous diffuse large B-cell lymphoma, leg type. The second most common type of cutaneous lymphoma, pcMZL, accounts for 25% of cases of pcBCL.¹ Primary cutaneous follicular center lymphoma makes up 60% of cutaneous lymphomas, and the remainder are primary cutaneous diffuse large B-cell lymphoma, leg type. All share a notable male predominance and onset most commonly in the sixth through eighth decades of life, although they also can occur in younger patients.¹

Histologically, pcMZL has 2 distinct subtypes: one resembling mucosal-associated lymphoid tissue lymphomas and a more clinically aggressive subtype with heavy chain class switching, although intermediate forms also exist. Both are characterized by diffuse and/or nodular infiltrates in the subcutis and dermis with sparing of the epidermis. Often, these infiltrates are more prominent in the deeper sections examined, and occasionally they may be accompanied by germinal center follicles. Immunohistochemical stains are key in determining the pcBCL subtype. Primary cutaneous marginal zone lymphoma will most commonly show a BCL2+, BCL6–, CD20+, and CD10– immunophenotype, as in our case. If a majority of cells have undergone plasmacytoid differentiation, loss of CD20 can occur, but retention of other B-cell markers, such as CD79a and CD19, will be seen. Proliferation fraction via Ki-67 commonly is low, reflecting the indolence of this subtype of lymphoma.¹

Monoclonal rearrangement of immunoglobulins also can occur, with IgH rearrangements detected in 60% to 80% of cases of pcMZL. Translocations are not a reliable method of diagnosis for pcMZL but can be present in a variable manner, with t(14;18), t(3;14), and t(11;18) reported in a subset of cases.² Leukemic infiltrates encountered on frozen sections should prompt the Mohs surgeon to consider the possibility of a concomitant leukemia or lymphoma. In one study, 36% (20/55) of patients with chronic lymphocytic leukemia (CLL) were found to have predominantly leukemic B-cell infiltrates on frozen sections.³ Numerous reports also exist of asymptomatic patients being diagnosed with CLL due to leukemic infiltrates identified during Mohs surgery.^4,5 Patients with systemic hematologic malignancies, including CLL and non-Hodgkin lymphoma, also are known to be at an increased risk for skin cancers, including keratinocyte cancers, melanoma, and Merkel cell carcinoma. This can be attributed partially to immunosuppression, a well-known risk factor for development of cutaneous malignancies.⁵ Padgett et al⁵ speculated that local immune suppression due to underlying pcBCL and reaction of lymphocytes to tumor antigens could have played a role in the development of BCC at this site. If a leukemic infiltrate is demonstrated, the surgeon should consider sending tissue for permanent section and immunostaining. This can be helpful to determine if it is a reactive or neoplastic process and aid in characterizing the leukemic infiltrate if it is suspected to be neoplastic in nature.

There are numerous reports of pcBCL imitating the cutaneous findings of BCC clinically, but this is quite uncommon on histopathology. As in our case, findings of sheets of dense, monomorphic lymphocytes; inability to clear inflammation on deeper Mohs sections; presence of primordial follicles; and atypical cytology, including predominance of blastic forms, plasmacytoid cells, or cleaved lymphocytes, should give the clinician pause to consider further evaluation through permanent sections as well as genetic and immunoglobulin studies by a dermatopathologist. This case highlights the importance of further evaluation when an atypical finding is encountered during Mohs surgery.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

THE DIAGNOSIS: Cutaneous Leishmaniasis

The biopsy results revealed amastigotes at the periphery of parasitized histiocytes, consistent with a diagnosis of cutaneous leishmaniasis. Polymerase chain reaction analysis revealed Leishmania guyanensis species complex, which includes both L guyanensis and Leishmania panamensis. In this case of disseminated cutaneous leishmaniasis (Figure 1), our patient received a prolonged course of systemic therapy with oral miltefosine 50 mg 3 times daily. At the most recent follow-up appointment, she showed ongoing resolution of ulcerations, subcutaneous plaques, and lymphadenopathy on the trunk and face, but development of subcutaneous nodules continued on the arms and legs. At the next follow-up, physical examination revealed that the lesions slowly started to fade.

Leishmania species are parasites transmitted by bites of female sand flies, which belong to the genera Phlebotomus (Old World, Eastern Hemisphere) and Lutzomyia (New World, Western Hemisphere) genera.¹ Leishmania species have a complex life cycle, propagating within human macrophages, ultimately leading to cutaneous, mucocutaneous, and visceral disease manifestations.² Cutaneous leishmaniasis manifests classically as scattered, painless, slow-healing ulcers.³ A biopsy taken from the edge of a cutaneous ulcer for hematoxylin and eosin processing is recommended for initial diagnosis, and subsequent polymerase chain reaction of the sample is required for speciation, which guides therapeutic options.^4,5 Classic hematoxylin and eosin and Giemsa stain findings include amastigotes lining the edges of parasitized histiocytes (Figure 2).

Systemic treatment options include sodium stibogluconate, amphotericin B, pentamidine, paromomycin, miltefosine, and azole antifungals.^2,5 Geography often plays a critical role in selecting treatment options due to resistance rates of individual Leishmania species; for example, paromomycin compounds are more effective for cutaneous disease caused by Leishmania major than Leishmania tropica. Miltefosine is not effective for treating Leishmania braziliensis which can be acquired outside Guatemala, and higher doses of amphotericin B are recommended for visceral disease from East Africa.^2,5 In patients with cutaneous leishmaniasis caused by L guyanensis, miltefosine remains a first-line option due to its oral formulation and long half-life within organisms, though there is a risk for teratogenicity.² Amphotericin B remains the most effective treatment for visceral leishmaniasis and can be used off label to treat mucocutaneous disease or when cutaneous disease is refractory to other treatment options.³

Given the potential of L guyanensis to progress to mucocutaneous disease, monitoring for mucosal involvement should be performed at regular intervals for 6 months to 1 year.² Treatment may be considered efficacious if no new skin lesions occur after 4 to 6 weeks of therapy; existing skin lesions should be re-epithelializing and reduced by 50% in size, with most cutaneous disease adequately controlled after 3 months of therapy.²

THE DIAGNOSIS: Cutaneous Leishmaniasis

The biopsy results revealed amastigotes at the periphery of parasitized histiocytes, consistent with a diagnosis of cutaneous leishmaniasis. Polymerase chain reaction analysis revealed Leishmania guyanensis species complex, which includes both L guyanensis and Leishmania panamensis. In this case of disseminated cutaneous leishmaniasis (Figure 1), our patient received a prolonged course of systemic therapy with oral miltefosine 50 mg 3 times daily. At the most recent follow-up appointment, she showed ongoing resolution of ulcerations, subcutaneous plaques, and lymphadenopathy on the trunk and face, but development of subcutaneous nodules continued on the arms and legs. At the next follow-up, physical examination revealed that the lesions slowly started to fade.

Leishmania species are parasites transmitted by bites of female sand flies, which belong to the genera Phlebotomus (Old World, Eastern Hemisphere) and Lutzomyia (New World, Western Hemisphere) genera.¹ Leishmania species have a complex life cycle, propagating within human macrophages, ultimately leading to cutaneous, mucocutaneous, and visceral disease manifestations.² Cutaneous leishmaniasis manifests classically as scattered, painless, slow-healing ulcers.³ A biopsy taken from the edge of a cutaneous ulcer for hematoxylin and eosin processing is recommended for initial diagnosis, and subsequent polymerase chain reaction of the sample is required for speciation, which guides therapeutic options.^4,5 Classic hematoxylin and eosin and Giemsa stain findings include amastigotes lining the edges of parasitized histiocytes (Figure 2).

Systemic treatment options include sodium stibogluconate, amphotericin B, pentamidine, paromomycin, miltefosine, and azole antifungals.^2,5 Geography often plays a critical role in selecting treatment options due to resistance rates of individual Leishmania species; for example, paromomycin compounds are more effective for cutaneous disease caused by Leishmania major than Leishmania tropica. Miltefosine is not effective for treating Leishmania braziliensis which can be acquired outside Guatemala, and higher doses of amphotericin B are recommended for visceral disease from East Africa.^2,5 In patients with cutaneous leishmaniasis caused by L guyanensis, miltefosine remains a first-line option due to its oral formulation and long half-life within organisms, though there is a risk for teratogenicity.² Amphotericin B remains the most effective treatment for visceral leishmaniasis and can be used off label to treat mucocutaneous disease or when cutaneous disease is refractory to other treatment options.³

Given the potential of L guyanensis to progress to mucocutaneous disease, monitoring for mucosal involvement should be performed at regular intervals for 6 months to 1 year.² Treatment may be considered efficacious if no new skin lesions occur after 4 to 6 weeks of therapy; existing skin lesions should be re-epithelializing and reduced by 50% in size, with most cutaneous disease adequately controlled after 3 months of therapy.²

THE DIAGNOSIS: Cutaneous Leishmaniasis

The biopsy results revealed amastigotes at the periphery of parasitized histiocytes, consistent with a diagnosis of cutaneous leishmaniasis. Polymerase chain reaction analysis revealed Leishmania guyanensis species complex, which includes both L guyanensis and Leishmania panamensis. In this case of disseminated cutaneous leishmaniasis (Figure 1), our patient received a prolonged course of systemic therapy with oral miltefosine 50 mg 3 times daily. At the most recent follow-up appointment, she showed ongoing resolution of ulcerations, subcutaneous plaques, and lymphadenopathy on the trunk and face, but development of subcutaneous nodules continued on the arms and legs. At the next follow-up, physical examination revealed that the lesions slowly started to fade.

Leishmania species are parasites transmitted by bites of female sand flies, which belong to the genera Phlebotomus (Old World, Eastern Hemisphere) and Lutzomyia (New World, Western Hemisphere) genera.¹ Leishmania species have a complex life cycle, propagating within human macrophages, ultimately leading to cutaneous, mucocutaneous, and visceral disease manifestations.² Cutaneous leishmaniasis manifests classically as scattered, painless, slow-healing ulcers.³ A biopsy taken from the edge of a cutaneous ulcer for hematoxylin and eosin processing is recommended for initial diagnosis, and subsequent polymerase chain reaction of the sample is required for speciation, which guides therapeutic options.^4,5 Classic hematoxylin and eosin and Giemsa stain findings include amastigotes lining the edges of parasitized histiocytes (Figure 2).

Systemic treatment options include sodium stibogluconate, amphotericin B, pentamidine, paromomycin, miltefosine, and azole antifungals.^2,5 Geography often plays a critical role in selecting treatment options due to resistance rates of individual Leishmania species; for example, paromomycin compounds are more effective for cutaneous disease caused by Leishmania major than Leishmania tropica. Miltefosine is not effective for treating Leishmania braziliensis which can be acquired outside Guatemala, and higher doses of amphotericin B are recommended for visceral disease from East Africa.^2,5 In patients with cutaneous leishmaniasis caused by L guyanensis, miltefosine remains a first-line option due to its oral formulation and long half-life within organisms, though there is a risk for teratogenicity.² Amphotericin B remains the most effective treatment for visceral leishmaniasis and can be used off label to treat mucocutaneous disease or when cutaneous disease is refractory to other treatment options.³

Given the potential of L guyanensis to progress to mucocutaneous disease, monitoring for mucosal involvement should be performed at regular intervals for 6 months to 1 year.² Treatment may be considered efficacious if no new skin lesions occur after 4 to 6 weeks of therapy; existing skin lesions should be re-epithelializing and reduced by 50% in size, with most cutaneous disease adequately controlled after 3 months of therapy.²

THE DIAGNOSIS: Pacemaker Extrusion

The lesion crust was easily scraped away to reveal extrusion of the permanent pacemaker (PPM) through the skin with a visible overlying gelatinous biofilm (Figure). The patient subsequently completed a 2-week course of clindamycin 300 mg 3 times daily followed by generator and lead removal, with reimplantation of the PPM into the right chest, as is the standard of care in the treatment of pacemaker extrusion.¹

Ours is the first known reported case of pacemaker extrusion referred to dermatology with a primary concern for cutaneous malignancy. Pacemaker extrusion through the skin is not common, but it is the most common complication of PPM implantation, followed by infection.¹ Pacemaker extrusion results from pressure necrosis and occurs when the PPM emerges through erythematous skin.^1,2 Pacemaker extrusions generally are diagnosed by cardiology; however, it is important for dermatologists to recognize this phenomenon and differentiate it from other cutaneous pathologies, as the morphology of skin changes related to pacemaker extrusion through the skin can mimic cutaneous malignancy or other primary skin disease, especially if the outer layer of a biofilm that forms around the PPM hardens to form a crust. Our case emphasizes the importance of removing crusts when evaluating lesions.³

THE DIAGNOSIS: Pacemaker Extrusion

The lesion crust was easily scraped away to reveal extrusion of the permanent pacemaker (PPM) through the skin with a visible overlying gelatinous biofilm (Figure). The patient subsequently completed a 2-week course of clindamycin 300 mg 3 times daily followed by generator and lead removal, with reimplantation of the PPM into the right chest, as is the standard of care in the treatment of pacemaker extrusion.¹

Ours is the first known reported case of pacemaker extrusion referred to dermatology with a primary concern for cutaneous malignancy. Pacemaker extrusion through the skin is not common, but it is the most common complication of PPM implantation, followed by infection.¹ Pacemaker extrusion results from pressure necrosis and occurs when the PPM emerges through erythematous skin.^1,2 Pacemaker extrusions generally are diagnosed by cardiology; however, it is important for dermatologists to recognize this phenomenon and differentiate it from other cutaneous pathologies, as the morphology of skin changes related to pacemaker extrusion through the skin can mimic cutaneous malignancy or other primary skin disease, especially if the outer layer of a biofilm that forms around the PPM hardens to form a crust. Our case emphasizes the importance of removing crusts when evaluating lesions.³

THE DIAGNOSIS: Pacemaker Extrusion

The lesion crust was easily scraped away to reveal extrusion of the permanent pacemaker (PPM) through the skin with a visible overlying gelatinous biofilm (Figure). The patient subsequently completed a 2-week course of clindamycin 300 mg 3 times daily followed by generator and lead removal, with reimplantation of the PPM into the right chest, as is the standard of care in the treatment of pacemaker extrusion.¹

Ours is the first known reported case of pacemaker extrusion referred to dermatology with a primary concern for cutaneous malignancy. Pacemaker extrusion through the skin is not common, but it is the most common complication of PPM implantation, followed by infection.¹ Pacemaker extrusion results from pressure necrosis and occurs when the PPM emerges through erythematous skin.^1,2 Pacemaker extrusions generally are diagnosed by cardiology; however, it is important for dermatologists to recognize this phenomenon and differentiate it from other cutaneous pathologies, as the morphology of skin changes related to pacemaker extrusion through the skin can mimic cutaneous malignancy or other primary skin disease, especially if the outer layer of a biofilm that forms around the PPM hardens to form a crust. Our case emphasizes the importance of removing crusts when evaluating lesions.³

Squamous cell carcinoma (SCC) is the malignant proliferation of keratinocytes in the epidermis of the skin. Most SCCs are caused by UV light exposure, with sex and increased age acting as the primary known risk factors: SCCs are nearly twice as prevalent in men vs women, and the average age of presentation is the middle of the seventh decade of life.¹ In the United States, there are an estimated 1.8 million new SCC cases annually.² Although not usually life threatening, if left untreated, SCC can metastasize, thereby reducing the 10-year survival rate from above 90% with treatment to 16%.^3-6

Most invasive SCC lesions are treated surgically, but intralesional methotrexate (IL-MTX) has emerged as an alternative treatment for cutaneous SCC. It offers the potential for lower-cost, efficacious outpatient treatment.^7-12 Methotrexate competitively inhibits the enzyme dihydrofolate reductase, which converts dihydrofolate into tetrahydrofolate.¹³ In doing so, MTX indirectly prevents the synthesis of thymine, a nucleotide required for DNA synthesis. Thus, MTX can halt DNA synthesis and consequently, cell division. Intralesional MTX has been shown to successfully treat keratoacanthomas, lymphomas, and various inflammatory dermatologic conditions.^8-12 

Surgical options include standard excision, Mohs micrographic surgery, or electrodesiccation and curettage. Surgical treatment has high (92% to 99%) cure rates and typically requires only 1 or 2 appointments.^14,15 Although costs can vary, one 2012 study using Medicare fee schedules found that total costs (including primary procedure, biopsy, follow-up appointments through 2 months, and other associated costs) for cutaneous SCC were $475 for electrodesiccation and curettage, $1302.92 for excision, and $2093.14 for Mohs micrographic surgery.¹⁶ For some patients, surgery is not an ideal option due to the tumor location, poor wound healing, anticoagulation, and cost. In these patients, photodynamic therapy, topical therapy with 5-fluorouracil or imiquimod, radiation, and cryotherapy are options listed in the American Academy of Dermatology guidelines.¹⁵ Compared with surgery, radiation is more demanding on the patient, often requiring multiple visits a week and including common undesirable adverse effects such as radiation dermatitis and prolonged wounds on the lower legs.¹⁷ Radiation also can be costly, with one study reporting costs between $2559 and $3431 for SCC of the forearm.¹⁸ Furthermore, in young patients, radiotherapy can increase the risk for developing nonmelanoma skin cancer later in life.¹⁶ 

Intralesional MTX is a localized treatment option that avoids the high costs of surgery, the side effects of radiotherapy, prolonged healing, and the systemic effects of chemotherapy. Treatment with IL-MTX can vary depending on the number of treatments necessary but usually only costs a few hundred dollars, rarely costing more than $1000.⁷ Although IL-MTX is less expensive, it typically requires several follow-up visits, whereas surgical removal may only require 1 visit.

Prior research has noted the efficacy of IL-MTX as a neoadjuvant therapy, with one study finding that IL-MTX can reduce the size of SCC lesions by an average of 0.52 cm² prior to surgery.¹⁹ Several case studies also have documented the effectiveness of IL-MTX as a treatment for SCC.^20-22 However, larger studies involving multiple patients to evaluate the efficacy of IL-MTX as a sole treatment for SCC are lacking. Gualdi et al²³ looked at the outcomes (complete resolution, partial response, or no response) for SCC treated with IL-MTX and found that 62% (13/21) of patients experienced improvement, with 48% (10/21) experiencing at least 50% improvement. Although these results are promising, further research is needed.

Our study sought to examine IL-MTX efficacy as well as evaluate the dosage and number of appointments/­sessions needed to achieve resolution of the lesions.

Methods

We conducted a retrospective chart review of patients who received only IL-MTX for clinically evident or biopsy-proven SCC at US Dermatology Partners clinics in Phoenix, Arizona, from January 1, 2022, to June 30, 2023. Patients aged 18 to 89 years were included, and they had not received other treatment for their SCC lesions such as radiation or systemic chemotherapy. Each patient received at least 1 dose of IL-MTX, beginning with a concentration of 12.5 mg/mL and with all subsequent doses at a concentration of 25 mg/mL (low dose vs high dose). Lesion resolution was categorized as no gross clinical tumor on follow-up. Patients received additional doses of IL-MTX based on the clinical appearance of their lesion(s).

Patient-level descriptive statistics are reported as mean (SD) or median (interquartile range [IQR]) for continuous variables as well as frequency and percentage for categorical variables. To account for the correlation of multiple lesions within individual patients, marginal Cox proportional hazard models were used. Time as well as cumulative dose to lesion resolution were evaluated and presented via the cumulative hazard function, while differences in resolution were estimated using separate Cox models for age, sex, and initial dose.

Results

In total, 107 different lesions from 21 patients were included in the analysis. The median number of lesions was 4 per patient (range, 1-15; IQR, 2-7), with a mean (SD) age of 80 (6) years. Patients were primarily female (81% [17/21]). From the data provided, the majority of lesions (83% [89/107]) resolved with IL-MTX. Of the 18 unresolved lesions, 5 (5%) were referred for a different procedure, and the remaining 13 (12%) were censored (lost to follow-up). Figure 1 provides the cumulative incidence function for lesion resolution. Approximately 50% of patient lesions resolved by the second appointment. Similarly, Figure 2 provides the cumulative dose function for lesion resolution; the median cumulative total dose for resolution was 5 mg (IQR, 2.5–12.5). Finally, concerning the ratio for case resolution, no difference in hazard ratio (HR) was observed for age (female vs male, HR: 1.01; 95% CI: 0.96-1.06), biological sex (HR, 1.01; 95% CI, 0.63-1.63), or initial dose (high vs low, HR: 1.13; 95% CI: 0.77-1.65).

Comment

Results of this study demonstrate the efficacy of IL-MTX for the treatment of cutaneous SCC. More than 80% of the lesions resolved by IL-MTX alone. This treatment approach is more cost-effective with fewer adverse effects when compared to other options. In our study, treatment with IL-MTX also proved to be reasonable in terms of the number of appointments and total dose required, with more than 50% of lesions resolving within 2 appointments and a median cumulative total dose of 5 mg. Intralesional MTX appears to be similarly efficacious in men and women, and the concentration of the initial dose (12.5 mg/mL vs 25 mg/mL) does not change the treatment outcome.

Although these data are encouraging for the use of IL-MTX in the treatment of SCC, future work should consider the relationships between lesion characteristics (such as size and location) and case resolution with IL-MTX as well as recurrence rates with lesions treated by IL-MTX compared to other treatment options.

Conclusion

This study demonstrated the efficacy of IL-MTX as a treatment for SCC that is cost-effective, avoids bothersome side effects, and can be accomplished in relatively few appointments. However, more data are needed to characterize the lesion type best suited to this treatment.

Squamous cell carcinoma (SCC) is the malignant proliferation of keratinocytes in the epidermis of the skin. Most SCCs are caused by UV light exposure, with sex and increased age acting as the primary known risk factors: SCCs are nearly twice as prevalent in men vs women, and the average age of presentation is the middle of the seventh decade of life.¹ In the United States, there are an estimated 1.8 million new SCC cases annually.² Although not usually life threatening, if left untreated, SCC can metastasize, thereby reducing the 10-year survival rate from above 90% with treatment to 16%.^3-6

Most invasive SCC lesions are treated surgically, but intralesional methotrexate (IL-MTX) has emerged as an alternative treatment for cutaneous SCC. It offers the potential for lower-cost, efficacious outpatient treatment.^7-12 Methotrexate competitively inhibits the enzyme dihydrofolate reductase, which converts dihydrofolate into tetrahydrofolate.¹³ In doing so, MTX indirectly prevents the synthesis of thymine, a nucleotide required for DNA synthesis. Thus, MTX can halt DNA synthesis and consequently, cell division. Intralesional MTX has been shown to successfully treat keratoacanthomas, lymphomas, and various inflammatory dermatologic conditions.^8-12 

Surgical options include standard excision, Mohs micrographic surgery, or electrodesiccation and curettage. Surgical treatment has high (92% to 99%) cure rates and typically requires only 1 or 2 appointments.^14,15 Although costs can vary, one 2012 study using Medicare fee schedules found that total costs (including primary procedure, biopsy, follow-up appointments through 2 months, and other associated costs) for cutaneous SCC were $475 for electrodesiccation and curettage, $1302.92 for excision, and $2093.14 for Mohs micrographic surgery.¹⁶ For some patients, surgery is not an ideal option due to the tumor location, poor wound healing, anticoagulation, and cost. In these patients, photodynamic therapy, topical therapy with 5-fluorouracil or imiquimod, radiation, and cryotherapy are options listed in the American Academy of Dermatology guidelines.¹⁵ Compared with surgery, radiation is more demanding on the patient, often requiring multiple visits a week and including common undesirable adverse effects such as radiation dermatitis and prolonged wounds on the lower legs.¹⁷ Radiation also can be costly, with one study reporting costs between $2559 and $3431 for SCC of the forearm.¹⁸ Furthermore, in young patients, radiotherapy can increase the risk for developing nonmelanoma skin cancer later in life.¹⁶ 

Intralesional MTX is a localized treatment option that avoids the high costs of surgery, the side effects of radiotherapy, prolonged healing, and the systemic effects of chemotherapy. Treatment with IL-MTX can vary depending on the number of treatments necessary but usually only costs a few hundred dollars, rarely costing more than $1000.⁷ Although IL-MTX is less expensive, it typically requires several follow-up visits, whereas surgical removal may only require 1 visit.

Prior research has noted the efficacy of IL-MTX as a neoadjuvant therapy, with one study finding that IL-MTX can reduce the size of SCC lesions by an average of 0.52 cm² prior to surgery.¹⁹ Several case studies also have documented the effectiveness of IL-MTX as a treatment for SCC.^20-22 However, larger studies involving multiple patients to evaluate the efficacy of IL-MTX as a sole treatment for SCC are lacking. Gualdi et al²³ looked at the outcomes (complete resolution, partial response, or no response) for SCC treated with IL-MTX and found that 62% (13/21) of patients experienced improvement, with 48% (10/21) experiencing at least 50% improvement. Although these results are promising, further research is needed.

Our study sought to examine IL-MTX efficacy as well as evaluate the dosage and number of appointments/­sessions needed to achieve resolution of the lesions.

Methods

We conducted a retrospective chart review of patients who received only IL-MTX for clinically evident or biopsy-proven SCC at US Dermatology Partners clinics in Phoenix, Arizona, from January 1, 2022, to June 30, 2023. Patients aged 18 to 89 years were included, and they had not received other treatment for their SCC lesions such as radiation or systemic chemotherapy. Each patient received at least 1 dose of IL-MTX, beginning with a concentration of 12.5 mg/mL and with all subsequent doses at a concentration of 25 mg/mL (low dose vs high dose). Lesion resolution was categorized as no gross clinical tumor on follow-up. Patients received additional doses of IL-MTX based on the clinical appearance of their lesion(s).

Patient-level descriptive statistics are reported as mean (SD) or median (interquartile range [IQR]) for continuous variables as well as frequency and percentage for categorical variables. To account for the correlation of multiple lesions within individual patients, marginal Cox proportional hazard models were used. Time as well as cumulative dose to lesion resolution were evaluated and presented via the cumulative hazard function, while differences in resolution were estimated using separate Cox models for age, sex, and initial dose.

Results

In total, 107 different lesions from 21 patients were included in the analysis. The median number of lesions was 4 per patient (range, 1-15; IQR, 2-7), with a mean (SD) age of 80 (6) years. Patients were primarily female (81% [17/21]). From the data provided, the majority of lesions (83% [89/107]) resolved with IL-MTX. Of the 18 unresolved lesions, 5 (5%) were referred for a different procedure, and the remaining 13 (12%) were censored (lost to follow-up). Figure 1 provides the cumulative incidence function for lesion resolution. Approximately 50% of patient lesions resolved by the second appointment. Similarly, Figure 2 provides the cumulative dose function for lesion resolution; the median cumulative total dose for resolution was 5 mg (IQR, 2.5–12.5). Finally, concerning the ratio for case resolution, no difference in hazard ratio (HR) was observed for age (female vs male, HR: 1.01; 95% CI: 0.96-1.06), biological sex (HR, 1.01; 95% CI, 0.63-1.63), or initial dose (high vs low, HR: 1.13; 95% CI: 0.77-1.65).

Comment

Results of this study demonstrate the efficacy of IL-MTX for the treatment of cutaneous SCC. More than 80% of the lesions resolved by IL-MTX alone. This treatment approach is more cost-effective with fewer adverse effects when compared to other options. In our study, treatment with IL-MTX also proved to be reasonable in terms of the number of appointments and total dose required, with more than 50% of lesions resolving within 2 appointments and a median cumulative total dose of 5 mg. Intralesional MTX appears to be similarly efficacious in men and women, and the concentration of the initial dose (12.5 mg/mL vs 25 mg/mL) does not change the treatment outcome.

Although these data are encouraging for the use of IL-MTX in the treatment of SCC, future work should consider the relationships between lesion characteristics (such as size and location) and case resolution with IL-MTX as well as recurrence rates with lesions treated by IL-MTX compared to other treatment options.

Conclusion

This study demonstrated the efficacy of IL-MTX as a treatment for SCC that is cost-effective, avoids bothersome side effects, and can be accomplished in relatively few appointments. However, more data are needed to characterize the lesion type best suited to this treatment.

Squamous cell carcinoma (SCC) is the malignant proliferation of keratinocytes in the epidermis of the skin. Most SCCs are caused by UV light exposure, with sex and increased age acting as the primary known risk factors: SCCs are nearly twice as prevalent in men vs women, and the average age of presentation is the middle of the seventh decade of life.¹ In the United States, there are an estimated 1.8 million new SCC cases annually.² Although not usually life threatening, if left untreated, SCC can metastasize, thereby reducing the 10-year survival rate from above 90% with treatment to 16%.^3-6

Most invasive SCC lesions are treated surgically, but intralesional methotrexate (IL-MTX) has emerged as an alternative treatment for cutaneous SCC. It offers the potential for lower-cost, efficacious outpatient treatment.^7-12 Methotrexate competitively inhibits the enzyme dihydrofolate reductase, which converts dihydrofolate into tetrahydrofolate.¹³ In doing so, MTX indirectly prevents the synthesis of thymine, a nucleotide required for DNA synthesis. Thus, MTX can halt DNA synthesis and consequently, cell division. Intralesional MTX has been shown to successfully treat keratoacanthomas, lymphomas, and various inflammatory dermatologic conditions.^8-12 

Surgical options include standard excision, Mohs micrographic surgery, or electrodesiccation and curettage. Surgical treatment has high (92% to 99%) cure rates and typically requires only 1 or 2 appointments.^14,15 Although costs can vary, one 2012 study using Medicare fee schedules found that total costs (including primary procedure, biopsy, follow-up appointments through 2 months, and other associated costs) for cutaneous SCC were $475 for electrodesiccation and curettage, $1302.92 for excision, and $2093.14 for Mohs micrographic surgery.¹⁶ For some patients, surgery is not an ideal option due to the tumor location, poor wound healing, anticoagulation, and cost. In these patients, photodynamic therapy, topical therapy with 5-fluorouracil or imiquimod, radiation, and cryotherapy are options listed in the American Academy of Dermatology guidelines.¹⁵ Compared with surgery, radiation is more demanding on the patient, often requiring multiple visits a week and including common undesirable adverse effects such as radiation dermatitis and prolonged wounds on the lower legs.¹⁷ Radiation also can be costly, with one study reporting costs between $2559 and $3431 for SCC of the forearm.¹⁸ Furthermore, in young patients, radiotherapy can increase the risk for developing nonmelanoma skin cancer later in life.¹⁶ 

Intralesional MTX is a localized treatment option that avoids the high costs of surgery, the side effects of radiotherapy, prolonged healing, and the systemic effects of chemotherapy. Treatment with IL-MTX can vary depending on the number of treatments necessary but usually only costs a few hundred dollars, rarely costing more than $1000.⁷ Although IL-MTX is less expensive, it typically requires several follow-up visits, whereas surgical removal may only require 1 visit.

Prior research has noted the efficacy of IL-MTX as a neoadjuvant therapy, with one study finding that IL-MTX can reduce the size of SCC lesions by an average of 0.52 cm² prior to surgery.¹⁹ Several case studies also have documented the effectiveness of IL-MTX as a treatment for SCC.^20-22 However, larger studies involving multiple patients to evaluate the efficacy of IL-MTX as a sole treatment for SCC are lacking. Gualdi et al²³ looked at the outcomes (complete resolution, partial response, or no response) for SCC treated with IL-MTX and found that 62% (13/21) of patients experienced improvement, with 48% (10/21) experiencing at least 50% improvement. Although these results are promising, further research is needed.

Our study sought to examine IL-MTX efficacy as well as evaluate the dosage and number of appointments/­sessions needed to achieve resolution of the lesions.

Methods

We conducted a retrospective chart review of patients who received only IL-MTX for clinically evident or biopsy-proven SCC at US Dermatology Partners clinics in Phoenix, Arizona, from January 1, 2022, to June 30, 2023. Patients aged 18 to 89 years were included, and they had not received other treatment for their SCC lesions such as radiation or systemic chemotherapy. Each patient received at least 1 dose of IL-MTX, beginning with a concentration of 12.5 mg/mL and with all subsequent doses at a concentration of 25 mg/mL (low dose vs high dose). Lesion resolution was categorized as no gross clinical tumor on follow-up. Patients received additional doses of IL-MTX based on the clinical appearance of their lesion(s).

Patient-level descriptive statistics are reported as mean (SD) or median (interquartile range [IQR]) for continuous variables as well as frequency and percentage for categorical variables. To account for the correlation of multiple lesions within individual patients, marginal Cox proportional hazard models were used. Time as well as cumulative dose to lesion resolution were evaluated and presented via the cumulative hazard function, while differences in resolution were estimated using separate Cox models for age, sex, and initial dose.

Results

In total, 107 different lesions from 21 patients were included in the analysis. The median number of lesions was 4 per patient (range, 1-15; IQR, 2-7), with a mean (SD) age of 80 (6) years. Patients were primarily female (81% [17/21]). From the data provided, the majority of lesions (83% [89/107]) resolved with IL-MTX. Of the 18 unresolved lesions, 5 (5%) were referred for a different procedure, and the remaining 13 (12%) were censored (lost to follow-up). Figure 1 provides the cumulative incidence function for lesion resolution. Approximately 50% of patient lesions resolved by the second appointment. Similarly, Figure 2 provides the cumulative dose function for lesion resolution; the median cumulative total dose for resolution was 5 mg (IQR, 2.5–12.5). Finally, concerning the ratio for case resolution, no difference in hazard ratio (HR) was observed for age (female vs male, HR: 1.01; 95% CI: 0.96-1.06), biological sex (HR, 1.01; 95% CI, 0.63-1.63), or initial dose (high vs low, HR: 1.13; 95% CI: 0.77-1.65).

Comment

Results of this study demonstrate the efficacy of IL-MTX for the treatment of cutaneous SCC. More than 80% of the lesions resolved by IL-MTX alone. This treatment approach is more cost-effective with fewer adverse effects when compared to other options. In our study, treatment with IL-MTX also proved to be reasonable in terms of the number of appointments and total dose required, with more than 50% of lesions resolving within 2 appointments and a median cumulative total dose of 5 mg. Intralesional MTX appears to be similarly efficacious in men and women, and the concentration of the initial dose (12.5 mg/mL vs 25 mg/mL) does not change the treatment outcome.

Although these data are encouraging for the use of IL-MTX in the treatment of SCC, future work should consider the relationships between lesion characteristics (such as size and location) and case resolution with IL-MTX as well as recurrence rates with lesions treated by IL-MTX compared to other treatment options.

Conclusion

This study demonstrated the efficacy of IL-MTX as a treatment for SCC that is cost-effective, avoids bothersome side effects, and can be accomplished in relatively few appointments. However, more data are needed to characterize the lesion type best suited to this treatment.

Choosing your first job out of residency can be overwhelming. The things you need to consider go way beyond the job itself: things like geography, work/life balance, and practice focus (eg, skin cancer, cosmetics, medical dermatology, pediatrics) are all relatively independent factors from the specific practice you join. About 1 in 6 dermatologists change practices every year, with even higher rates for new graduates.¹

Drawing from my 20 years of experience as a dermatologist (10 in academia and 10 in 3 different private group practice settings—one that was independently owned and 2 with private equity owners, of which I am one), I have seen firsthand what matters and what does not when it comes to joining a group practice, both in my own career and in watching the careers of many young dermatologists. I will do my best to summarize that experience into useful advice.

Important Factors to Consider When Choosing a Practice

As a second- or third-year resident, you likely are excited but nervous about leaping into practice. To approach it with confidence, allow me to outline certain factors that apply to all dermatology practices that you may consider joining as you start your career and beyond.

• Every Practice Owner Has to Prioritize Profit. Independent owners need to build the value of their main asset, academics need to fund research and teaching, and private equity owners need to drive returns for their investors. In other words, there are lots of negative situations in academic and independently owned groups, although private equity gets all the bad press.^2-5 Nothing inherently makes one type of practice setting better; it depends on the specific organization. Owners do care about other things beyond just profit (eg, providing quality care, performing cutting-edge research), but when the rubber meets the road, if a practice is providing amazing quality care but losing money doing so, in a short time it won’t be providing any care at all.
• There Is No Free Money. Your long-term compensation will 100% be determined by how much revenue you generate minus the overhead. There is no magic fund to boost your pay long term, no matter how badly the practice needs or wants you. Be clear and even blunt: ask how the practice is going to profit from you. Ask how they plan to make back any signing bonus or guaranteed salary. If they are paying you a higher percentage of collections, ask them how they are able to pay more than competitors. If they say it is because they are more efficient with lower overhead, make sure that increased efficiency does not translate into less support.
• Percent of Collections Is Irrelevant. OK, perhaps not completely irrelevant, but it is one of the least important aspects in determining how much you will make or how happy you will be. Percent of collections is the percentage of the money that the practice actually collects that is paid out to you as compensation. For example, if your percentage of collections is 40%, that means that if the practice collects $1,000,000 for the care you deliver, you will be compensated $400,000. Read on to find out why it is not as important as it seems.
• Don’t Get Too Hung Up on the Details of the Contract. I have seen so many young dermatologists spend enormous amounts of time and money on attorneys and negotiating the fine points of the contract, but not a single one has ever said later that because of all that negotiation they were protected or treated well when things got contentious. What it comes down to is that, if the practice wants to treat you well, they will. If they want to treat you badly, no contract on earth can protect you from all the ways they can do so. And if you leave, no matter what the contract says, they can do whatever they want unless you are willing to spend hundreds of thousands of dollars to fight them in court. So review the contract with an attorney and know what it says, but don’t sweat every period and clause. It isn’t worth it.
• Your Day-to-Day Is Everything. The practice you join may be the best-run practice in the world in every way, except that the office you happen to be going to work in is the one office in the practice that has 2 providers who are jerks and everyone dreads coming to work every morning. There are so many other examples of ways one location can be a disaster even in a great practice—and unfortunately, even great locations can change. The best you can do is to make sure you know where you will be working and with whom. Go and visit the actual office and spend a day shadowing to feel what the vibe is.

What Really Matters

If factors like the percentage of collections you keep are not the big things, what are? The good and bad news is that there isn’t a single answer to this question. Rather, the fundamental question is whether the practice’s plan to maximize profit includes having satisfied, motivated, and engaged long-term providers. Obviously every group practice says this is fundamental to them, but often it isn’t true. Your real job is to find out whether or not it is. The second fundamental question is whether or not the leadership and members of a group practice are competent. It doesn’t matter if they want and intend to do everything right; if the practice is not competent at getting it done, your life practicing dermatology there is not going to be good.

As a dermatologist who has practiced for 20 years in multiple settings, here are some of the questions I would ask when assessing a practice setting I might consider joining. The practice should be able to easily answer all of these questions. If they won’t, can’t, or don’t—or if they answer but don’t give you clear, concrete responses—it is a huge red flag. It could be that they know you won’t like the answers or it could be that they don’t know the answers, but either reason indicates a big problem.

• How do the contracted rates compare to other practices? Pick 5 to 10 Current Procedural Terminology codes you expect to bill the most and ask the practice to tell you the contracted rates for each of those codes with their top 5 payers. Get the same information from all the practices you are considering joining and compare them. The variation between 2 practices in the same market can be as high as 30%. That means that for doing the same work at Practice A you could collect $800,000 and at Practice B in the same market you could collect more than $1,000,000. Getting 45% of your collection from Practice A is a losing proposition compared to getting 40% at Practice B.
• What is the collection rate? If the practice has great contracted rates but terrible revenue cycle management operations, the rates don’t matter. For example, maybe their contracted rate for a given code is $150, compared to another practice whose contracted rate is $125. But if their collection rate is only 60% and the other practice has a collection rate of 80%, they are only getting $90 while the practice with the lower contracted rate is getting $100.
• What billing and coding support does the practice offer? Are you expected to know and keep up with all the procedure codes, modifiers, etc, and use them correctly yourself or do they have professional coders who review every visit? Do they appeal every denied claim? Will you get reports on what charges get denied and why so that you can adjust your practices to avoid further denials?
• How do they train and assign medical assistants (MAs)? The single biggest determinant of your day-to-day productivity and happiness will be your MAs. Having 3 experienced, efficient MAs will allow you to see 50 patients per day with less effort and more fun than seeing 30 patients per day with 2 inexperienced, inefficient MAs. Seeing 50 patients per day at 40% of collections leads to you earning a lot more than seeing 30 per day at 50% of collections. Beyond the basic question of how many MAs you will have, also ask: Will you be expected to train them yourself, or does the practice have a formal training program? Who assesses how well they are performing? Will you have the same MAs every day? When more senior providers have MAs call off sick or leave the practice, will your MAs be pulled to cover their clinics? If that happens, will you be compensated in some way? Get the answers in writing.
• What is the “feel” of the office you will be working in? Ideally you will go and spend a day seeing patients in the office with one of the existing providers to get a sense of whether it’s a place you will be excited to come to every morning. Do you like the other providers? Is there someone who could act as a mentor for you? Does the staff seem happy? Will the physical layout and square footage accommodate the way you imagine practicing? Are the sociodemographics of the patients a fit for what you want?
• Who will be the office manager responsible for your personal practice? Some practices have an on-site manager for every location; others have district or regional managers who are split between multiple practices. Some have both. All can work, but having a competent, supportive office manager with whom you get along with whom and who “gets it” is crucial. You should ask about office manager turnover (high rates are bad, of course) and should ask to meet and interview the office manager who will be the boots on the ground for the practice in your location.
• How much demand for services is there and how are new patients scheduled? If the new hire gets all the hair loss, acne, and eczema cases and the established providers get all the skin cancer/Medicare patients, you are not going to have a balanced patient mix, and you are not going to meet productivity goals because you won’t be doing enough procedures. If there is not enough demand to fill your schedule, what kind of marketing support does the practice offer and what other approaches might they take? If you want to do cosmetics, how are they going to help you grow in that area? Are there other providers who don’t do cosmetics and will refer to you? Is there already someone in the practice who all the referrals go to? Is your percentage of collections based on total collections or on collections after the cost of injectables is deducted?
• What educational support does the practice offer? Do they have an annual meeting for networking and continuing medical education (CME)? If so, will you be expected to use your CME budget to pay to attend? Are there restrictions on what you can use your CME budget for? Is your CME budget considered part of your percentage of collections? Are there experts in the practice you can go to if you have a challenging case or difficult situation?
• Are physician associates and nurse practitioners a big part of the practice? Will you have the opportunity to increase your compensation by supervising them? If so, what is expected of supervising physicians and how are they compensated (flat fee vs percentage of collections vs another model)?
• What does the noncompete say? Obviously the shorter the time period and the smaller the distance, the better. For most practices, a noncompete is nonnegotiable. But there are some nuances to consider: Is the restricted distance from any location that the practice has in the market, or from any location(s) in which you personally have practiced, or from the primary location(s) in which you have practiced? If it is from the primary location(s), get details on how this term is defined: How much do you have to be at a location before it is considered primary? If you stop going to a location, after what period of time is it no longer considered a primary location? Additional questions to ask about noncompetes include: Is there a nonsolicitation clause for employees or patients? Will the practice include a buy-out clause in which you can pay them a set amount to waive the noncompete? Will they make the noncompete time dependent? In other words, if it is a terrible fit and you want to leave in the first year, there is very little justification for them to enforce a noncompete—but unless it is in your contract that they won’t enforce it if you leave before a certain amount of time, they will enforce it.
• Is there a path to having equity in the practice? In academia, this obviously is not a possibility. In independent practices it generally is referred to as an ownership stake or becoming a partner, and in private-equity groups it is literally referred to as “equity,” but they mean essentially the same thing for our purposes. It benefits the practice if you have equity because it gives you a reason to work to help increase the value of the practice. It benefits you to have equity because it means you have more input into decisions that will affect you (and the influence is proportional to how much equity you have) and the equity is an asset that can become very valuable.

The primary advice I have when it comes to being promised an opportunity to become an owner/partner in an independent group is to get the timing and conditions under which you can become an owner in the contract and strongly advocate for a clause that states that if you are not offered the opportunity as defined in the contract that you will be compensated. Also consider what happens if the current owner(s) sell the practice before you become an owner.

In private-equity groups, ask how many of the current providers have equity and ask how the equity is currently divided (what percentage is held by the private equity group, what percentage is held by the CEO and other executives, and what percentage is held by providers). The more equity held by the executive leadership and providers the better, as that means more people are on the same team of trying to increase the value of the practice. Find out how and when you will be able to buy in and try to get this in the contract or at least in writing. Also ask for a guarantee that your equity will not decrease in value. There are instances in which the practice loses value over time due to mismanagement, and the legal structure typically prioritizes the equity of the private-equity owners over the equity of providers. This is called an equity waterfall. Equity that providers were told was worth millions can literally be worth nothing.

One Key Thing You Need to Know

More important than the formal interviews and meetings that will provide you with answers to the questions outlined here, you need to know if you can trust the answers and you need to know the overall culture of the organization. Are they truly pro-provider, and do they believe that engaged and supported providers are the best route to long-term profit maximization? Or do they see providers primarily as replaceable adversaries who need to be placated and managed in order to minimize overhead? The only way to find out is to talk to providers already working there.

If you ask the practice for contact information for providers you can talk to, they likely will put you in touch with those who they know are going to talk about the practice in the best possible light. Be aware that providers may speak positively about a practice for a few different reasons other than that they are actually happy. Maybe the provider has an ownership stake in the practice and will benefit financially if you join. Keep in mind that, if a friend or colleague introduced you to the practice, they are almost certainly getting a substantial referral bonus if you join, so they may not be unbiased; however, if they are an actual friend, the last thing they want is for you to join and be unhappy in the practice because they didn’t tell the truth.

To learn about the experiences of others in your situation who have joined the practice, go to the website and look through the list of providers. Ideally, look for people who are in their first 3 years out of residency who have been there long enough to know the ins and outs but who still are considered newbies and almost certainly don’t have a meaningful ownership stake or strong allegiance to the practice. If it is a geographically widespread practice, focus on people in the region you will be in, but also talk to at least one person from a distant site.

Next, go to the American Academy of Dermatology’s website to find the email addresses for the providers you want to contact in the member directory. Send them an email explaining that you are thinking about joining the practice and that you would like to have an off-the-record phone conversation with them about their experiences. If they decline or don’t respond, it could be a red flag that likely means they don’t think they can speak positively about the practice. If they do agree to speak with you, you can reiterate at that time that the conversation is off the record and that you won’t relay your discussion to anyone at the practice.

Here is a sample email you can use to reach out to providers from a practice you are considering joining:

Subject: Advice on Joining [Practice Name]

Dear Dr. [Name],

I’m a dermatology resident considering joining [Practice Name] and came across your profile. Would you be willing to have a brief (5 to 10 minutes), off-the-record call about your experience? I’d value your perspective and won’t share our conversation with the practice. Thank you!

Best, [Your Name]

Start the conversation with open-ended questions and see where it goes. Some things to ask might be, are you glad you joined the practice? Was there anything that surprised you after you joined? Is there anything you wish you would have asked or known before you joined? I would recommend not asking specifically about their compensation, as it likely will be different from what you are being offered due to variations in location and current market situations.

Final Thoughts

There is no perfect dermatology practice, but the approach outlined here—rooted in first principles and real-world experience—will help you find one that is right for you. Ask tough questions, talk to other providers, and trust your instincts.

Choosing your first job out of residency can be overwhelming. The things you need to consider go way beyond the job itself: things like geography, work/life balance, and practice focus (eg, skin cancer, cosmetics, medical dermatology, pediatrics) are all relatively independent factors from the specific practice you join. About 1 in 6 dermatologists change practices every year, with even higher rates for new graduates.¹

Drawing from my 20 years of experience as a dermatologist (10 in academia and 10 in 3 different private group practice settings—one that was independently owned and 2 with private equity owners, of which I am one), I have seen firsthand what matters and what does not when it comes to joining a group practice, both in my own career and in watching the careers of many young dermatologists. I will do my best to summarize that experience into useful advice.

Important Factors to Consider When Choosing a Practice

As a second- or third-year resident, you likely are excited but nervous about leaping into practice. To approach it with confidence, allow me to outline certain factors that apply to all dermatology practices that you may consider joining as you start your career and beyond.

• Every Practice Owner Has to Prioritize Profit. Independent owners need to build the value of their main asset, academics need to fund research and teaching, and private equity owners need to drive returns for their investors. In other words, there are lots of negative situations in academic and independently owned groups, although private equity gets all the bad press.^2-5 Nothing inherently makes one type of practice setting better; it depends on the specific organization. Owners do care about other things beyond just profit (eg, providing quality care, performing cutting-edge research), but when the rubber meets the road, if a practice is providing amazing quality care but losing money doing so, in a short time it won’t be providing any care at all.
• There Is No Free Money. Your long-term compensation will 100% be determined by how much revenue you generate minus the overhead. There is no magic fund to boost your pay long term, no matter how badly the practice needs or wants you. Be clear and even blunt: ask how the practice is going to profit from you. Ask how they plan to make back any signing bonus or guaranteed salary. If they are paying you a higher percentage of collections, ask them how they are able to pay more than competitors. If they say it is because they are more efficient with lower overhead, make sure that increased efficiency does not translate into less support.
• Percent of Collections Is Irrelevant. OK, perhaps not completely irrelevant, but it is one of the least important aspects in determining how much you will make or how happy you will be. Percent of collections is the percentage of the money that the practice actually collects that is paid out to you as compensation. For example, if your percentage of collections is 40%, that means that if the practice collects $1,000,000 for the care you deliver, you will be compensated $400,000. Read on to find out why it is not as important as it seems.
• Don’t Get Too Hung Up on the Details of the Contract. I have seen so many young dermatologists spend enormous amounts of time and money on attorneys and negotiating the fine points of the contract, but not a single one has ever said later that because of all that negotiation they were protected or treated well when things got contentious. What it comes down to is that, if the practice wants to treat you well, they will. If they want to treat you badly, no contract on earth can protect you from all the ways they can do so. And if you leave, no matter what the contract says, they can do whatever they want unless you are willing to spend hundreds of thousands of dollars to fight them in court. So review the contract with an attorney and know what it says, but don’t sweat every period and clause. It isn’t worth it.
• Your Day-to-Day Is Everything. The practice you join may be the best-run practice in the world in every way, except that the office you happen to be going to work in is the one office in the practice that has 2 providers who are jerks and everyone dreads coming to work every morning. There are so many other examples of ways one location can be a disaster even in a great practice—and unfortunately, even great locations can change. The best you can do is to make sure you know where you will be working and with whom. Go and visit the actual office and spend a day shadowing to feel what the vibe is.

What Really Matters

If factors like the percentage of collections you keep are not the big things, what are? The good and bad news is that there isn’t a single answer to this question. Rather, the fundamental question is whether the practice’s plan to maximize profit includes having satisfied, motivated, and engaged long-term providers. Obviously every group practice says this is fundamental to them, but often it isn’t true. Your real job is to find out whether or not it is. The second fundamental question is whether or not the leadership and members of a group practice are competent. It doesn’t matter if they want and intend to do everything right; if the practice is not competent at getting it done, your life practicing dermatology there is not going to be good.

As a dermatologist who has practiced for 20 years in multiple settings, here are some of the questions I would ask when assessing a practice setting I might consider joining. The practice should be able to easily answer all of these questions. If they won’t, can’t, or don’t—or if they answer but don’t give you clear, concrete responses—it is a huge red flag. It could be that they know you won’t like the answers or it could be that they don’t know the answers, but either reason indicates a big problem.

• How do the contracted rates compare to other practices? Pick 5 to 10 Current Procedural Terminology codes you expect to bill the most and ask the practice to tell you the contracted rates for each of those codes with their top 5 payers. Get the same information from all the practices you are considering joining and compare them. The variation between 2 practices in the same market can be as high as 30%. That means that for doing the same work at Practice A you could collect $800,000 and at Practice B in the same market you could collect more than $1,000,000. Getting 45% of your collection from Practice A is a losing proposition compared to getting 40% at Practice B.
• What is the collection rate? If the practice has great contracted rates but terrible revenue cycle management operations, the rates don’t matter. For example, maybe their contracted rate for a given code is $150, compared to another practice whose contracted rate is $125. But if their collection rate is only 60% and the other practice has a collection rate of 80%, they are only getting $90 while the practice with the lower contracted rate is getting $100.
• What billing and coding support does the practice offer? Are you expected to know and keep up with all the procedure codes, modifiers, etc, and use them correctly yourself or do they have professional coders who review every visit? Do they appeal every denied claim? Will you get reports on what charges get denied and why so that you can adjust your practices to avoid further denials?
• How do they train and assign medical assistants (MAs)? The single biggest determinant of your day-to-day productivity and happiness will be your MAs. Having 3 experienced, efficient MAs will allow you to see 50 patients per day with less effort and more fun than seeing 30 patients per day with 2 inexperienced, inefficient MAs. Seeing 50 patients per day at 40% of collections leads to you earning a lot more than seeing 30 per day at 50% of collections. Beyond the basic question of how many MAs you will have, also ask: Will you be expected to train them yourself, or does the practice have a formal training program? Who assesses how well they are performing? Will you have the same MAs every day? When more senior providers have MAs call off sick or leave the practice, will your MAs be pulled to cover their clinics? If that happens, will you be compensated in some way? Get the answers in writing.
• What is the “feel” of the office you will be working in? Ideally you will go and spend a day seeing patients in the office with one of the existing providers to get a sense of whether it’s a place you will be excited to come to every morning. Do you like the other providers? Is there someone who could act as a mentor for you? Does the staff seem happy? Will the physical layout and square footage accommodate the way you imagine practicing? Are the sociodemographics of the patients a fit for what you want?
• Who will be the office manager responsible for your personal practice? Some practices have an on-site manager for every location; others have district or regional managers who are split between multiple practices. Some have both. All can work, but having a competent, supportive office manager with whom you get along with whom and who “gets it” is crucial. You should ask about office manager turnover (high rates are bad, of course) and should ask to meet and interview the office manager who will be the boots on the ground for the practice in your location.
• How much demand for services is there and how are new patients scheduled? If the new hire gets all the hair loss, acne, and eczema cases and the established providers get all the skin cancer/Medicare patients, you are not going to have a balanced patient mix, and you are not going to meet productivity goals because you won’t be doing enough procedures. If there is not enough demand to fill your schedule, what kind of marketing support does the practice offer and what other approaches might they take? If you want to do cosmetics, how are they going to help you grow in that area? Are there other providers who don’t do cosmetics and will refer to you? Is there already someone in the practice who all the referrals go to? Is your percentage of collections based on total collections or on collections after the cost of injectables is deducted?
• What educational support does the practice offer? Do they have an annual meeting for networking and continuing medical education (CME)? If so, will you be expected to use your CME budget to pay to attend? Are there restrictions on what you can use your CME budget for? Is your CME budget considered part of your percentage of collections? Are there experts in the practice you can go to if you have a challenging case or difficult situation?
• Are physician associates and nurse practitioners a big part of the practice? Will you have the opportunity to increase your compensation by supervising them? If so, what is expected of supervising physicians and how are they compensated (flat fee vs percentage of collections vs another model)?
• What does the noncompete say? Obviously the shorter the time period and the smaller the distance, the better. For most practices, a noncompete is nonnegotiable. But there are some nuances to consider: Is the restricted distance from any location that the practice has in the market, or from any location(s) in which you personally have practiced, or from the primary location(s) in which you have practiced? If it is from the primary location(s), get details on how this term is defined: How much do you have to be at a location before it is considered primary? If you stop going to a location, after what period of time is it no longer considered a primary location? Additional questions to ask about noncompetes include: Is there a nonsolicitation clause for employees or patients? Will the practice include a buy-out clause in which you can pay them a set amount to waive the noncompete? Will they make the noncompete time dependent? In other words, if it is a terrible fit and you want to leave in the first year, there is very little justification for them to enforce a noncompete—but unless it is in your contract that they won’t enforce it if you leave before a certain amount of time, they will enforce it.
• Is there a path to having equity in the practice? In academia, this obviously is not a possibility. In independent practices it generally is referred to as an ownership stake or becoming a partner, and in private-equity groups it is literally referred to as “equity,” but they mean essentially the same thing for our purposes. It benefits the practice if you have equity because it gives you a reason to work to help increase the value of the practice. It benefits you to have equity because it means you have more input into decisions that will affect you (and the influence is proportional to how much equity you have) and the equity is an asset that can become very valuable.

The primary advice I have when it comes to being promised an opportunity to become an owner/partner in an independent group is to get the timing and conditions under which you can become an owner in the contract and strongly advocate for a clause that states that if you are not offered the opportunity as defined in the contract that you will be compensated. Also consider what happens if the current owner(s) sell the practice before you become an owner.

In private-equity groups, ask how many of the current providers have equity and ask how the equity is currently divided (what percentage is held by the private equity group, what percentage is held by the CEO and other executives, and what percentage is held by providers). The more equity held by the executive leadership and providers the better, as that means more people are on the same team of trying to increase the value of the practice. Find out how and when you will be able to buy in and try to get this in the contract or at least in writing. Also ask for a guarantee that your equity will not decrease in value. There are instances in which the practice loses value over time due to mismanagement, and the legal structure typically prioritizes the equity of the private-equity owners over the equity of providers. This is called an equity waterfall. Equity that providers were told was worth millions can literally be worth nothing.

One Key Thing You Need to Know

More important than the formal interviews and meetings that will provide you with answers to the questions outlined here, you need to know if you can trust the answers and you need to know the overall culture of the organization. Are they truly pro-provider, and do they believe that engaged and supported providers are the best route to long-term profit maximization? Or do they see providers primarily as replaceable adversaries who need to be placated and managed in order to minimize overhead? The only way to find out is to talk to providers already working there.

If you ask the practice for contact information for providers you can talk to, they likely will put you in touch with those who they know are going to talk about the practice in the best possible light. Be aware that providers may speak positively about a practice for a few different reasons other than that they are actually happy. Maybe the provider has an ownership stake in the practice and will benefit financially if you join. Keep in mind that, if a friend or colleague introduced you to the practice, they are almost certainly getting a substantial referral bonus if you join, so they may not be unbiased; however, if they are an actual friend, the last thing they want is for you to join and be unhappy in the practice because they didn’t tell the truth.

To learn about the experiences of others in your situation who have joined the practice, go to the website and look through the list of providers. Ideally, look for people who are in their first 3 years out of residency who have been there long enough to know the ins and outs but who still are considered newbies and almost certainly don’t have a meaningful ownership stake or strong allegiance to the practice. If it is a geographically widespread practice, focus on people in the region you will be in, but also talk to at least one person from a distant site.

Next, go to the American Academy of Dermatology’s website to find the email addresses for the providers you want to contact in the member directory. Send them an email explaining that you are thinking about joining the practice and that you would like to have an off-the-record phone conversation with them about their experiences. If they decline or don’t respond, it could be a red flag that likely means they don’t think they can speak positively about the practice. If they do agree to speak with you, you can reiterate at that time that the conversation is off the record and that you won’t relay your discussion to anyone at the practice.

Here is a sample email you can use to reach out to providers from a practice you are considering joining:

Subject: Advice on Joining [Practice Name]

Dear Dr. [Name],

I’m a dermatology resident considering joining [Practice Name] and came across your profile. Would you be willing to have a brief (5 to 10 minutes), off-the-record call about your experience? I’d value your perspective and won’t share our conversation with the practice. Thank you!

Best, [Your Name]

Start the conversation with open-ended questions and see where it goes. Some things to ask might be, are you glad you joined the practice? Was there anything that surprised you after you joined? Is there anything you wish you would have asked or known before you joined? I would recommend not asking specifically about their compensation, as it likely will be different from what you are being offered due to variations in location and current market situations.

Final Thoughts

There is no perfect dermatology practice, but the approach outlined here—rooted in first principles and real-world experience—will help you find one that is right for you. Ask tough questions, talk to other providers, and trust your instincts.

Choosing your first job out of residency can be overwhelming. The things you need to consider go way beyond the job itself: things like geography, work/life balance, and practice focus (eg, skin cancer, cosmetics, medical dermatology, pediatrics) are all relatively independent factors from the specific practice you join. About 1 in 6 dermatologists change practices every year, with even higher rates for new graduates.¹

Drawing from my 20 years of experience as a dermatologist (10 in academia and 10 in 3 different private group practice settings—one that was independently owned and 2 with private equity owners, of which I am one), I have seen firsthand what matters and what does not when it comes to joining a group practice, both in my own career and in watching the careers of many young dermatologists. I will do my best to summarize that experience into useful advice.

Important Factors to Consider When Choosing a Practice

As a second- or third-year resident, you likely are excited but nervous about leaping into practice. To approach it with confidence, allow me to outline certain factors that apply to all dermatology practices that you may consider joining as you start your career and beyond.

• Every Practice Owner Has to Prioritize Profit. Independent owners need to build the value of their main asset, academics need to fund research and teaching, and private equity owners need to drive returns for their investors. In other words, there are lots of negative situations in academic and independently owned groups, although private equity gets all the bad press.^2-5 Nothing inherently makes one type of practice setting better; it depends on the specific organization. Owners do care about other things beyond just profit (eg, providing quality care, performing cutting-edge research), but when the rubber meets the road, if a practice is providing amazing quality care but losing money doing so, in a short time it won’t be providing any care at all.
• There Is No Free Money. Your long-term compensation will 100% be determined by how much revenue you generate minus the overhead. There is no magic fund to boost your pay long term, no matter how badly the practice needs or wants you. Be clear and even blunt: ask how the practice is going to profit from you. Ask how they plan to make back any signing bonus or guaranteed salary. If they are paying you a higher percentage of collections, ask them how they are able to pay more than competitors. If they say it is because they are more efficient with lower overhead, make sure that increased efficiency does not translate into less support.
• Percent of Collections Is Irrelevant. OK, perhaps not completely irrelevant, but it is one of the least important aspects in determining how much you will make or how happy you will be. Percent of collections is the percentage of the money that the practice actually collects that is paid out to you as compensation. For example, if your percentage of collections is 40%, that means that if the practice collects $1,000,000 for the care you deliver, you will be compensated $400,000. Read on to find out why it is not as important as it seems.
• Don’t Get Too Hung Up on the Details of the Contract. I have seen so many young dermatologists spend enormous amounts of time and money on attorneys and negotiating the fine points of the contract, but not a single one has ever said later that because of all that negotiation they were protected or treated well when things got contentious. What it comes down to is that, if the practice wants to treat you well, they will. If they want to treat you badly, no contract on earth can protect you from all the ways they can do so. And if you leave, no matter what the contract says, they can do whatever they want unless you are willing to spend hundreds of thousands of dollars to fight them in court. So review the contract with an attorney and know what it says, but don’t sweat every period and clause. It isn’t worth it.
• Your Day-to-Day Is Everything. The practice you join may be the best-run practice in the world in every way, except that the office you happen to be going to work in is the one office in the practice that has 2 providers who are jerks and everyone dreads coming to work every morning. There are so many other examples of ways one location can be a disaster even in a great practice—and unfortunately, even great locations can change. The best you can do is to make sure you know where you will be working and with whom. Go and visit the actual office and spend a day shadowing to feel what the vibe is.

What Really Matters

If factors like the percentage of collections you keep are not the big things, what are? The good and bad news is that there isn’t a single answer to this question. Rather, the fundamental question is whether the practice’s plan to maximize profit includes having satisfied, motivated, and engaged long-term providers. Obviously every group practice says this is fundamental to them, but often it isn’t true. Your real job is to find out whether or not it is. The second fundamental question is whether or not the leadership and members of a group practice are competent. It doesn’t matter if they want and intend to do everything right; if the practice is not competent at getting it done, your life practicing dermatology there is not going to be good.

As a dermatologist who has practiced for 20 years in multiple settings, here are some of the questions I would ask when assessing a practice setting I might consider joining. The practice should be able to easily answer all of these questions. If they won’t, can’t, or don’t—or if they answer but don’t give you clear, concrete responses—it is a huge red flag. It could be that they know you won’t like the answers or it could be that they don’t know the answers, but either reason indicates a big problem.

• How do the contracted rates compare to other practices? Pick 5 to 10 Current Procedural Terminology codes you expect to bill the most and ask the practice to tell you the contracted rates for each of those codes with their top 5 payers. Get the same information from all the practices you are considering joining and compare them. The variation between 2 practices in the same market can be as high as 30%. That means that for doing the same work at Practice A you could collect $800,000 and at Practice B in the same market you could collect more than $1,000,000. Getting 45% of your collection from Practice A is a losing proposition compared to getting 40% at Practice B.
• What is the collection rate? If the practice has great contracted rates but terrible revenue cycle management operations, the rates don’t matter. For example, maybe their contracted rate for a given code is $150, compared to another practice whose contracted rate is $125. But if their collection rate is only 60% and the other practice has a collection rate of 80%, they are only getting $90 while the practice with the lower contracted rate is getting $100.
• What billing and coding support does the practice offer? Are you expected to know and keep up with all the procedure codes, modifiers, etc, and use them correctly yourself or do they have professional coders who review every visit? Do they appeal every denied claim? Will you get reports on what charges get denied and why so that you can adjust your practices to avoid further denials?
• How do they train and assign medical assistants (MAs)? The single biggest determinant of your day-to-day productivity and happiness will be your MAs. Having 3 experienced, efficient MAs will allow you to see 50 patients per day with less effort and more fun than seeing 30 patients per day with 2 inexperienced, inefficient MAs. Seeing 50 patients per day at 40% of collections leads to you earning a lot more than seeing 30 per day at 50% of collections. Beyond the basic question of how many MAs you will have, also ask: Will you be expected to train them yourself, or does the practice have a formal training program? Who assesses how well they are performing? Will you have the same MAs every day? When more senior providers have MAs call off sick or leave the practice, will your MAs be pulled to cover their clinics? If that happens, will you be compensated in some way? Get the answers in writing.
• What is the “feel” of the office you will be working in? Ideally you will go and spend a day seeing patients in the office with one of the existing providers to get a sense of whether it’s a place you will be excited to come to every morning. Do you like the other providers? Is there someone who could act as a mentor for you? Does the staff seem happy? Will the physical layout and square footage accommodate the way you imagine practicing? Are the sociodemographics of the patients a fit for what you want?
• Who will be the office manager responsible for your personal practice? Some practices have an on-site manager for every location; others have district or regional managers who are split between multiple practices. Some have both. All can work, but having a competent, supportive office manager with whom you get along with whom and who “gets it” is crucial. You should ask about office manager turnover (high rates are bad, of course) and should ask to meet and interview the office manager who will be the boots on the ground for the practice in your location.
• How much demand for services is there and how are new patients scheduled? If the new hire gets all the hair loss, acne, and eczema cases and the established providers get all the skin cancer/Medicare patients, you are not going to have a balanced patient mix, and you are not going to meet productivity goals because you won’t be doing enough procedures. If there is not enough demand to fill your schedule, what kind of marketing support does the practice offer and what other approaches might they take? If you want to do cosmetics, how are they going to help you grow in that area? Are there other providers who don’t do cosmetics and will refer to you? Is there already someone in the practice who all the referrals go to? Is your percentage of collections based on total collections or on collections after the cost of injectables is deducted?
• What educational support does the practice offer? Do they have an annual meeting for networking and continuing medical education (CME)? If so, will you be expected to use your CME budget to pay to attend? Are there restrictions on what you can use your CME budget for? Is your CME budget considered part of your percentage of collections? Are there experts in the practice you can go to if you have a challenging case or difficult situation?
• Are physician associates and nurse practitioners a big part of the practice? Will you have the opportunity to increase your compensation by supervising them? If so, what is expected of supervising physicians and how are they compensated (flat fee vs percentage of collections vs another model)?
• What does the noncompete say? Obviously the shorter the time period and the smaller the distance, the better. For most practices, a noncompete is nonnegotiable. But there are some nuances to consider: Is the restricted distance from any location that the practice has in the market, or from any location(s) in which you personally have practiced, or from the primary location(s) in which you have practiced? If it is from the primary location(s), get details on how this term is defined: How much do you have to be at a location before it is considered primary? If you stop going to a location, after what period of time is it no longer considered a primary location? Additional questions to ask about noncompetes include: Is there a nonsolicitation clause for employees or patients? Will the practice include a buy-out clause in which you can pay them a set amount to waive the noncompete? Will they make the noncompete time dependent? In other words, if it is a terrible fit and you want to leave in the first year, there is very little justification for them to enforce a noncompete—but unless it is in your contract that they won’t enforce it if you leave before a certain amount of time, they will enforce it.
• Is there a path to having equity in the practice? In academia, this obviously is not a possibility. In independent practices it generally is referred to as an ownership stake or becoming a partner, and in private-equity groups it is literally referred to as “equity,” but they mean essentially the same thing for our purposes. It benefits the practice if you have equity because it gives you a reason to work to help increase the value of the practice. It benefits you to have equity because it means you have more input into decisions that will affect you (and the influence is proportional to how much equity you have) and the equity is an asset that can become very valuable.

The primary advice I have when it comes to being promised an opportunity to become an owner/partner in an independent group is to get the timing and conditions under which you can become an owner in the contract and strongly advocate for a clause that states that if you are not offered the opportunity as defined in the contract that you will be compensated. Also consider what happens if the current owner(s) sell the practice before you become an owner.

In private-equity groups, ask how many of the current providers have equity and ask how the equity is currently divided (what percentage is held by the private equity group, what percentage is held by the CEO and other executives, and what percentage is held by providers). The more equity held by the executive leadership and providers the better, as that means more people are on the same team of trying to increase the value of the practice. Find out how and when you will be able to buy in and try to get this in the contract or at least in writing. Also ask for a guarantee that your equity will not decrease in value. There are instances in which the practice loses value over time due to mismanagement, and the legal structure typically prioritizes the equity of the private-equity owners over the equity of providers. This is called an equity waterfall. Equity that providers were told was worth millions can literally be worth nothing.

One Key Thing You Need to Know

More important than the formal interviews and meetings that will provide you with answers to the questions outlined here, you need to know if you can trust the answers and you need to know the overall culture of the organization. Are they truly pro-provider, and do they believe that engaged and supported providers are the best route to long-term profit maximization? Or do they see providers primarily as replaceable adversaries who need to be placated and managed in order to minimize overhead? The only way to find out is to talk to providers already working there.

If you ask the practice for contact information for providers you can talk to, they likely will put you in touch with those who they know are going to talk about the practice in the best possible light. Be aware that providers may speak positively about a practice for a few different reasons other than that they are actually happy. Maybe the provider has an ownership stake in the practice and will benefit financially if you join. Keep in mind that, if a friend or colleague introduced you to the practice, they are almost certainly getting a substantial referral bonus if you join, so they may not be unbiased; however, if they are an actual friend, the last thing they want is for you to join and be unhappy in the practice because they didn’t tell the truth.

To learn about the experiences of others in your situation who have joined the practice, go to the website and look through the list of providers. Ideally, look for people who are in their first 3 years out of residency who have been there long enough to know the ins and outs but who still are considered newbies and almost certainly don’t have a meaningful ownership stake or strong allegiance to the practice. If it is a geographically widespread practice, focus on people in the region you will be in, but also talk to at least one person from a distant site.

Next, go to the American Academy of Dermatology’s website to find the email addresses for the providers you want to contact in the member directory. Send them an email explaining that you are thinking about joining the practice and that you would like to have an off-the-record phone conversation with them about their experiences. If they decline or don’t respond, it could be a red flag that likely means they don’t think they can speak positively about the practice. If they do agree to speak with you, you can reiterate at that time that the conversation is off the record and that you won’t relay your discussion to anyone at the practice.

Here is a sample email you can use to reach out to providers from a practice you are considering joining:

Subject: Advice on Joining [Practice Name]

Dear Dr. [Name],

I’m a dermatology resident considering joining [Practice Name] and came across your profile. Would you be willing to have a brief (5 to 10 minutes), off-the-record call about your experience? I’d value your perspective and won’t share our conversation with the practice. Thank you!

Best, [Your Name]

Start the conversation with open-ended questions and see where it goes. Some things to ask might be, are you glad you joined the practice? Was there anything that surprised you after you joined? Is there anything you wish you would have asked or known before you joined? I would recommend not asking specifically about their compensation, as it likely will be different from what you are being offered due to variations in location and current market situations.

Final Thoughts

There is no perfect dermatology practice, but the approach outlined here—rooted in first principles and real-world experience—will help you find one that is right for you. Ask tough questions, talk to other providers, and trust your instincts.