Schield Wikas, DO

To the Editor:

A 46-year-old overweight woman presented with a rash in the axillae of 2 months’ duration. She did not report any additional symptoms such as pruritus or pain. She reported changing her deodorant recently from Secret Original to Secret Clinical Strength (both Procter & Gamble). Her medical history was remarkable for asthma and gastroesophageal reflux disease. Clinical examination revealed erythematous-brown, stuccolike, hyperkeratotic papules coalescing into plaques in recently shaved axillae, affecting the left axilla more than the right axilla (Figure 1). The clinical differential diagnosis included granular parakeratosis, intertrigo, Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, acanthosis nigricans, seborrheic keratoses, and irritant or allergic contact dermatitis. A punch biopsy revealed a marked compact parakeratotic horn with retention of keratohyalin granules (Figure 2). The subjacent epidermis showed some acanthosis and spongiosis with mild chronic inflammation of the dermal rim. Based on histopathology, granular parakeratosis was diagnosed.

At a subsequent visit 2 weeks later, we prescribed glycolic acid lotion 10% applied to the axillae twice daily, plus tretinoin gel 0.05% applied to the axillae each evening. She reported clearing after 1 week of therapy. She also had changed her deodorant from Secret Clinical Strength back to the usual Secret Original. The patient discontinued topical treatment after clearing of the lesions. Three weeks later, clinical examination revealed postinflammatory hyperpigmentation in the axillae, and the prior lesions had resolved (Figure 3).

Granular parakeratosis is an unusual condition most commonly presenting in middle-aged women in the axillae, with a clinical presentation of erythematous to brownish hyperkeratotic papules coalescing into plaques. Although few cases have been reported, granular parakeratosis likely is more common than has been reported. There have been reports involving the scalp, cheeks, abdomen, thighs, and other intertriginous areas including inguinal folds and the submammary region.^1-4 There also is an infantile form related to diapers and zinc oxide paste.⁵ Although uncommon, granular parakeratosis can occur as a single papule or plaque and is termed granular parakeratotic acanthoma.⁶ Lesions may persist for months, spontaneously resolve and recur, and occasionally evolve into fissures and erosions due to irritation. Pruritus is a common concern. Histology of granular parakeratosis reveals hyperkeratosis with eosinophilic staining, compact parakeratosis with retention of basophilic keratohyalin granules, and vascular proliferation and ectasia.⁵

The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.^5,7 Cases indicate a link to obesity. Hypotheses as to the etiology include the disruption of cornification. Normally, filaggrin maintains the keratohyaline granules in the stratum corneum during cornification. Therefore, the retention of keratohyaline granules in granular parakeratosis may be due to a defect in processing profilaggrin to filaggrin, which has been proposed based on ultrastructural and immunohistochemical studies.⁸

The differential diagnosis includes granular parakeratosis, intertrigo (caused by seborrheic dermatitis, candidiasis, inverse psoriasis, or erythrasma), Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, and irritant or allergic contact dermatitis. The papules may resemble seborrheic keratoses, while the plaques can be mistaken for acanthosis nigricans.

Therapeutic success has been reported with topical corticosteroids, vitamin D analogues, topical or oral retinoids, ammonium lactate, calcineurin inhibitors, topical or oral antifungals, cryotherapy, and botulinum toxin injections.^3,9-11 In addition, parakeratosis has decreased in biopsies from psoriatic patients after acitretin, methotrexate, and phototherapy, which may be alternative treatments for unusually difficult or recalcitrant cases of granular parakeratosis. To minimize side effects and resolve the papules quickly, we combined 2 synergistic agents—glycolic acid and tretinoin—each with different mechanisms of action, and we observed excellent clinical response.

Granular parakeratosis is possibly related to a combination of topical products that potentiate irritation, rubbing, and occlusion of sweat. Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products. Our patient’s change in deodorant may have been the inciting factor for the disease. Withdrawal of the Secret Clinical Strength deodorant prompted clearing, though topical retinoid and glycolic acid acted as facilitating therapies for timely results. A thorough history, as highlighted by this case, may help pinpoint etiologic factors. By identifying a seemingly innocuous change in hygienic routine, we were able to minimize the need for ongoing therapy.

To the Editor:

A 46-year-old overweight woman presented with a rash in the axillae of 2 months’ duration. She did not report any additional symptoms such as pruritus or pain. She reported changing her deodorant recently from Secret Original to Secret Clinical Strength (both Procter & Gamble). Her medical history was remarkable for asthma and gastroesophageal reflux disease. Clinical examination revealed erythematous-brown, stuccolike, hyperkeratotic papules coalescing into plaques in recently shaved axillae, affecting the left axilla more than the right axilla (Figure 1). The clinical differential diagnosis included granular parakeratosis, intertrigo, Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, acanthosis nigricans, seborrheic keratoses, and irritant or allergic contact dermatitis. A punch biopsy revealed a marked compact parakeratotic horn with retention of keratohyalin granules (Figure 2). The subjacent epidermis showed some acanthosis and spongiosis with mild chronic inflammation of the dermal rim. Based on histopathology, granular parakeratosis was diagnosed.

At a subsequent visit 2 weeks later, we prescribed glycolic acid lotion 10% applied to the axillae twice daily, plus tretinoin gel 0.05% applied to the axillae each evening. She reported clearing after 1 week of therapy. She also had changed her deodorant from Secret Clinical Strength back to the usual Secret Original. The patient discontinued topical treatment after clearing of the lesions. Three weeks later, clinical examination revealed postinflammatory hyperpigmentation in the axillae, and the prior lesions had resolved (Figure 3).

Granular parakeratosis is an unusual condition most commonly presenting in middle-aged women in the axillae, with a clinical presentation of erythematous to brownish hyperkeratotic papules coalescing into plaques. Although few cases have been reported, granular parakeratosis likely is more common than has been reported. There have been reports involving the scalp, cheeks, abdomen, thighs, and other intertriginous areas including inguinal folds and the submammary region.^1-4 There also is an infantile form related to diapers and zinc oxide paste.⁵ Although uncommon, granular parakeratosis can occur as a single papule or plaque and is termed granular parakeratotic acanthoma.⁶ Lesions may persist for months, spontaneously resolve and recur, and occasionally evolve into fissures and erosions due to irritation. Pruritus is a common concern. Histology of granular parakeratosis reveals hyperkeratosis with eosinophilic staining, compact parakeratosis with retention of basophilic keratohyalin granules, and vascular proliferation and ectasia.⁵

The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.^5,7 Cases indicate a link to obesity. Hypotheses as to the etiology include the disruption of cornification. Normally, filaggrin maintains the keratohyaline granules in the stratum corneum during cornification. Therefore, the retention of keratohyaline granules in granular parakeratosis may be due to a defect in processing profilaggrin to filaggrin, which has been proposed based on ultrastructural and immunohistochemical studies.⁸

The differential diagnosis includes granular parakeratosis, intertrigo (caused by seborrheic dermatitis, candidiasis, inverse psoriasis, or erythrasma), Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, and irritant or allergic contact dermatitis. The papules may resemble seborrheic keratoses, while the plaques can be mistaken for acanthosis nigricans.

Therapeutic success has been reported with topical corticosteroids, vitamin D analogues, topical or oral retinoids, ammonium lactate, calcineurin inhibitors, topical or oral antifungals, cryotherapy, and botulinum toxin injections.^3,9-11 In addition, parakeratosis has decreased in biopsies from psoriatic patients after acitretin, methotrexate, and phototherapy, which may be alternative treatments for unusually difficult or recalcitrant cases of granular parakeratosis. To minimize side effects and resolve the papules quickly, we combined 2 synergistic agents—glycolic acid and tretinoin—each with different mechanisms of action, and we observed excellent clinical response.

Granular parakeratosis is possibly related to a combination of topical products that potentiate irritation, rubbing, and occlusion of sweat. Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products. Our patient’s change in deodorant may have been the inciting factor for the disease. Withdrawal of the Secret Clinical Strength deodorant prompted clearing, though topical retinoid and glycolic acid acted as facilitating therapies for timely results. A thorough history, as highlighted by this case, may help pinpoint etiologic factors. By identifying a seemingly innocuous change in hygienic routine, we were able to minimize the need for ongoing therapy.

To the Editor:

A 46-year-old overweight woman presented with a rash in the axillae of 2 months’ duration. She did not report any additional symptoms such as pruritus or pain. She reported changing her deodorant recently from Secret Original to Secret Clinical Strength (both Procter & Gamble). Her medical history was remarkable for asthma and gastroesophageal reflux disease. Clinical examination revealed erythematous-brown, stuccolike, hyperkeratotic papules coalescing into plaques in recently shaved axillae, affecting the left axilla more than the right axilla (Figure 1). The clinical differential diagnosis included granular parakeratosis, intertrigo, Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, acanthosis nigricans, seborrheic keratoses, and irritant or allergic contact dermatitis. A punch biopsy revealed a marked compact parakeratotic horn with retention of keratohyalin granules (Figure 2). The subjacent epidermis showed some acanthosis and spongiosis with mild chronic inflammation of the dermal rim. Based on histopathology, granular parakeratosis was diagnosed.

At a subsequent visit 2 weeks later, we prescribed glycolic acid lotion 10% applied to the axillae twice daily, plus tretinoin gel 0.05% applied to the axillae each evening. She reported clearing after 1 week of therapy. She also had changed her deodorant from Secret Clinical Strength back to the usual Secret Original. The patient discontinued topical treatment after clearing of the lesions. Three weeks later, clinical examination revealed postinflammatory hyperpigmentation in the axillae, and the prior lesions had resolved (Figure 3).

Granular parakeratosis is an unusual condition most commonly presenting in middle-aged women in the axillae, with a clinical presentation of erythematous to brownish hyperkeratotic papules coalescing into plaques. Although few cases have been reported, granular parakeratosis likely is more common than has been reported. There have been reports involving the scalp, cheeks, abdomen, thighs, and other intertriginous areas including inguinal folds and the submammary region.^1-4 There also is an infantile form related to diapers and zinc oxide paste.⁵ Although uncommon, granular parakeratosis can occur as a single papule or plaque and is termed granular parakeratotic acanthoma.⁶ Lesions may persist for months, spontaneously resolve and recur, and occasionally evolve into fissures and erosions due to irritation. Pruritus is a common concern. Histology of granular parakeratosis reveals hyperkeratosis with eosinophilic staining, compact parakeratosis with retention of basophilic keratohyalin granules, and vascular proliferation and ectasia.⁵

The cause is unknown but possibly related to irritation from rubbing, occlusion, sweating, or deodorants.^5,7 Cases indicate a link to obesity. Hypotheses as to the etiology include the disruption of cornification. Normally, filaggrin maintains the keratohyaline granules in the stratum corneum during cornification. Therefore, the retention of keratohyaline granules in granular parakeratosis may be due to a defect in processing profilaggrin to filaggrin, which has been proposed based on ultrastructural and immunohistochemical studies.⁸

The differential diagnosis includes granular parakeratosis, intertrigo (caused by seborrheic dermatitis, candidiasis, inverse psoriasis, or erythrasma), Hailey-Hailey disease, Darier disease, pemphigus vegetans, confluent and reticulated papillomatosis, and irritant or allergic contact dermatitis. The papules may resemble seborrheic keratoses, while the plaques can be mistaken for acanthosis nigricans.

Therapeutic success has been reported with topical corticosteroids, vitamin D analogues, topical or oral retinoids, ammonium lactate, calcineurin inhibitors, topical or oral antifungals, cryotherapy, and botulinum toxin injections.^3,9-11 In addition, parakeratosis has decreased in biopsies from psoriatic patients after acitretin, methotrexate, and phototherapy, which may be alternative treatments for unusually difficult or recalcitrant cases of granular parakeratosis. To minimize side effects and resolve the papules quickly, we combined 2 synergistic agents—glycolic acid and tretinoin—each with different mechanisms of action, and we observed excellent clinical response.

Granular parakeratosis is possibly related to a combination of topical products that potentiate irritation, rubbing, and occlusion of sweat. Multiple treatment modalities likely contribute to clearing, the most important being removal of any triggering topical products. Our patient’s change in deodorant may have been the inciting factor for the disease. Withdrawal of the Secret Clinical Strength deodorant prompted clearing, though topical retinoid and glycolic acid acted as facilitating therapies for timely results. A thorough history, as highlighted by this case, may help pinpoint etiologic factors. By identifying a seemingly innocuous change in hygienic routine, we were able to minimize the need for ongoing therapy.

To the Editor:

A 17-year-old adolescent girl presented to the dermatology clinic with a tender pruritic rash on the left wrist that was spreading to the bilateral arms and legs of several years’ duration. An area of a prior biopsy on the left wrist was healing well with use of petroleum jelly and halcinonide cream. The patient denied any constitutional symptoms.

Physical examination revealed numerous erythematous papules coalescing into plaques on the bilateral anterior and posterior arms and legs, including some erythematous macules and papules on the palms and soles. The original area of involvement on the left dorsal medial wrist demonstrated a background of erythema with overlying peripheral scaling and resolving violaceous to erythematous papules with signs of serosanguineous crusting (Figure 1). Scattered perifollicular erythema was present on the posterior aspects of the bilateral thighs and arms (Figure 2). Baseline complete blood cell count and complete metabolic panel were within reference range.

Clinical histopathology showed evidence of a pustular superficial dermatophyte infection, and Grocott-Gomori methenamine-silver stain demonstrated numerous fungal hyphae within subcorneal pustules, indicating pustular tinea. Based on the clinicopathologic correlation, the initial presentation was diagnosed as pustular tinea of the entire left wrist, followed by a generalized id reaction 1 week later.

The patient was prescribed oral terbinafine 250 mg once daily to treat the diffuse involvement of the pustular tinea as well as once-daily oral cetirizine, once-daily oral diphenhydramine, a topical emollient, and a topical nonsteroidal antipruritic gel.

Tinea is a superficial fungal infection commonly caused by the dermatophytes Epidermophyton, Trichophyton, and Microsporum. It has a variety of clinical presentations based on the anatomic location, including tinea capitis (hair/scalp), tinea pedis (feet), tinea corporis (face/trunk/extremities), tinea cruris (groin), and tinea unguium (nails).¹ Tinea infections occur in the stratum corneum, hair, and nails, thriving on dead keratin in these areas.² Tinea corporis usually appears as an erythematous ring-shaped lesion with a scaly border, but atypical cases presenting with vesicles, pustules, and bullae also have been reported.³ Additionally, secondary eruptions called id reactions, or autoeczematization, can present in the setting of dermatophyte infections. Such outbreaks may be due to a delayed hypersensitivity reaction to the fungal antigens. Id reactions can manifest in many forms of tinea with patients generally exhibiting pruritic papulovesicular lesions that can present far from the site of origin.⁴

Patients with id reactions can have atypical and varied presentations. In a case of id reaction due to tinea corporis, a patient presented with vesicles and pustules that grew in number and coalesced to form annular lesions.⁵ A case of an id reaction caused by tinea pedis also noted the presence of pustules, which are atypical in this form of tinea.⁶ In another case of tinea pedis, a generalized id reaction was noted, illustrating that such eruptions do not necessarily appear at the original site of infection.⁷ Additionally, in a rare presentation of tinea invading the nares, a patient developed an erythema multiforme id reaction.⁸ Id reactions also were noted in 14 patients with refractory otitis externa, illustrating the ability of this fungal infection to persist and infect distant locations.⁹

Because the differential diagnoses for tinea infection are extensive, pathology or laboratory confirmation is necessary for diagnosis, and potassium hydroxide preparation often is used to diagnose dermatophyte infections.^1,2 Additionally, the possibility of a hypersensitivity drug rash should remain in the differential if the patient received allergy-inducing medications prior to the outbreak, which may in turn complicate the diagnosis.

Tinea infections typically can be treated with topical antifungals such as terbinafine, butenafine,¹ and luliconazole¹⁰; however, more involved cases may require oral antifungal treatment.¹ Systemic treatment of tinea corporis includes itraconazole, terbinafine, and fluconazole,¹¹ all of which exhibit fewer side effects and greater efficacy when compared to griseofulvin.^12-15

Treatment of id reactions centers on the proper clearance of the dermatophyte infection, and treatment with oral antifungals generally is sufficient. In the cases of id reaction in patients with refractory otitis, some success was achieved with treatment involving immunotherapy with dermatophyte and dust mite allergen extracts coupled with a yeast elimination diet.⁹ In acute id reactions, topical corticosteroids and antipruritic agents can be applied.⁴ Rarely, systemic glucocorticoids are required, such as in cases in which the id reaction persists despite proper treatment of the primary infection.¹⁶

To the Editor:

A 17-year-old adolescent girl presented to the dermatology clinic with a tender pruritic rash on the left wrist that was spreading to the bilateral arms and legs of several years’ duration. An area of a prior biopsy on the left wrist was healing well with use of petroleum jelly and halcinonide cream. The patient denied any constitutional symptoms.

Physical examination revealed numerous erythematous papules coalescing into plaques on the bilateral anterior and posterior arms and legs, including some erythematous macules and papules on the palms and soles. The original area of involvement on the left dorsal medial wrist demonstrated a background of erythema with overlying peripheral scaling and resolving violaceous to erythematous papules with signs of serosanguineous crusting (Figure 1). Scattered perifollicular erythema was present on the posterior aspects of the bilateral thighs and arms (Figure 2). Baseline complete blood cell count and complete metabolic panel were within reference range.

Clinical histopathology showed evidence of a pustular superficial dermatophyte infection, and Grocott-Gomori methenamine-silver stain demonstrated numerous fungal hyphae within subcorneal pustules, indicating pustular tinea. Based on the clinicopathologic correlation, the initial presentation was diagnosed as pustular tinea of the entire left wrist, followed by a generalized id reaction 1 week later.

The patient was prescribed oral terbinafine 250 mg once daily to treat the diffuse involvement of the pustular tinea as well as once-daily oral cetirizine, once-daily oral diphenhydramine, a topical emollient, and a topical nonsteroidal antipruritic gel.

Tinea is a superficial fungal infection commonly caused by the dermatophytes Epidermophyton, Trichophyton, and Microsporum. It has a variety of clinical presentations based on the anatomic location, including tinea capitis (hair/scalp), tinea pedis (feet), tinea corporis (face/trunk/extremities), tinea cruris (groin), and tinea unguium (nails).¹ Tinea infections occur in the stratum corneum, hair, and nails, thriving on dead keratin in these areas.² Tinea corporis usually appears as an erythematous ring-shaped lesion with a scaly border, but atypical cases presenting with vesicles, pustules, and bullae also have been reported.³ Additionally, secondary eruptions called id reactions, or autoeczematization, can present in the setting of dermatophyte infections. Such outbreaks may be due to a delayed hypersensitivity reaction to the fungal antigens. Id reactions can manifest in many forms of tinea with patients generally exhibiting pruritic papulovesicular lesions that can present far from the site of origin.⁴

Patients with id reactions can have atypical and varied presentations. In a case of id reaction due to tinea corporis, a patient presented with vesicles and pustules that grew in number and coalesced to form annular lesions.⁵ A case of an id reaction caused by tinea pedis also noted the presence of pustules, which are atypical in this form of tinea.⁶ In another case of tinea pedis, a generalized id reaction was noted, illustrating that such eruptions do not necessarily appear at the original site of infection.⁷ Additionally, in a rare presentation of tinea invading the nares, a patient developed an erythema multiforme id reaction.⁸ Id reactions also were noted in 14 patients with refractory otitis externa, illustrating the ability of this fungal infection to persist and infect distant locations.⁹

Because the differential diagnoses for tinea infection are extensive, pathology or laboratory confirmation is necessary for diagnosis, and potassium hydroxide preparation often is used to diagnose dermatophyte infections.^1,2 Additionally, the possibility of a hypersensitivity drug rash should remain in the differential if the patient received allergy-inducing medications prior to the outbreak, which may in turn complicate the diagnosis.

Tinea infections typically can be treated with topical antifungals such as terbinafine, butenafine,¹ and luliconazole¹⁰; however, more involved cases may require oral antifungal treatment.¹ Systemic treatment of tinea corporis includes itraconazole, terbinafine, and fluconazole,¹¹ all of which exhibit fewer side effects and greater efficacy when compared to griseofulvin.^12-15

Treatment of id reactions centers on the proper clearance of the dermatophyte infection, and treatment with oral antifungals generally is sufficient. In the cases of id reaction in patients with refractory otitis, some success was achieved with treatment involving immunotherapy with dermatophyte and dust mite allergen extracts coupled with a yeast elimination diet.⁹ In acute id reactions, topical corticosteroids and antipruritic agents can be applied.⁴ Rarely, systemic glucocorticoids are required, such as in cases in which the id reaction persists despite proper treatment of the primary infection.¹⁶

To the Editor:

A 17-year-old adolescent girl presented to the dermatology clinic with a tender pruritic rash on the left wrist that was spreading to the bilateral arms and legs of several years’ duration. An area of a prior biopsy on the left wrist was healing well with use of petroleum jelly and halcinonide cream. The patient denied any constitutional symptoms.

Physical examination revealed numerous erythematous papules coalescing into plaques on the bilateral anterior and posterior arms and legs, including some erythematous macules and papules on the palms and soles. The original area of involvement on the left dorsal medial wrist demonstrated a background of erythema with overlying peripheral scaling and resolving violaceous to erythematous papules with signs of serosanguineous crusting (Figure 1). Scattered perifollicular erythema was present on the posterior aspects of the bilateral thighs and arms (Figure 2). Baseline complete blood cell count and complete metabolic panel were within reference range.

Clinical histopathology showed evidence of a pustular superficial dermatophyte infection, and Grocott-Gomori methenamine-silver stain demonstrated numerous fungal hyphae within subcorneal pustules, indicating pustular tinea. Based on the clinicopathologic correlation, the initial presentation was diagnosed as pustular tinea of the entire left wrist, followed by a generalized id reaction 1 week later.

The patient was prescribed oral terbinafine 250 mg once daily to treat the diffuse involvement of the pustular tinea as well as once-daily oral cetirizine, once-daily oral diphenhydramine, a topical emollient, and a topical nonsteroidal antipruritic gel.

Tinea is a superficial fungal infection commonly caused by the dermatophytes Epidermophyton, Trichophyton, and Microsporum. It has a variety of clinical presentations based on the anatomic location, including tinea capitis (hair/scalp), tinea pedis (feet), tinea corporis (face/trunk/extremities), tinea cruris (groin), and tinea unguium (nails).¹ Tinea infections occur in the stratum corneum, hair, and nails, thriving on dead keratin in these areas.² Tinea corporis usually appears as an erythematous ring-shaped lesion with a scaly border, but atypical cases presenting with vesicles, pustules, and bullae also have been reported.³ Additionally, secondary eruptions called id reactions, or autoeczematization, can present in the setting of dermatophyte infections. Such outbreaks may be due to a delayed hypersensitivity reaction to the fungal antigens. Id reactions can manifest in many forms of tinea with patients generally exhibiting pruritic papulovesicular lesions that can present far from the site of origin.⁴

Patients with id reactions can have atypical and varied presentations. In a case of id reaction due to tinea corporis, a patient presented with vesicles and pustules that grew in number and coalesced to form annular lesions.⁵ A case of an id reaction caused by tinea pedis also noted the presence of pustules, which are atypical in this form of tinea.⁶ In another case of tinea pedis, a generalized id reaction was noted, illustrating that such eruptions do not necessarily appear at the original site of infection.⁷ Additionally, in a rare presentation of tinea invading the nares, a patient developed an erythema multiforme id reaction.⁸ Id reactions also were noted in 14 patients with refractory otitis externa, illustrating the ability of this fungal infection to persist and infect distant locations.⁹

Because the differential diagnoses for tinea infection are extensive, pathology or laboratory confirmation is necessary for diagnosis, and potassium hydroxide preparation often is used to diagnose dermatophyte infections.^1,2 Additionally, the possibility of a hypersensitivity drug rash should remain in the differential if the patient received allergy-inducing medications prior to the outbreak, which may in turn complicate the diagnosis.

Tinea infections typically can be treated with topical antifungals such as terbinafine, butenafine,¹ and luliconazole¹⁰; however, more involved cases may require oral antifungal treatment.¹ Systemic treatment of tinea corporis includes itraconazole, terbinafine, and fluconazole,¹¹ all of which exhibit fewer side effects and greater efficacy when compared to griseofulvin.^12-15

Treatment of id reactions centers on the proper clearance of the dermatophyte infection, and treatment with oral antifungals generally is sufficient. In the cases of id reaction in patients with refractory otitis, some success was achieved with treatment involving immunotherapy with dermatophyte and dust mite allergen extracts coupled with a yeast elimination diet.⁹ In acute id reactions, topical corticosteroids and antipruritic agents can be applied.⁴ Rarely, systemic glucocorticoids are required, such as in cases in which the id reaction persists despite proper treatment of the primary infection.¹⁶