Article

Bullous pemphigoid (BP) is a chronic autoimmune skin condition characterized by large, fluid-filled blisters (bullae) on the skin. There usually is severe itching, which may antedate the bullae by several weeks. Bullous pemphigoid most commonly affects adults aged 60 years and older with comorbidities such as metabolic syndrome or other autoimmune diseases. The typical blistering is subepidermal, and its occurrence seems to be driven by autoantibodies targeting the epidermal basement membrane zone.

Conventional treatment for BP has long included systemic corticosteroids and immunosuppressants; this combination of drugs effectively controls inflammation but also is associated with considerable risks such as infection, hyperglycemia with worsening diabetes, hypertension, osteoporosis and fracture risk, and delirium, particularly in older patients. Recent developments in biologic therapy have supported the utilization of potentially safer alternatives. Specifically, dupilumab has demonstrated efficacy in the treatment of atopic dermatitis. Case reports and small research studies included in a recent review have suggested that dupilumab could be effective in managing BP, potentially offering a safer treatment option.¹ Importantly, dupilumab recently was approved for BP by the US Food and Drug Administration, making it the first biologic approved for treating this condition.² In this article, we discuss dupilumab as an option for clinicians to prescribe as an initial therapy for BP.

Pathophysiology of Bullous Pemphigoid and Dupilumab

Bullous pemphigoid pathophysiology is driven by 2 main components: immunologic and inflammatory processes. The immune-mediated attack consists of autoantibodies against the hemidesmosomal proteins BP180 and BP230 in the basement membrane zone, which anchor the epidermis to the dermis.¹ When these proteins are targeted, a cascade of responses is triggered, including the release of inflammatory cells, particularly eosinophils and neutrophils, into the skin. These cells release inflammatory mediators that break down the basement membrane, resulting in the separation of the epidermis from the dermis and leading to subepidermal blister formation.

The inflammation associated with BP largely is driven by a T helper 2–dominant immune response, with increased levels of cytokines such as interleukin (IL) 4 and IL-13.¹ The chronic inflammation contributes to the characteristic blisters and intense pruritus seen in patients with BP. Traditional treatments such as corticosteroids work broadly to suppress this inflammation by reducing the production of all proinflammatory cytokines; however, they lack specificity, which dampens the targeted immune response against BP and broadly suppresses the immune system, increasing the risk for infection and other adverse effects. For older patients with multiple health conditions, these adverse effects can impact quality of life and pose health risks.

Interleukin 4 and IL-13 contribute to eosinophilia by upregulating the expression of eosinophil chemoattractant cytokines that promote eosinophil migration and adhesion.¹ This is where dupilumab presents a promising alternative. Dupilumab is a monoclonal antibody that selectively targets the key cytokines implicated in BP. It binds to the IL-4 receptor alpha subunit, which IL-4 and IL-13 share, thereby inhibiting the signaling of both cytokines.¹

Dupilumab Reports and Case Series

Current evidence supporting the use of dupilumab for BP consists primarily of case series and uncontrolled clinical observations, both of which are useful to formulate but not to test hypotheses.³ One case series of 13 patients diagnosed with BP reported that 92.3% (12/13) of patients achieved disease clearance or satisfactory control, with 53.8% (7/13) achieving total lesion clearance and no adverse events observed.⁴ In a larger case series, 87.0% of 146 patients achieved disease control with an initial dose of dupilumab 600 mg followed by 300 mg every 2 weeks for 4 weeks, though the study also looked at secondary outcomes for up to 64 weeks.⁵ Both these findings are compatible with the idea that dupilumab has efficacy in BP, but they cannot be used to test hypotheses.^3,4

In a single case report of refractory BP, the combination of dupilumab and omalizumab—a monoclonal antibody that blocks the binding of IgE to mast cells, basophils, and dendritic cells—has shown efficacy, particularly when BP is unresponsive to standard therapies.⁶ The case involved a 72-year-old woman with unresponsive BP who was treated with a combination of dupilumab and omalizumab. She experienced marked improvement in pruritus and bullae accompanied by normalization of anti-BP180 autoantibody levels. This result points to the possibility that IL-4 and IL-13 blockade could influence autoantibody production. The authors attributed the reduction in pruritus to dupilumab, although the drug was administered in combination with omalizumab.⁶

Small Randomized Trial of Dupilumab

In addition to these uncontrolled clinical observations, dupilumab recently demonstrated positive results in a small randomized trial.⁷ Patients who were assigned to receive dupilumab were 5 times more likely to achieve sustained remission compared to those assigned to a placebo. All randomized patients also were treated with a standard-of-care oral corticosteroid regimen, which complicated the ability to isolate the specific effects of dupilumab.⁷ Finally, a completed totality of evidence on the prescription of dupilumab for refractory BP should include more reliable results from larger randomized trials.⁸

Final Thoughts

Dupilumab is now approved by the US Food and Drug Administration for the treatment of BP, marking an important milestone as the first targeted biologic therapy for this condition. While the totality of evidence is still evolving, the available data indicate both efficacy and a favorable safety profile when compared to traditional corticosteroids and immunosuppressants. Based on the available data, we suggest that health care providers consider dupilumab as a first-line monotherapy in appropriate patients with BP without specific contraindications, particularly as a practical and safe alternative to corticosteroids and immunosuppressive therapies in older adults with comorbidities. If the patient demonstrates clinical improvement in symptom relief, the therapy can be continued. This strategy minimizes initial exposure to more potent biologics or therapies with higher toxicity profiles. For patients without adequate disease control or with severe initial presentations requiring rapid improvement, clinicians may consider escalation to adjunctive or alternative therapies, such as rituximab, omalizumab, or a short course of systemic corticosteroids for acute management.

Emerging data suggest that dupilumab is a promising therapy for BP. We suggest that it may be a safer targeted alternative to traditional corticosteroids and immunosuppressive therapies. The ability of dupilumab to mitigate inflammation without broadly suppressing the immune system suggests that it may turn out to be an especially valuable option for older patients and those with comorbid conditions.

Acknowledgement—The authors thank Jodi Fiedler, MD (Boca Raton, FL), for her expert advice and assistance.

Bullous pemphigoid (BP) is a chronic autoimmune skin condition characterized by large, fluid-filled blisters (bullae) on the skin. There usually is severe itching, which may antedate the bullae by several weeks. Bullous pemphigoid most commonly affects adults aged 60 years and older with comorbidities such as metabolic syndrome or other autoimmune diseases. The typical blistering is subepidermal, and its occurrence seems to be driven by autoantibodies targeting the epidermal basement membrane zone.

Conventional treatment for BP has long included systemic corticosteroids and immunosuppressants; this combination of drugs effectively controls inflammation but also is associated with considerable risks such as infection, hyperglycemia with worsening diabetes, hypertension, osteoporosis and fracture risk, and delirium, particularly in older patients. Recent developments in biologic therapy have supported the utilization of potentially safer alternatives. Specifically, dupilumab has demonstrated efficacy in the treatment of atopic dermatitis. Case reports and small research studies included in a recent review have suggested that dupilumab could be effective in managing BP, potentially offering a safer treatment option.¹ Importantly, dupilumab recently was approved for BP by the US Food and Drug Administration, making it the first biologic approved for treating this condition.² In this article, we discuss dupilumab as an option for clinicians to prescribe as an initial therapy for BP.

Pathophysiology of Bullous Pemphigoid and Dupilumab

Bullous pemphigoid pathophysiology is driven by 2 main components: immunologic and inflammatory processes. The immune-mediated attack consists of autoantibodies against the hemidesmosomal proteins BP180 and BP230 in the basement membrane zone, which anchor the epidermis to the dermis.¹ When these proteins are targeted, a cascade of responses is triggered, including the release of inflammatory cells, particularly eosinophils and neutrophils, into the skin. These cells release inflammatory mediators that break down the basement membrane, resulting in the separation of the epidermis from the dermis and leading to subepidermal blister formation.

The inflammation associated with BP largely is driven by a T helper 2–dominant immune response, with increased levels of cytokines such as interleukin (IL) 4 and IL-13.¹ The chronic inflammation contributes to the characteristic blisters and intense pruritus seen in patients with BP. Traditional treatments such as corticosteroids work broadly to suppress this inflammation by reducing the production of all proinflammatory cytokines; however, they lack specificity, which dampens the targeted immune response against BP and broadly suppresses the immune system, increasing the risk for infection and other adverse effects. For older patients with multiple health conditions, these adverse effects can impact quality of life and pose health risks.

Interleukin 4 and IL-13 contribute to eosinophilia by upregulating the expression of eosinophil chemoattractant cytokines that promote eosinophil migration and adhesion.¹ This is where dupilumab presents a promising alternative. Dupilumab is a monoclonal antibody that selectively targets the key cytokines implicated in BP. It binds to the IL-4 receptor alpha subunit, which IL-4 and IL-13 share, thereby inhibiting the signaling of both cytokines.¹

Dupilumab Reports and Case Series

Current evidence supporting the use of dupilumab for BP consists primarily of case series and uncontrolled clinical observations, both of which are useful to formulate but not to test hypotheses.³ One case series of 13 patients diagnosed with BP reported that 92.3% (12/13) of patients achieved disease clearance or satisfactory control, with 53.8% (7/13) achieving total lesion clearance and no adverse events observed.⁴ In a larger case series, 87.0% of 146 patients achieved disease control with an initial dose of dupilumab 600 mg followed by 300 mg every 2 weeks for 4 weeks, though the study also looked at secondary outcomes for up to 64 weeks.⁵ Both these findings are compatible with the idea that dupilumab has efficacy in BP, but they cannot be used to test hypotheses.^3,4

In a single case report of refractory BP, the combination of dupilumab and omalizumab—a monoclonal antibody that blocks the binding of IgE to mast cells, basophils, and dendritic cells—has shown efficacy, particularly when BP is unresponsive to standard therapies.⁶ The case involved a 72-year-old woman with unresponsive BP who was treated with a combination of dupilumab and omalizumab. She experienced marked improvement in pruritus and bullae accompanied by normalization of anti-BP180 autoantibody levels. This result points to the possibility that IL-4 and IL-13 blockade could influence autoantibody production. The authors attributed the reduction in pruritus to dupilumab, although the drug was administered in combination with omalizumab.⁶

Small Randomized Trial of Dupilumab

In addition to these uncontrolled clinical observations, dupilumab recently demonstrated positive results in a small randomized trial.⁷ Patients who were assigned to receive dupilumab were 5 times more likely to achieve sustained remission compared to those assigned to a placebo. All randomized patients also were treated with a standard-of-care oral corticosteroid regimen, which complicated the ability to isolate the specific effects of dupilumab.⁷ Finally, a completed totality of evidence on the prescription of dupilumab for refractory BP should include more reliable results from larger randomized trials.⁸

Final Thoughts

Dupilumab is now approved by the US Food and Drug Administration for the treatment of BP, marking an important milestone as the first targeted biologic therapy for this condition. While the totality of evidence is still evolving, the available data indicate both efficacy and a favorable safety profile when compared to traditional corticosteroids and immunosuppressants. Based on the available data, we suggest that health care providers consider dupilumab as a first-line monotherapy in appropriate patients with BP without specific contraindications, particularly as a practical and safe alternative to corticosteroids and immunosuppressive therapies in older adults with comorbidities. If the patient demonstrates clinical improvement in symptom relief, the therapy can be continued. This strategy minimizes initial exposure to more potent biologics or therapies with higher toxicity profiles. For patients without adequate disease control or with severe initial presentations requiring rapid improvement, clinicians may consider escalation to adjunctive or alternative therapies, such as rituximab, omalizumab, or a short course of systemic corticosteroids for acute management.

Emerging data suggest that dupilumab is a promising therapy for BP. We suggest that it may be a safer targeted alternative to traditional corticosteroids and immunosuppressive therapies. The ability of dupilumab to mitigate inflammation without broadly suppressing the immune system suggests that it may turn out to be an especially valuable option for older patients and those with comorbid conditions.

Acknowledgement—The authors thank Jodi Fiedler, MD (Boca Raton, FL), for her expert advice and assistance.

Bullous pemphigoid (BP) is a chronic autoimmune skin condition characterized by large, fluid-filled blisters (bullae) on the skin. There usually is severe itching, which may antedate the bullae by several weeks. Bullous pemphigoid most commonly affects adults aged 60 years and older with comorbidities such as metabolic syndrome or other autoimmune diseases. The typical blistering is subepidermal, and its occurrence seems to be driven by autoantibodies targeting the epidermal basement membrane zone.

Conventional treatment for BP has long included systemic corticosteroids and immunosuppressants; this combination of drugs effectively controls inflammation but also is associated with considerable risks such as infection, hyperglycemia with worsening diabetes, hypertension, osteoporosis and fracture risk, and delirium, particularly in older patients. Recent developments in biologic therapy have supported the utilization of potentially safer alternatives. Specifically, dupilumab has demonstrated efficacy in the treatment of atopic dermatitis. Case reports and small research studies included in a recent review have suggested that dupilumab could be effective in managing BP, potentially offering a safer treatment option.¹ Importantly, dupilumab recently was approved for BP by the US Food and Drug Administration, making it the first biologic approved for treating this condition.² In this article, we discuss dupilumab as an option for clinicians to prescribe as an initial therapy for BP.

Pathophysiology of Bullous Pemphigoid and Dupilumab

Bullous pemphigoid pathophysiology is driven by 2 main components: immunologic and inflammatory processes. The immune-mediated attack consists of autoantibodies against the hemidesmosomal proteins BP180 and BP230 in the basement membrane zone, which anchor the epidermis to the dermis.¹ When these proteins are targeted, a cascade of responses is triggered, including the release of inflammatory cells, particularly eosinophils and neutrophils, into the skin. These cells release inflammatory mediators that break down the basement membrane, resulting in the separation of the epidermis from the dermis and leading to subepidermal blister formation.

The inflammation associated with BP largely is driven by a T helper 2–dominant immune response, with increased levels of cytokines such as interleukin (IL) 4 and IL-13.¹ The chronic inflammation contributes to the characteristic blisters and intense pruritus seen in patients with BP. Traditional treatments such as corticosteroids work broadly to suppress this inflammation by reducing the production of all proinflammatory cytokines; however, they lack specificity, which dampens the targeted immune response against BP and broadly suppresses the immune system, increasing the risk for infection and other adverse effects. For older patients with multiple health conditions, these adverse effects can impact quality of life and pose health risks.

Interleukin 4 and IL-13 contribute to eosinophilia by upregulating the expression of eosinophil chemoattractant cytokines that promote eosinophil migration and adhesion.¹ This is where dupilumab presents a promising alternative. Dupilumab is a monoclonal antibody that selectively targets the key cytokines implicated in BP. It binds to the IL-4 receptor alpha subunit, which IL-4 and IL-13 share, thereby inhibiting the signaling of both cytokines.¹

Dupilumab Reports and Case Series

Current evidence supporting the use of dupilumab for BP consists primarily of case series and uncontrolled clinical observations, both of which are useful to formulate but not to test hypotheses.³ One case series of 13 patients diagnosed with BP reported that 92.3% (12/13) of patients achieved disease clearance or satisfactory control, with 53.8% (7/13) achieving total lesion clearance and no adverse events observed.⁴ In a larger case series, 87.0% of 146 patients achieved disease control with an initial dose of dupilumab 600 mg followed by 300 mg every 2 weeks for 4 weeks, though the study also looked at secondary outcomes for up to 64 weeks.⁵ Both these findings are compatible with the idea that dupilumab has efficacy in BP, but they cannot be used to test hypotheses.^3,4

In a single case report of refractory BP, the combination of dupilumab and omalizumab—a monoclonal antibody that blocks the binding of IgE to mast cells, basophils, and dendritic cells—has shown efficacy, particularly when BP is unresponsive to standard therapies.⁶ The case involved a 72-year-old woman with unresponsive BP who was treated with a combination of dupilumab and omalizumab. She experienced marked improvement in pruritus and bullae accompanied by normalization of anti-BP180 autoantibody levels. This result points to the possibility that IL-4 and IL-13 blockade could influence autoantibody production. The authors attributed the reduction in pruritus to dupilumab, although the drug was administered in combination with omalizumab.⁶

Small Randomized Trial of Dupilumab

In addition to these uncontrolled clinical observations, dupilumab recently demonstrated positive results in a small randomized trial.⁷ Patients who were assigned to receive dupilumab were 5 times more likely to achieve sustained remission compared to those assigned to a placebo. All randomized patients also were treated with a standard-of-care oral corticosteroid regimen, which complicated the ability to isolate the specific effects of dupilumab.⁷ Finally, a completed totality of evidence on the prescription of dupilumab for refractory BP should include more reliable results from larger randomized trials.⁸

Final Thoughts

Dupilumab is now approved by the US Food and Drug Administration for the treatment of BP, marking an important milestone as the first targeted biologic therapy for this condition. While the totality of evidence is still evolving, the available data indicate both efficacy and a favorable safety profile when compared to traditional corticosteroids and immunosuppressants. Based on the available data, we suggest that health care providers consider dupilumab as a first-line monotherapy in appropriate patients with BP without specific contraindications, particularly as a practical and safe alternative to corticosteroids and immunosuppressive therapies in older adults with comorbidities. If the patient demonstrates clinical improvement in symptom relief, the therapy can be continued. This strategy minimizes initial exposure to more potent biologics or therapies with higher toxicity profiles. For patients without adequate disease control or with severe initial presentations requiring rapid improvement, clinicians may consider escalation to adjunctive or alternative therapies, such as rituximab, omalizumab, or a short course of systemic corticosteroids for acute management.

Emerging data suggest that dupilumab is a promising therapy for BP. We suggest that it may be a safer targeted alternative to traditional corticosteroids and immunosuppressive therapies. The ability of dupilumab to mitigate inflammation without broadly suppressing the immune system suggests that it may turn out to be an especially valuable option for older patients and those with comorbid conditions.

Acknowledgement—The authors thank Jodi Fiedler, MD (Boca Raton, FL), for her expert advice and assistance.

Social drivers of health (SDH) describe the conditions in which an individual is born, grows, lives, works, and ages—all of which collectively influence their health. Examples of SDH include employment status, literacy level, education level, housing status, food access, income level, and social cohesion. Social drivers of health are critical catalysts to attaining health equity. Effectively applying an understanding of how SDH affect the care of all patients is an essential competency for physicians practicing in the modern era of rising income inequality and housing instability and increasing racial, ethnic, language, religious, and cultural diversity in the United States; however, in dermatology residency, this skill set often is developed by the hidden curriculum (ie, the informal curriculum that is based on what patient scenarios a resident happens to face) rather than one represented by formal educational objectives.²

Adding to this challenge of limited formal curricula is that caring for minoritized, marginalized, and other populations facing specific barriers can evoke feelings of frustration, helplessness, and even anger. These feelings can test the limits of a physician’s identity as a healer, leading to burnout and self-protective attitudes such as distancing (emotionally, physically, or both) from these patients.³ This is particularly relevant given that the majority (76%-79% each year from 2007-2019) of medical student matriculants come from families with incomes in the top 2 quintiles nationwide, and fewer than 6% come from the lowest quintile earners.^4,5 These data indicate that most trainees have not experienced (and may even have a hard time imagining) the degree of economic and housing instability faced by many of their low-income patients, the care of whom disproportionately falls to large academic medical centers, which sponsor dermatology training programs.⁶ Many trainees may feel uncomfortable communicating across the broad range of racial, socioeconomic, linguistic, and cultural differences they encounter during training and in practice. Structured opportunities to provide care in a supervised supportive environment combined with didactics that emphasize practical, evidence-based strategies can build empathy, improve attitudes toward patients from diverse backgrounds, and strengthen self-efficacy in challenging scenarios.³

In the past decade, there has been a push toward integrating our understanding of SDH into formal medical training.⁷ Other specialty training programs—including psychiatry,⁸ internal medicine,⁹ pediatrics,¹⁰ and family medicine¹¹—have incorporated these elements into their curricula and competency evaluations. In dermatology, as in other specialties, making and implementing effective, patient-centered care plans requires attention to the various social and structural drivers that may influence outcomes. Dermatologists therefore should be educated about SDH during their training programs and empowered to address the ways they affect patient care.

At the University of California San Francisco (UCSF)(San Francisco, California), our dermatology trainees care for patients in several hospital systems citywide, including a tertiary academic medical center with multiple locations, a county hospital, and a Veterans Affairs medical center. Given the diversity of patient populations across our training sites—including many racially and ethnically minoritized individuals, immigrants, patients with limited English proficiency, people experiencing homelessness, and sexual and gender diverse individuals—we identified a critical opportunity to enhance our training through formal didactics and hands-on experiences that integrate SDH into existing curricula and strengthen trainees’ ability to provide high-quality care to all patients.

Implementing an SDH Curriculum

In May 2020, UCSF dermatology faculty with an interest in SDH collaborated with departmental educational leadership to develop a formal SDH curriculum centered around 8 core learning objectives for residents (eTable 1). To achieve these objectives, we organized a 3-year didactic and experiential curriculum consisting of lectures (eTable 2), grand rounds sessions, journal clubs, and community engagement opportunities. Residents also spend 7 months during their training rotating at San Francisco’s city and county hospital (Zuckerberg San Francisco General Hospital [San Francisco, California]) where all faculty are members of the core SDH curriculum development team and where residents can put into practice many of the skills learned in formal didactics to develop patient-centered care plans for low-income patients, approximately 40% of whom have limited English proficiency.

To further center the importance of SDH and health equity in our training program, we developed a Health Equity Chief leadership role for senior dermatology residents. Each year, 2 to 4 residents volunteer for and serve in this role, wherein they work with core faculty to review and improve SDH curriculum elements. They also work to enhance community engagement opportunities for residents (eg, pathway programs aimed at diversifying the dermatology workforce by introducing historically excluded local high school and college students to dermatology as a career path) and improve dermatology trainees’ awareness of the history and health needs of the specific communities we serve in San Francisco. They also are prepared to become leaders in the field of health equity and to improve the care of diverse patient populations after residency. Our faculty curriculum leaders meet quarterly with our Health Equity Chiefs to review their individual and collective goals and strategize ways to improve learner and community engagement. Departmental funds are made available to support these efforts.

Leadership at our safety-net county hospital also developed a patient navigator position to improve our ability to care for patients with the most complex medical conditions and social needs. This role is held by a medical student taking a funded gap year and incorporates aspects of social work (eg, identifying barriers to care and connecting patients with resources such as transportation), quality improvement, and clinical research.¹²

Assessing Residents’ Experience of a New SDH Curriculum

Prior to curriculum implementation, we surveyed graduating UCSF dermatology residents in June 2020 to assess their familiarity with SDH and the social and medical needs of various populations facing barriers to care, their comfort level with specific challenging clinical situations, and their desire for additional training. Responses were measured using a 5-part Likert scale, with additional options for free-text response. After initiating the SDH curriculum in July 2020, we sent the same survey each year to all senior residents immediately prior to their graduation, offering a small financial incentive ($15 cash gift card) to those who completed the survey. We obtained UCSF Institutional Review Board approval to utilize these survey data to better understand and to enhance residents’ experience of the SDH curriculum.

All 8 residents invited in 2020 completed the survey assessing curriculum efficacy (100% response rate). For the 2023 and 2024 classes, data were analyzed in aggregate (n=14), with a 50% response rate. After implementation of the SDH curriculum, there was improvement in learners’ awareness of challenges faced by every patient population, from a mean (SD) of 3.12 (0.66) to 4.52 (SD, 0.69)(P<.05). Learners were more comfortable handling hypothetical clinical scenarios requiring them to identify and address specific SDH after vs before implementation of the curriculum (mean [SD], 3.5 [1.06] before vs 4.0 [1.16] after)(P>.05), though this difference was not statistically learners’ awareness of challenges faced by every patient population, from a mean (SD) of 3.12 (0.66) to 4.52 (0.69)(P<.05). Learners were more comfortable handling hypothetical clinical scenarios requiring them to identify and address specific SDH after vs before implementation of the curriculum (mean [SD], 3.5 [1.06] before vs 4.0 [1.16] after)(P>.05), though this difference was not statistically significant. Finally, many respondents expressed appreciation that our curriculum improved their ability to care for patients in complex social circumstances. Residents suggested in the free-text responses that learning more about the historical underpinnings of health disparities, opportunities for grassroots activism, and how to provide more culturally competent care of Native American populations could improve our curriculum.

Implications for Dermatology Training

Our survey results indicate that a formal SDH curriculum can improve dermatology residents’ ability to care for populations with complex social needs. We advocate for implementing SDH curricula into dermatology training programs nationwide, as has been recommended by others.^13,14 We also propose that structural competency should eventually be a key dermatologic competency as determined by the Accreditation Council for Graduate Medical Education, in line with the American Medical Association’s recommendation that structural competency is a learned skill required to end health inequity.¹⁵ The Accreditation Council for Graduate Medical Education specialty program requirements currently are being revised; interested individuals can engage in this process by submitting this suggestion for public comment (https://www.acgme.org/programs-and-institutions/programs/review-and-comment/).

Limitations of a survey include the relatively small sample size (7-8 per year) and variable response rates. In addition, we did not survey each class of residents at the beginning and end of their training; our comparisons therefore were limited by comparing different individuals with distinct backgrounds and experiences. Furthermore, we acknowledge that the experience of developing this curriculum in San Francisco may be distinct from other communities, where access to dermatologic care may vary according to both the availability of public health insurance and the treatments covered by public insurers. In San Francisco, insurance coverage is near universal, such that residents in our training program regularly care for undocumented immigrants, persons experiencing homelessness, and other populations that might find it challenging to present to dermatology clinics in other settings nationwide.

Final Thoughts

Future directions of our curriculum include exploration of novel curriculum delivery methods (including a problem-based curriculum approach and other more experiential didactics), increased opportunities for community engagement, greater focus on advocacy with an emphasis on broader social and structural policies and their downstream effects, and focusing more specifically on the history and needs of specific low-income San Francisco neighborhoods and diverse patient populations.

Social drivers of health (SDH) describe the conditions in which an individual is born, grows, lives, works, and ages—all of which collectively influence their health. Examples of SDH include employment status, literacy level, education level, housing status, food access, income level, and social cohesion. Social drivers of health are critical catalysts to attaining health equity. Effectively applying an understanding of how SDH affect the care of all patients is an essential competency for physicians practicing in the modern era of rising income inequality and housing instability and increasing racial, ethnic, language, religious, and cultural diversity in the United States; however, in dermatology residency, this skill set often is developed by the hidden curriculum (ie, the informal curriculum that is based on what patient scenarios a resident happens to face) rather than one represented by formal educational objectives.²

Adding to this challenge of limited formal curricula is that caring for minoritized, marginalized, and other populations facing specific barriers can evoke feelings of frustration, helplessness, and even anger. These feelings can test the limits of a physician’s identity as a healer, leading to burnout and self-protective attitudes such as distancing (emotionally, physically, or both) from these patients.³ This is particularly relevant given that the majority (76%-79% each year from 2007-2019) of medical student matriculants come from families with incomes in the top 2 quintiles nationwide, and fewer than 6% come from the lowest quintile earners.^4,5 These data indicate that most trainees have not experienced (and may even have a hard time imagining) the degree of economic and housing instability faced by many of their low-income patients, the care of whom disproportionately falls to large academic medical centers, which sponsor dermatology training programs.⁶ Many trainees may feel uncomfortable communicating across the broad range of racial, socioeconomic, linguistic, and cultural differences they encounter during training and in practice. Structured opportunities to provide care in a supervised supportive environment combined with didactics that emphasize practical, evidence-based strategies can build empathy, improve attitudes toward patients from diverse backgrounds, and strengthen self-efficacy in challenging scenarios.³

In the past decade, there has been a push toward integrating our understanding of SDH into formal medical training.⁷ Other specialty training programs—including psychiatry,⁸ internal medicine,⁹ pediatrics,¹⁰ and family medicine¹¹—have incorporated these elements into their curricula and competency evaluations. In dermatology, as in other specialties, making and implementing effective, patient-centered care plans requires attention to the various social and structural drivers that may influence outcomes. Dermatologists therefore should be educated about SDH during their training programs and empowered to address the ways they affect patient care.

At the University of California San Francisco (UCSF)(San Francisco, California), our dermatology trainees care for patients in several hospital systems citywide, including a tertiary academic medical center with multiple locations, a county hospital, and a Veterans Affairs medical center. Given the diversity of patient populations across our training sites—including many racially and ethnically minoritized individuals, immigrants, patients with limited English proficiency, people experiencing homelessness, and sexual and gender diverse individuals—we identified a critical opportunity to enhance our training through formal didactics and hands-on experiences that integrate SDH into existing curricula and strengthen trainees’ ability to provide high-quality care to all patients.

Implementing an SDH Curriculum

In May 2020, UCSF dermatology faculty with an interest in SDH collaborated with departmental educational leadership to develop a formal SDH curriculum centered around 8 core learning objectives for residents (eTable 1). To achieve these objectives, we organized a 3-year didactic and experiential curriculum consisting of lectures (eTable 2), grand rounds sessions, journal clubs, and community engagement opportunities. Residents also spend 7 months during their training rotating at San Francisco’s city and county hospital (Zuckerberg San Francisco General Hospital [San Francisco, California]) where all faculty are members of the core SDH curriculum development team and where residents can put into practice many of the skills learned in formal didactics to develop patient-centered care plans for low-income patients, approximately 40% of whom have limited English proficiency.

To further center the importance of SDH and health equity in our training program, we developed a Health Equity Chief leadership role for senior dermatology residents. Each year, 2 to 4 residents volunteer for and serve in this role, wherein they work with core faculty to review and improve SDH curriculum elements. They also work to enhance community engagement opportunities for residents (eg, pathway programs aimed at diversifying the dermatology workforce by introducing historically excluded local high school and college students to dermatology as a career path) and improve dermatology trainees’ awareness of the history and health needs of the specific communities we serve in San Francisco. They also are prepared to become leaders in the field of health equity and to improve the care of diverse patient populations after residency. Our faculty curriculum leaders meet quarterly with our Health Equity Chiefs to review their individual and collective goals and strategize ways to improve learner and community engagement. Departmental funds are made available to support these efforts.

Leadership at our safety-net county hospital also developed a patient navigator position to improve our ability to care for patients with the most complex medical conditions and social needs. This role is held by a medical student taking a funded gap year and incorporates aspects of social work (eg, identifying barriers to care and connecting patients with resources such as transportation), quality improvement, and clinical research.¹²

Assessing Residents’ Experience of a New SDH Curriculum

Prior to curriculum implementation, we surveyed graduating UCSF dermatology residents in June 2020 to assess their familiarity with SDH and the social and medical needs of various populations facing barriers to care, their comfort level with specific challenging clinical situations, and their desire for additional training. Responses were measured using a 5-part Likert scale, with additional options for free-text response. After initiating the SDH curriculum in July 2020, we sent the same survey each year to all senior residents immediately prior to their graduation, offering a small financial incentive ($15 cash gift card) to those who completed the survey. We obtained UCSF Institutional Review Board approval to utilize these survey data to better understand and to enhance residents’ experience of the SDH curriculum.

All 8 residents invited in 2020 completed the survey assessing curriculum efficacy (100% response rate). For the 2023 and 2024 classes, data were analyzed in aggregate (n=14), with a 50% response rate. After implementation of the SDH curriculum, there was improvement in learners’ awareness of challenges faced by every patient population, from a mean (SD) of 3.12 (0.66) to 4.52 (SD, 0.69)(P<.05). Learners were more comfortable handling hypothetical clinical scenarios requiring them to identify and address specific SDH after vs before implementation of the curriculum (mean [SD], 3.5 [1.06] before vs 4.0 [1.16] after)(P>.05), though this difference was not statistically learners’ awareness of challenges faced by every patient population, from a mean (SD) of 3.12 (0.66) to 4.52 (0.69)(P<.05). Learners were more comfortable handling hypothetical clinical scenarios requiring them to identify and address specific SDH after vs before implementation of the curriculum (mean [SD], 3.5 [1.06] before vs 4.0 [1.16] after)(P>.05), though this difference was not statistically significant. Finally, many respondents expressed appreciation that our curriculum improved their ability to care for patients in complex social circumstances. Residents suggested in the free-text responses that learning more about the historical underpinnings of health disparities, opportunities for grassroots activism, and how to provide more culturally competent care of Native American populations could improve our curriculum.

Implications for Dermatology Training

Our survey results indicate that a formal SDH curriculum can improve dermatology residents’ ability to care for populations with complex social needs. We advocate for implementing SDH curricula into dermatology training programs nationwide, as has been recommended by others.^13,14 We also propose that structural competency should eventually be a key dermatologic competency as determined by the Accreditation Council for Graduate Medical Education, in line with the American Medical Association’s recommendation that structural competency is a learned skill required to end health inequity.¹⁵ The Accreditation Council for Graduate Medical Education specialty program requirements currently are being revised; interested individuals can engage in this process by submitting this suggestion for public comment (https://www.acgme.org/programs-and-institutions/programs/review-and-comment/).

Limitations of a survey include the relatively small sample size (7-8 per year) and variable response rates. In addition, we did not survey each class of residents at the beginning and end of their training; our comparisons therefore were limited by comparing different individuals with distinct backgrounds and experiences. Furthermore, we acknowledge that the experience of developing this curriculum in San Francisco may be distinct from other communities, where access to dermatologic care may vary according to both the availability of public health insurance and the treatments covered by public insurers. In San Francisco, insurance coverage is near universal, such that residents in our training program regularly care for undocumented immigrants, persons experiencing homelessness, and other populations that might find it challenging to present to dermatology clinics in other settings nationwide.

Final Thoughts

Future directions of our curriculum include exploration of novel curriculum delivery methods (including a problem-based curriculum approach and other more experiential didactics), increased opportunities for community engagement, greater focus on advocacy with an emphasis on broader social and structural policies and their downstream effects, and focusing more specifically on the history and needs of specific low-income San Francisco neighborhoods and diverse patient populations.

Social drivers of health (SDH) describe the conditions in which an individual is born, grows, lives, works, and ages—all of which collectively influence their health. Examples of SDH include employment status, literacy level, education level, housing status, food access, income level, and social cohesion. Social drivers of health are critical catalysts to attaining health equity. Effectively applying an understanding of how SDH affect the care of all patients is an essential competency for physicians practicing in the modern era of rising income inequality and housing instability and increasing racial, ethnic, language, religious, and cultural diversity in the United States; however, in dermatology residency, this skill set often is developed by the hidden curriculum (ie, the informal curriculum that is based on what patient scenarios a resident happens to face) rather than one represented by formal educational objectives.²

Adding to this challenge of limited formal curricula is that caring for minoritized, marginalized, and other populations facing specific barriers can evoke feelings of frustration, helplessness, and even anger. These feelings can test the limits of a physician’s identity as a healer, leading to burnout and self-protective attitudes such as distancing (emotionally, physically, or both) from these patients.³ This is particularly relevant given that the majority (76%-79% each year from 2007-2019) of medical student matriculants come from families with incomes in the top 2 quintiles nationwide, and fewer than 6% come from the lowest quintile earners.^4,5 These data indicate that most trainees have not experienced (and may even have a hard time imagining) the degree of economic and housing instability faced by many of their low-income patients, the care of whom disproportionately falls to large academic medical centers, which sponsor dermatology training programs.⁶ Many trainees may feel uncomfortable communicating across the broad range of racial, socioeconomic, linguistic, and cultural differences they encounter during training and in practice. Structured opportunities to provide care in a supervised supportive environment combined with didactics that emphasize practical, evidence-based strategies can build empathy, improve attitudes toward patients from diverse backgrounds, and strengthen self-efficacy in challenging scenarios.³

In the past decade, there has been a push toward integrating our understanding of SDH into formal medical training.⁷ Other specialty training programs—including psychiatry,⁸ internal medicine,⁹ pediatrics,¹⁰ and family medicine¹¹—have incorporated these elements into their curricula and competency evaluations. In dermatology, as in other specialties, making and implementing effective, patient-centered care plans requires attention to the various social and structural drivers that may influence outcomes. Dermatologists therefore should be educated about SDH during their training programs and empowered to address the ways they affect patient care.

At the University of California San Francisco (UCSF)(San Francisco, California), our dermatology trainees care for patients in several hospital systems citywide, including a tertiary academic medical center with multiple locations, a county hospital, and a Veterans Affairs medical center. Given the diversity of patient populations across our training sites—including many racially and ethnically minoritized individuals, immigrants, patients with limited English proficiency, people experiencing homelessness, and sexual and gender diverse individuals—we identified a critical opportunity to enhance our training through formal didactics and hands-on experiences that integrate SDH into existing curricula and strengthen trainees’ ability to provide high-quality care to all patients.

Implementing an SDH Curriculum

In May 2020, UCSF dermatology faculty with an interest in SDH collaborated with departmental educational leadership to develop a formal SDH curriculum centered around 8 core learning objectives for residents (eTable 1). To achieve these objectives, we organized a 3-year didactic and experiential curriculum consisting of lectures (eTable 2), grand rounds sessions, journal clubs, and community engagement opportunities. Residents also spend 7 months during their training rotating at San Francisco’s city and county hospital (Zuckerberg San Francisco General Hospital [San Francisco, California]) where all faculty are members of the core SDH curriculum development team and where residents can put into practice many of the skills learned in formal didactics to develop patient-centered care plans for low-income patients, approximately 40% of whom have limited English proficiency.

To further center the importance of SDH and health equity in our training program, we developed a Health Equity Chief leadership role for senior dermatology residents. Each year, 2 to 4 residents volunteer for and serve in this role, wherein they work with core faculty to review and improve SDH curriculum elements. They also work to enhance community engagement opportunities for residents (eg, pathway programs aimed at diversifying the dermatology workforce by introducing historically excluded local high school and college students to dermatology as a career path) and improve dermatology trainees’ awareness of the history and health needs of the specific communities we serve in San Francisco. They also are prepared to become leaders in the field of health equity and to improve the care of diverse patient populations after residency. Our faculty curriculum leaders meet quarterly with our Health Equity Chiefs to review their individual and collective goals and strategize ways to improve learner and community engagement. Departmental funds are made available to support these efforts.

Leadership at our safety-net county hospital also developed a patient navigator position to improve our ability to care for patients with the most complex medical conditions and social needs. This role is held by a medical student taking a funded gap year and incorporates aspects of social work (eg, identifying barriers to care and connecting patients with resources such as transportation), quality improvement, and clinical research.¹²

Assessing Residents’ Experience of a New SDH Curriculum

Prior to curriculum implementation, we surveyed graduating UCSF dermatology residents in June 2020 to assess their familiarity with SDH and the social and medical needs of various populations facing barriers to care, their comfort level with specific challenging clinical situations, and their desire for additional training. Responses were measured using a 5-part Likert scale, with additional options for free-text response. After initiating the SDH curriculum in July 2020, we sent the same survey each year to all senior residents immediately prior to their graduation, offering a small financial incentive ($15 cash gift card) to those who completed the survey. We obtained UCSF Institutional Review Board approval to utilize these survey data to better understand and to enhance residents’ experience of the SDH curriculum.

All 8 residents invited in 2020 completed the survey assessing curriculum efficacy (100% response rate). For the 2023 and 2024 classes, data were analyzed in aggregate (n=14), with a 50% response rate. After implementation of the SDH curriculum, there was improvement in learners’ awareness of challenges faced by every patient population, from a mean (SD) of 3.12 (0.66) to 4.52 (SD, 0.69)(P<.05). Learners were more comfortable handling hypothetical clinical scenarios requiring them to identify and address specific SDH after vs before implementation of the curriculum (mean [SD], 3.5 [1.06] before vs 4.0 [1.16] after)(P>.05), though this difference was not statistically learners’ awareness of challenges faced by every patient population, from a mean (SD) of 3.12 (0.66) to 4.52 (0.69)(P<.05). Learners were more comfortable handling hypothetical clinical scenarios requiring them to identify and address specific SDH after vs before implementation of the curriculum (mean [SD], 3.5 [1.06] before vs 4.0 [1.16] after)(P>.05), though this difference was not statistically significant. Finally, many respondents expressed appreciation that our curriculum improved their ability to care for patients in complex social circumstances. Residents suggested in the free-text responses that learning more about the historical underpinnings of health disparities, opportunities for grassroots activism, and how to provide more culturally competent care of Native American populations could improve our curriculum.

Implications for Dermatology Training

Our survey results indicate that a formal SDH curriculum can improve dermatology residents’ ability to care for populations with complex social needs. We advocate for implementing SDH curricula into dermatology training programs nationwide, as has been recommended by others.^13,14 We also propose that structural competency should eventually be a key dermatologic competency as determined by the Accreditation Council for Graduate Medical Education, in line with the American Medical Association’s recommendation that structural competency is a learned skill required to end health inequity.¹⁵ The Accreditation Council for Graduate Medical Education specialty program requirements currently are being revised; interested individuals can engage in this process by submitting this suggestion for public comment (https://www.acgme.org/programs-and-institutions/programs/review-and-comment/).

Limitations of a survey include the relatively small sample size (7-8 per year) and variable response rates. In addition, we did not survey each class of residents at the beginning and end of their training; our comparisons therefore were limited by comparing different individuals with distinct backgrounds and experiences. Furthermore, we acknowledge that the experience of developing this curriculum in San Francisco may be distinct from other communities, where access to dermatologic care may vary according to both the availability of public health insurance and the treatments covered by public insurers. In San Francisco, insurance coverage is near universal, such that residents in our training program regularly care for undocumented immigrants, persons experiencing homelessness, and other populations that might find it challenging to present to dermatology clinics in other settings nationwide.

Final Thoughts

Future directions of our curriculum include exploration of novel curriculum delivery methods (including a problem-based curriculum approach and other more experiential didactics), increased opportunities for community engagement, greater focus on advocacy with an emphasis on broader social and structural policies and their downstream effects, and focusing more specifically on the history and needs of specific low-income San Francisco neighborhoods and diverse patient populations.

Choosing an electronic medical record (EMR) is one of the most important clinical and financial decisions a dermatology practice will make. An effective system can help streamline workflows, support high-quality patient care, and protect revenue, while the wrong choice can slow clinicians down and add to the administrative burden.

Dermatology workflows involve unique documentation, imaging, and billing needs that are not always well served by generic EMR platforms. To help guide the selection of an EMR, the following framework outlines key features and practice considerations specific to dermatology practices.

Dermatology-Specific Charting

While many general EMRs offer customization, dermatology practices benefit greatly from ready-built, specialty-specific documentation tools. Key elements to evaluate include the following:

• Preconfigured dermatology templates for common conditions and procedures (eg, acne, psoriasis, melanoma, biopsies, cosmetic treatments)
• Smart-phrase libraries tailored to dermatologic language and examinations
• Ability to create, modify, and share custom templates across providers

Why It Matters—Efficient charting reduces documentation time, improves consistency, and supports accurate coding.

Clinical Photography and Imaging

Dermatology is a highly visual specialty, making clinical photography and image management essential. Important capabilities of an EMR include the following:

• Easy capture, annotation, and longitudinal tracking of clinical images
• Seamless embedding of photographs directly into the patient chart
• Side-by-side comparison of current and prior images
• Secure image storage and camera integration
• Body-mapping tools to mark and track lesion locations visually

Why It Matters—A high-quality image workflow supports diagnosis, treatment planning, patient education, and medicolegal documentation.

Coding, Billing, and Revenue Cycle Support

For insurance-based practices, robust billing and revenue cycle management (RCM) tools are critical. For direct-care models, some of these items may be prioritized lower. Key features to compare include the following:

• Support for International Classification of Diseases, 10th Revision, Clinical Modification; Current Procedural Terminology; and dermatology-specific code sets
• Automated coding suggestions tied to clinical documentation
• Reviewing claims for errors and inconsistencies prior to submitting to payers’ insurance eligibility verification
• Electronic Remittance Advice/Explanation of Benefits posting and denial management workflows
• Support for cosmetic and self-pay billing
• Ability to generate superbills (itemized receipts for medical services that include International Classification of Diseases Tenth Revision and Current Procedural Terminology codes; patients can submit these directly to their insurance company for reimbursement) for direct-pay practices

Why It Matters—Strong RCM functionality protects revenue, reduces denials, and minimizes staff workload.

Scheduling and Practice Integration

The most effective EMRs tightly integrate clinical charting with daily practice operations. Features to evaluate include the following:

• Integrated scheduling with color-coded calendars
• Appointment-type templates and block scheduling
• Automated patient reminders via text or email
• Support for multiprovider and multilocation practices
• Integration with outside pathology or lab services

Why It Matters—Clear and templated scheduling and practice integration help practices run more smoothly by reducing administrative workload and errors and coordinating communication between providers and even ancillary services.

Telehealth and Patient Communication Tools

Patient communication and virtual care are increasingly important in dermatology. When evaluating EMRs, compare the following:

• Built-in telehealth functionality vs third-party integrations
• Automated appointment reminders
• Patient portal features (forms, messaging, results)
• Online booking capabilities

Why It Matters—Integrated telehealth and patient communication tools improve access to care, enhance patient engagement, and streamline scheduling, messaging, and virtual visits within dermatology workflows.

Reporting and Analytics

Reporting capabilities support clinical quality, compliance, and business decision-making. Key reporting areas include the following:

• Clinical reports (outcomes, lesion tracking, disease management)
• Financial reports (revenue per provider, payer mix, visit types)
• Customizable or exportable reporting tools

Why It Matters—Robust reporting and analytics help dermatology practices track clinical outcomes, monitor financial performance, and make data-driven decisions to improve both patient care and practice management.

Support, Training, and User Community

The user experience after implementation of the EMR is just as important as the software itself. Evaluate the following after the EMR is implemented:

• Initial training and onboarding resources
• Availability of dermatology-specific support teams
• Ongoing education, help centers, or user communities
• Access to dedicated implementation or success managers

Why It Matters—Strong training and support resources help ensure a smoother EMR implementation, faster staff adoption, and ongoing optimization of the system for dermatology workflows.

Cost and Overall Value

Finally, look beyond the sticker price. The total cost of ownership includes far more than monthly fees. Compare the following:

• Upfront costs (implementation, data migration, training)
• Subscription pricing (per provider or per user)
• Billing or RCM fees (including percentages of collections if applicable) and payment processing fees
• Costs for add-on modules (telehealth, imaging, analytics)
• Contract length and termination terms

Why It Matters—Understanding the full cost of ownership helps dermatology practices choose an EMR that fits their budget long-term while avoiding unexpected fees and contractual limitations.

Final Thoughts

There is no single “best” EMR for every dermatology practice. The right choice depends on your practice model, payer mix, clinical focus, and growth plans. By evaluating EMRs through a dermatology-specific lens and asking the right questions, you can choose a system that supports both excellent patient care and long-term practice success.

Choosing an electronic medical record (EMR) is one of the most important clinical and financial decisions a dermatology practice will make. An effective system can help streamline workflows, support high-quality patient care, and protect revenue, while the wrong choice can slow clinicians down and add to the administrative burden.

Dermatology workflows involve unique documentation, imaging, and billing needs that are not always well served by generic EMR platforms. To help guide the selection of an EMR, the following framework outlines key features and practice considerations specific to dermatology practices.

Dermatology-Specific Charting

While many general EMRs offer customization, dermatology practices benefit greatly from ready-built, specialty-specific documentation tools. Key elements to evaluate include the following:

• Preconfigured dermatology templates for common conditions and procedures (eg, acne, psoriasis, melanoma, biopsies, cosmetic treatments)
• Smart-phrase libraries tailored to dermatologic language and examinations
• Ability to create, modify, and share custom templates across providers

Why It Matters—Efficient charting reduces documentation time, improves consistency, and supports accurate coding.

Clinical Photography and Imaging

Dermatology is a highly visual specialty, making clinical photography and image management essential. Important capabilities of an EMR include the following:

• Easy capture, annotation, and longitudinal tracking of clinical images
• Seamless embedding of photographs directly into the patient chart
• Side-by-side comparison of current and prior images
• Secure image storage and camera integration
• Body-mapping tools to mark and track lesion locations visually

Why It Matters—A high-quality image workflow supports diagnosis, treatment planning, patient education, and medicolegal documentation.

Coding, Billing, and Revenue Cycle Support

For insurance-based practices, robust billing and revenue cycle management (RCM) tools are critical. For direct-care models, some of these items may be prioritized lower. Key features to compare include the following:

• Support for International Classification of Diseases, 10th Revision, Clinical Modification; Current Procedural Terminology; and dermatology-specific code sets
• Automated coding suggestions tied to clinical documentation
• Reviewing claims for errors and inconsistencies prior to submitting to payers’ insurance eligibility verification
• Electronic Remittance Advice/Explanation of Benefits posting and denial management workflows
• Support for cosmetic and self-pay billing
• Ability to generate superbills (itemized receipts for medical services that include International Classification of Diseases Tenth Revision and Current Procedural Terminology codes; patients can submit these directly to their insurance company for reimbursement) for direct-pay practices

Why It Matters—Strong RCM functionality protects revenue, reduces denials, and minimizes staff workload.

Scheduling and Practice Integration

The most effective EMRs tightly integrate clinical charting with daily practice operations. Features to evaluate include the following:

• Integrated scheduling with color-coded calendars
• Appointment-type templates and block scheduling
• Automated patient reminders via text or email
• Support for multiprovider and multilocation practices
• Integration with outside pathology or lab services

Why It Matters—Clear and templated scheduling and practice integration help practices run more smoothly by reducing administrative workload and errors and coordinating communication between providers and even ancillary services.

Telehealth and Patient Communication Tools

Patient communication and virtual care are increasingly important in dermatology. When evaluating EMRs, compare the following:

• Built-in telehealth functionality vs third-party integrations
• Automated appointment reminders
• Patient portal features (forms, messaging, results)
• Online booking capabilities

Why It Matters—Integrated telehealth and patient communication tools improve access to care, enhance patient engagement, and streamline scheduling, messaging, and virtual visits within dermatology workflows.

Reporting and Analytics

Reporting capabilities support clinical quality, compliance, and business decision-making. Key reporting areas include the following:

• Clinical reports (outcomes, lesion tracking, disease management)
• Financial reports (revenue per provider, payer mix, visit types)
• Customizable or exportable reporting tools

Why It Matters—Robust reporting and analytics help dermatology practices track clinical outcomes, monitor financial performance, and make data-driven decisions to improve both patient care and practice management.

Support, Training, and User Community

The user experience after implementation of the EMR is just as important as the software itself. Evaluate the following after the EMR is implemented:

• Initial training and onboarding resources
• Availability of dermatology-specific support teams
• Ongoing education, help centers, or user communities
• Access to dedicated implementation or success managers

Why It Matters—Strong training and support resources help ensure a smoother EMR implementation, faster staff adoption, and ongoing optimization of the system for dermatology workflows.

Cost and Overall Value

Finally, look beyond the sticker price. The total cost of ownership includes far more than monthly fees. Compare the following:

• Upfront costs (implementation, data migration, training)
• Subscription pricing (per provider or per user)
• Billing or RCM fees (including percentages of collections if applicable) and payment processing fees
• Costs for add-on modules (telehealth, imaging, analytics)
• Contract length and termination terms

Why It Matters—Understanding the full cost of ownership helps dermatology practices choose an EMR that fits their budget long-term while avoiding unexpected fees and contractual limitations.

Final Thoughts

There is no single “best” EMR for every dermatology practice. The right choice depends on your practice model, payer mix, clinical focus, and growth plans. By evaluating EMRs through a dermatology-specific lens and asking the right questions, you can choose a system that supports both excellent patient care and long-term practice success.

Choosing an electronic medical record (EMR) is one of the most important clinical and financial decisions a dermatology practice will make. An effective system can help streamline workflows, support high-quality patient care, and protect revenue, while the wrong choice can slow clinicians down and add to the administrative burden.

Dermatology workflows involve unique documentation, imaging, and billing needs that are not always well served by generic EMR platforms. To help guide the selection of an EMR, the following framework outlines key features and practice considerations specific to dermatology practices.

Dermatology-Specific Charting

While many general EMRs offer customization, dermatology practices benefit greatly from ready-built, specialty-specific documentation tools. Key elements to evaluate include the following:

• Preconfigured dermatology templates for common conditions and procedures (eg, acne, psoriasis, melanoma, biopsies, cosmetic treatments)
• Smart-phrase libraries tailored to dermatologic language and examinations
• Ability to create, modify, and share custom templates across providers

Why It Matters—Efficient charting reduces documentation time, improves consistency, and supports accurate coding.

Clinical Photography and Imaging

Dermatology is a highly visual specialty, making clinical photography and image management essential. Important capabilities of an EMR include the following:

• Easy capture, annotation, and longitudinal tracking of clinical images
• Seamless embedding of photographs directly into the patient chart
• Side-by-side comparison of current and prior images
• Secure image storage and camera integration
• Body-mapping tools to mark and track lesion locations visually

Why It Matters—A high-quality image workflow supports diagnosis, treatment planning, patient education, and medicolegal documentation.

Coding, Billing, and Revenue Cycle Support

For insurance-based practices, robust billing and revenue cycle management (RCM) tools are critical. For direct-care models, some of these items may be prioritized lower. Key features to compare include the following:

• Support for International Classification of Diseases, 10th Revision, Clinical Modification; Current Procedural Terminology; and dermatology-specific code sets
• Automated coding suggestions tied to clinical documentation
• Reviewing claims for errors and inconsistencies prior to submitting to payers’ insurance eligibility verification
• Electronic Remittance Advice/Explanation of Benefits posting and denial management workflows
• Support for cosmetic and self-pay billing
• Ability to generate superbills (itemized receipts for medical services that include International Classification of Diseases Tenth Revision and Current Procedural Terminology codes; patients can submit these directly to their insurance company for reimbursement) for direct-pay practices

Why It Matters—Strong RCM functionality protects revenue, reduces denials, and minimizes staff workload.

Scheduling and Practice Integration

The most effective EMRs tightly integrate clinical charting with daily practice operations. Features to evaluate include the following:

• Integrated scheduling with color-coded calendars
• Appointment-type templates and block scheduling
• Automated patient reminders via text or email
• Support for multiprovider and multilocation practices
• Integration with outside pathology or lab services

Why It Matters—Clear and templated scheduling and practice integration help practices run more smoothly by reducing administrative workload and errors and coordinating communication between providers and even ancillary services.

Telehealth and Patient Communication Tools

Patient communication and virtual care are increasingly important in dermatology. When evaluating EMRs, compare the following:

• Built-in telehealth functionality vs third-party integrations
• Automated appointment reminders
• Patient portal features (forms, messaging, results)
• Online booking capabilities

Why It Matters—Integrated telehealth and patient communication tools improve access to care, enhance patient engagement, and streamline scheduling, messaging, and virtual visits within dermatology workflows.

Reporting and Analytics

Reporting capabilities support clinical quality, compliance, and business decision-making. Key reporting areas include the following:

• Clinical reports (outcomes, lesion tracking, disease management)
• Financial reports (revenue per provider, payer mix, visit types)
• Customizable or exportable reporting tools

Why It Matters—Robust reporting and analytics help dermatology practices track clinical outcomes, monitor financial performance, and make data-driven decisions to improve both patient care and practice management.

Support, Training, and User Community

The user experience after implementation of the EMR is just as important as the software itself. Evaluate the following after the EMR is implemented:

• Initial training and onboarding resources
• Availability of dermatology-specific support teams
• Ongoing education, help centers, or user communities
• Access to dedicated implementation or success managers

Why It Matters—Strong training and support resources help ensure a smoother EMR implementation, faster staff adoption, and ongoing optimization of the system for dermatology workflows.

Cost and Overall Value

Finally, look beyond the sticker price. The total cost of ownership includes far more than monthly fees. Compare the following:

• Upfront costs (implementation, data migration, training)
• Subscription pricing (per provider or per user)
• Billing or RCM fees (including percentages of collections if applicable) and payment processing fees
• Costs for add-on modules (telehealth, imaging, analytics)
• Contract length and termination terms

Why It Matters—Understanding the full cost of ownership helps dermatology practices choose an EMR that fits their budget long-term while avoiding unexpected fees and contractual limitations.

Final Thoughts

There is no single “best” EMR for every dermatology practice. The right choice depends on your practice model, payer mix, clinical focus, and growth plans. By evaluating EMRs through a dermatology-specific lens and asking the right questions, you can choose a system that supports both excellent patient care and long-term practice success.

Melasma is a chronic hyperpigmentation disorder with a high recurrence rate. Advances in pathogenesis, diagnosis, and treatment have shifted dermatologic approaches for both initial management and long-term care. These advances highlight the need to move beyond conventional paradigms for melasma to adopt a more comprehensive and holistic approach to evaluation and management.

Diagnosis: Beyond the Wood Lamp

Diagnosis of melasma is primarily clinical, based on visual examination, with tools such as a Wood lamp (320-400 nm) aiding in classification as epidermal, dermal, or mixed types.¹ Dermoscopy is another useful tool that commonly demonstrates a brown reticular pseudonetwork, vascular patterns, and brown clods.² Reflectance confocal microscopy allows detailed assessment of pigment distribution across skin layers and may serve as a useful diagnostic adjunct.³ Two-photon excitation microscopy also has shown concordance with reflectance confocal microscopy in identifying key pathologic features of melasma and allows quantitative assessment of pigment burden.^4,5 Biopsy remains warranted in cases when the diagnosis is unclear.^6,7 These advanced tools provide additional options for noninvasive imaging of melasma, which may be useful during both diagnosis and treatment.

Pathogenesis: Beyond the Melanocyte

Recent insights into pathogenesis have shifted the view of melasma from a purely melanocyte-driven disorder to one involving complex epidermal-dermal interactions influenced by chronic UV and visible light exposure and sustained cutaneous inflammation. Evidence suggests involvement of additional cell types and structural components, including epidermal barrier dysfunction, basement membrane alterations, senescent fibroblasts, mast cell activity, vascular remodeling, and dermal solar elastosis. Senescent fibroblasts secrete melanogenic and angiogenic mediators (including stem cell factor, vascular endothelial growth factor, endothelin 1, and matrix metalloproteinases) while mast cell degranulation releases histamine, tryptase, and other proteases that drive melanocyte activation, extracellular matrix degradation, and persistent hyperpigmentation.⁸ New research highlights the importance of epidermal-dermal communication in melasma disease activity.^8,9 Exposure to UV and visible light leads to keratinocyte injury and fibroblast dysfunction, promoting the release of inflammatory and melanogenic mediators that stimulate melanocytes and weaken the basement membrane.⁸ Mast cell activation and vascular signaling also have been implicated, reinforcing the contribution of inflammation and dermal remodeling to ongoing pigmentation.⁹ This broader understanding helps explain the difficulty of sustaining long-term remission.^8,9 The multifaceted and evolving understanding of melasma’s complex pathogenesis highlights areas for future therapeutic targets beyond melanin, which may help lead to greater clearance and remission periods.

Treatment: Beyond Hydroquinone

Melasma treatment has shifted toward a longitudinal approach reflecting its chronic relapsing nature. Effective management should include combination therapy of broad-spectrum photoprotection, topical therapies, systemic therapies (when appropriate), and adjunctive procedural modalities, while emphasizing the importance of maintenance therapy and relapse prevention.^10,11 Growing evidence demonstrates that UV and visible light contribute to melanogenesis and prolonged pigmentation, particularly in individuals with skin of color.^12,13 Visible light, particularly within the high-energy blue wavelength spectrum (400-500 nm), induces reactive oxygen species and stimulates melanogenesis, resulting in persistent hyperpigmentation and exacerbation of melasma in darker skin types.¹³ Iron oxide, a mineral-based physical filter commonly used in tinted mineral sunscreens, enhances protection from visible light, thus improving melasma outcomes.^12,13 In a randomized double-blind placebo-controlled trial, oral polypodium leucotomos extract, an antioxidant with photoprotective effects, improved Melasma Area and Severity Index (MASI)/modified MASI (mMASI) scores and melasma-rated quality of life measures when used as an adjunct to sunscreen with or without topical hydroquinone.¹⁴

Topical therapy serves as the mainstay of melasma treatment. Hydroquinone- and retinoid-based regimens including triple-combination therapy remain an effective gold standard for active disease; however, there still are concerns about irritant dermatitis with both as well as ochronosis with long-term use of hydroquinone.¹⁵ Recent studies highlight the efficacy of nonhydroquinone topical therapies such as azelaic acid, tranexamic acid (TXA), thiamidol, cysteamine, metformin, malassezin, ­2-mercaptonicotinoyl glycine, niacinamide, kojic acid, ascorbic acid, and botanical-derived compounds, many of which demonstrate reductions in disease severity and more favorable tolerability profiles.^16-19 Combinations of these ingredients can allow for addressing the various pathogenic factors of melasma beyond pigmentation, including vascularity, inflammation, and solar damage.

Systemic therapy, particularly oral TXA, has emerged as an option for patients with moderate to severe or refractory melasma. Clinical trials and observational studies demonstrate improvement with oral TXA; however, relapse after discontinuation is common, emphasizing the importance of careful patient selection, established treatment duration, and concurrent maintenance therapy.^16,20 Although it is well tolerated, adverse effects include gastrointestinal discomfort, menstrual irregularities, and headache. Additionally, prescreening for contraindications and clotting risk factors is needed to avoid thromboembolic events.²¹

Procedural interventions are best used as adjunctive therapies rather than primary treatment. Superficial and medium peels can be used depending on baseline skin type.²² Platelet-rich plasma is a promising adjunctive therapy for melasma, demonstrating reductions in MASI scores following intradermal or microneedling-assisted delivery, likely mediated through growth factor–driven inhibition of melanogenesis and modulation of tyrosinase activity. Platelet-rich plasma promotes dermal remodeling through angiogenesis, collagen synthesis, and extracellular matrix production improving skin texture and pigmentation.²³ Botulinum toxin A may improve pigmentation by modulating melanogenesis as well as inflammatory and vascular pathways.²⁴

Radiofrequency microneedling provides a dermal-targeting therapeutic approach, with some evidence showing that monthly treatments can help maintain improvements achieved with conventional therapy by modulating photoaged dermal structures impacted by melanogenic signaling.²⁵ Histopathologic correlation studies suggest that microneedling used alone or as a delivery platform alongside topical agents may be beneficial in dermal-predominant disease, while laser-based therapies should be reserved for recalcitrant cases due to the risk for postinflammatory hyperpigmentation and melasma recurrence, particularly in those with darker skin types.²⁶ Lasers such as Q-switched 1064-nm Nd:YAG as well as nonablative lasers used in conservative settings are options for melasma treatment, including in patients with skin of color.^26,27 Laser toning with serial low-fluence (<3 J/cm²), large-spot 1064-nm Nd:YAG has been used to reduce inflammation and risk for postinflammatory hyperpigmentation.²⁸ Additionally, randomized split-face data demonstrate that picosecond 1064-nm devices achieve comparable reductions in mMASI scores to traditional nanosecond devices, and combination strategies incorporating intense pulsed light (IPL) have shown greater MASI improvement compared with IPL alone.^28,29 However, IPL generally is limited to lighter skin phototypes due to the risk for postinflammatory hyperpigmentation in darker skin.³⁰

Lastly, long-term management requires patient education on the importance of year-round maintenance therapy, consistency, and compliance. Reinforcing adherence to photoprotection, supporting barrier repair, and setting expectations regarding prognosis are essential components to optimizing melasma treatment outcomes.¹²

Future Insights: Beyond the Current State of Melasma Research and Treatment

Future advances in melasma management likely will focus on improving disease assessment and long-term treatment durability. Tools such as the MASI and mMASI are widely used but are limited by interobserver variability and reduced sensitivity in darker skin types, highlighting the need to incorporate objective measures such as colorimetry.^10,26 There also is a need for studies that relate clinical improvement to underlying pathology. Histopathologic correlation remains limited across most therapeutic trials, and more studies should assess long-term outcomes and quality-of-life measures given the relapsing nature of melasma.²⁶

Future interventions will continue to move past the treatment of pigment alone. Increasing recognition of vascular, inflammatory, and barrier-related contributions to melasma, as well as targeting of other cell types affected by melasma, will be important considerations in future treatment innovations.^8,11 In summary, improved inclusion of patients with skin of color in clinical trials, expansion of clinical outcomes measures and objective parameters of disease evaluation, novel approaches to treatment and relapse prevention, and greater attention to patient adherence and education will be essential to achieving advancements in melasma care.¹²

Melasma is a chronic hyperpigmentation disorder with a high recurrence rate. Advances in pathogenesis, diagnosis, and treatment have shifted dermatologic approaches for both initial management and long-term care. These advances highlight the need to move beyond conventional paradigms for melasma to adopt a more comprehensive and holistic approach to evaluation and management.

Diagnosis: Beyond the Wood Lamp

Diagnosis of melasma is primarily clinical, based on visual examination, with tools such as a Wood lamp (320-400 nm) aiding in classification as epidermal, dermal, or mixed types.¹ Dermoscopy is another useful tool that commonly demonstrates a brown reticular pseudonetwork, vascular patterns, and brown clods.² Reflectance confocal microscopy allows detailed assessment of pigment distribution across skin layers and may serve as a useful diagnostic adjunct.³ Two-photon excitation microscopy also has shown concordance with reflectance confocal microscopy in identifying key pathologic features of melasma and allows quantitative assessment of pigment burden.^4,5 Biopsy remains warranted in cases when the diagnosis is unclear.^6,7 These advanced tools provide additional options for noninvasive imaging of melasma, which may be useful during both diagnosis and treatment.

Pathogenesis: Beyond the Melanocyte

Recent insights into pathogenesis have shifted the view of melasma from a purely melanocyte-driven disorder to one involving complex epidermal-dermal interactions influenced by chronic UV and visible light exposure and sustained cutaneous inflammation. Evidence suggests involvement of additional cell types and structural components, including epidermal barrier dysfunction, basement membrane alterations, senescent fibroblasts, mast cell activity, vascular remodeling, and dermal solar elastosis. Senescent fibroblasts secrete melanogenic and angiogenic mediators (including stem cell factor, vascular endothelial growth factor, endothelin 1, and matrix metalloproteinases) while mast cell degranulation releases histamine, tryptase, and other proteases that drive melanocyte activation, extracellular matrix degradation, and persistent hyperpigmentation.⁸ New research highlights the importance of epidermal-dermal communication in melasma disease activity.^8,9 Exposure to UV and visible light leads to keratinocyte injury and fibroblast dysfunction, promoting the release of inflammatory and melanogenic mediators that stimulate melanocytes and weaken the basement membrane.⁸ Mast cell activation and vascular signaling also have been implicated, reinforcing the contribution of inflammation and dermal remodeling to ongoing pigmentation.⁹ This broader understanding helps explain the difficulty of sustaining long-term remission.^8,9 The multifaceted and evolving understanding of melasma’s complex pathogenesis highlights areas for future therapeutic targets beyond melanin, which may help lead to greater clearance and remission periods.

Treatment: Beyond Hydroquinone

Melasma treatment has shifted toward a longitudinal approach reflecting its chronic relapsing nature. Effective management should include combination therapy of broad-spectrum photoprotection, topical therapies, systemic therapies (when appropriate), and adjunctive procedural modalities, while emphasizing the importance of maintenance therapy and relapse prevention.^10,11 Growing evidence demonstrates that UV and visible light contribute to melanogenesis and prolonged pigmentation, particularly in individuals with skin of color.^12,13 Visible light, particularly within the high-energy blue wavelength spectrum (400-500 nm), induces reactive oxygen species and stimulates melanogenesis, resulting in persistent hyperpigmentation and exacerbation of melasma in darker skin types.¹³ Iron oxide, a mineral-based physical filter commonly used in tinted mineral sunscreens, enhances protection from visible light, thus improving melasma outcomes.^12,13 In a randomized double-blind placebo-controlled trial, oral polypodium leucotomos extract, an antioxidant with photoprotective effects, improved Melasma Area and Severity Index (MASI)/modified MASI (mMASI) scores and melasma-rated quality of life measures when used as an adjunct to sunscreen with or without topical hydroquinone.¹⁴

Topical therapy serves as the mainstay of melasma treatment. Hydroquinone- and retinoid-based regimens including triple-combination therapy remain an effective gold standard for active disease; however, there still are concerns about irritant dermatitis with both as well as ochronosis with long-term use of hydroquinone.¹⁵ Recent studies highlight the efficacy of nonhydroquinone topical therapies such as azelaic acid, tranexamic acid (TXA), thiamidol, cysteamine, metformin, malassezin, ­2-mercaptonicotinoyl glycine, niacinamide, kojic acid, ascorbic acid, and botanical-derived compounds, many of which demonstrate reductions in disease severity and more favorable tolerability profiles.^16-19 Combinations of these ingredients can allow for addressing the various pathogenic factors of melasma beyond pigmentation, including vascularity, inflammation, and solar damage.

Systemic therapy, particularly oral TXA, has emerged as an option for patients with moderate to severe or refractory melasma. Clinical trials and observational studies demonstrate improvement with oral TXA; however, relapse after discontinuation is common, emphasizing the importance of careful patient selection, established treatment duration, and concurrent maintenance therapy.^16,20 Although it is well tolerated, adverse effects include gastrointestinal discomfort, menstrual irregularities, and headache. Additionally, prescreening for contraindications and clotting risk factors is needed to avoid thromboembolic events.²¹

Procedural interventions are best used as adjunctive therapies rather than primary treatment. Superficial and medium peels can be used depending on baseline skin type.²² Platelet-rich plasma is a promising adjunctive therapy for melasma, demonstrating reductions in MASI scores following intradermal or microneedling-assisted delivery, likely mediated through growth factor–driven inhibition of melanogenesis and modulation of tyrosinase activity. Platelet-rich plasma promotes dermal remodeling through angiogenesis, collagen synthesis, and extracellular matrix production improving skin texture and pigmentation.²³ Botulinum toxin A may improve pigmentation by modulating melanogenesis as well as inflammatory and vascular pathways.²⁴

Radiofrequency microneedling provides a dermal-targeting therapeutic approach, with some evidence showing that monthly treatments can help maintain improvements achieved with conventional therapy by modulating photoaged dermal structures impacted by melanogenic signaling.²⁵ Histopathologic correlation studies suggest that microneedling used alone or as a delivery platform alongside topical agents may be beneficial in dermal-predominant disease, while laser-based therapies should be reserved for recalcitrant cases due to the risk for postinflammatory hyperpigmentation and melasma recurrence, particularly in those with darker skin types.²⁶ Lasers such as Q-switched 1064-nm Nd:YAG as well as nonablative lasers used in conservative settings are options for melasma treatment, including in patients with skin of color.^26,27 Laser toning with serial low-fluence (<3 J/cm²), large-spot 1064-nm Nd:YAG has been used to reduce inflammation and risk for postinflammatory hyperpigmentation.²⁸ Additionally, randomized split-face data demonstrate that picosecond 1064-nm devices achieve comparable reductions in mMASI scores to traditional nanosecond devices, and combination strategies incorporating intense pulsed light (IPL) have shown greater MASI improvement compared with IPL alone.^28,29 However, IPL generally is limited to lighter skin phototypes due to the risk for postinflammatory hyperpigmentation in darker skin.³⁰

Lastly, long-term management requires patient education on the importance of year-round maintenance therapy, consistency, and compliance. Reinforcing adherence to photoprotection, supporting barrier repair, and setting expectations regarding prognosis are essential components to optimizing melasma treatment outcomes.¹²

Future Insights: Beyond the Current State of Melasma Research and Treatment

Future advances in melasma management likely will focus on improving disease assessment and long-term treatment durability. Tools such as the MASI and mMASI are widely used but are limited by interobserver variability and reduced sensitivity in darker skin types, highlighting the need to incorporate objective measures such as colorimetry.^10,26 There also is a need for studies that relate clinical improvement to underlying pathology. Histopathologic correlation remains limited across most therapeutic trials, and more studies should assess long-term outcomes and quality-of-life measures given the relapsing nature of melasma.²⁶

Future interventions will continue to move past the treatment of pigment alone. Increasing recognition of vascular, inflammatory, and barrier-related contributions to melasma, as well as targeting of other cell types affected by melasma, will be important considerations in future treatment innovations.^8,11 In summary, improved inclusion of patients with skin of color in clinical trials, expansion of clinical outcomes measures and objective parameters of disease evaluation, novel approaches to treatment and relapse prevention, and greater attention to patient adherence and education will be essential to achieving advancements in melasma care.¹²

Melasma is a chronic hyperpigmentation disorder with a high recurrence rate. Advances in pathogenesis, diagnosis, and treatment have shifted dermatologic approaches for both initial management and long-term care. These advances highlight the need to move beyond conventional paradigms for melasma to adopt a more comprehensive and holistic approach to evaluation and management.

Diagnosis: Beyond the Wood Lamp

Diagnosis of melasma is primarily clinical, based on visual examination, with tools such as a Wood lamp (320-400 nm) aiding in classification as epidermal, dermal, or mixed types.¹ Dermoscopy is another useful tool that commonly demonstrates a brown reticular pseudonetwork, vascular patterns, and brown clods.² Reflectance confocal microscopy allows detailed assessment of pigment distribution across skin layers and may serve as a useful diagnostic adjunct.³ Two-photon excitation microscopy also has shown concordance with reflectance confocal microscopy in identifying key pathologic features of melasma and allows quantitative assessment of pigment burden.^4,5 Biopsy remains warranted in cases when the diagnosis is unclear.^6,7 These advanced tools provide additional options for noninvasive imaging of melasma, which may be useful during both diagnosis and treatment.

Pathogenesis: Beyond the Melanocyte

Recent insights into pathogenesis have shifted the view of melasma from a purely melanocyte-driven disorder to one involving complex epidermal-dermal interactions influenced by chronic UV and visible light exposure and sustained cutaneous inflammation. Evidence suggests involvement of additional cell types and structural components, including epidermal barrier dysfunction, basement membrane alterations, senescent fibroblasts, mast cell activity, vascular remodeling, and dermal solar elastosis. Senescent fibroblasts secrete melanogenic and angiogenic mediators (including stem cell factor, vascular endothelial growth factor, endothelin 1, and matrix metalloproteinases) while mast cell degranulation releases histamine, tryptase, and other proteases that drive melanocyte activation, extracellular matrix degradation, and persistent hyperpigmentation.⁸ New research highlights the importance of epidermal-dermal communication in melasma disease activity.^8,9 Exposure to UV and visible light leads to keratinocyte injury and fibroblast dysfunction, promoting the release of inflammatory and melanogenic mediators that stimulate melanocytes and weaken the basement membrane.⁸ Mast cell activation and vascular signaling also have been implicated, reinforcing the contribution of inflammation and dermal remodeling to ongoing pigmentation.⁹ This broader understanding helps explain the difficulty of sustaining long-term remission.^8,9 The multifaceted and evolving understanding of melasma’s complex pathogenesis highlights areas for future therapeutic targets beyond melanin, which may help lead to greater clearance and remission periods.

Treatment: Beyond Hydroquinone

Melasma treatment has shifted toward a longitudinal approach reflecting its chronic relapsing nature. Effective management should include combination therapy of broad-spectrum photoprotection, topical therapies, systemic therapies (when appropriate), and adjunctive procedural modalities, while emphasizing the importance of maintenance therapy and relapse prevention.^10,11 Growing evidence demonstrates that UV and visible light contribute to melanogenesis and prolonged pigmentation, particularly in individuals with skin of color.^12,13 Visible light, particularly within the high-energy blue wavelength spectrum (400-500 nm), induces reactive oxygen species and stimulates melanogenesis, resulting in persistent hyperpigmentation and exacerbation of melasma in darker skin types.¹³ Iron oxide, a mineral-based physical filter commonly used in tinted mineral sunscreens, enhances protection from visible light, thus improving melasma outcomes.^12,13 In a randomized double-blind placebo-controlled trial, oral polypodium leucotomos extract, an antioxidant with photoprotective effects, improved Melasma Area and Severity Index (MASI)/modified MASI (mMASI) scores and melasma-rated quality of life measures when used as an adjunct to sunscreen with or without topical hydroquinone.¹⁴

Topical therapy serves as the mainstay of melasma treatment. Hydroquinone- and retinoid-based regimens including triple-combination therapy remain an effective gold standard for active disease; however, there still are concerns about irritant dermatitis with both as well as ochronosis with long-term use of hydroquinone.¹⁵ Recent studies highlight the efficacy of nonhydroquinone topical therapies such as azelaic acid, tranexamic acid (TXA), thiamidol, cysteamine, metformin, malassezin, ­2-mercaptonicotinoyl glycine, niacinamide, kojic acid, ascorbic acid, and botanical-derived compounds, many of which demonstrate reductions in disease severity and more favorable tolerability profiles.^16-19 Combinations of these ingredients can allow for addressing the various pathogenic factors of melasma beyond pigmentation, including vascularity, inflammation, and solar damage.

Systemic therapy, particularly oral TXA, has emerged as an option for patients with moderate to severe or refractory melasma. Clinical trials and observational studies demonstrate improvement with oral TXA; however, relapse after discontinuation is common, emphasizing the importance of careful patient selection, established treatment duration, and concurrent maintenance therapy.^16,20 Although it is well tolerated, adverse effects include gastrointestinal discomfort, menstrual irregularities, and headache. Additionally, prescreening for contraindications and clotting risk factors is needed to avoid thromboembolic events.²¹

Procedural interventions are best used as adjunctive therapies rather than primary treatment. Superficial and medium peels can be used depending on baseline skin type.²² Platelet-rich plasma is a promising adjunctive therapy for melasma, demonstrating reductions in MASI scores following intradermal or microneedling-assisted delivery, likely mediated through growth factor–driven inhibition of melanogenesis and modulation of tyrosinase activity. Platelet-rich plasma promotes dermal remodeling through angiogenesis, collagen synthesis, and extracellular matrix production improving skin texture and pigmentation.²³ Botulinum toxin A may improve pigmentation by modulating melanogenesis as well as inflammatory and vascular pathways.²⁴

Radiofrequency microneedling provides a dermal-targeting therapeutic approach, with some evidence showing that monthly treatments can help maintain improvements achieved with conventional therapy by modulating photoaged dermal structures impacted by melanogenic signaling.²⁵ Histopathologic correlation studies suggest that microneedling used alone or as a delivery platform alongside topical agents may be beneficial in dermal-predominant disease, while laser-based therapies should be reserved for recalcitrant cases due to the risk for postinflammatory hyperpigmentation and melasma recurrence, particularly in those with darker skin types.²⁶ Lasers such as Q-switched 1064-nm Nd:YAG as well as nonablative lasers used in conservative settings are options for melasma treatment, including in patients with skin of color.^26,27 Laser toning with serial low-fluence (<3 J/cm²), large-spot 1064-nm Nd:YAG has been used to reduce inflammation and risk for postinflammatory hyperpigmentation.²⁸ Additionally, randomized split-face data demonstrate that picosecond 1064-nm devices achieve comparable reductions in mMASI scores to traditional nanosecond devices, and combination strategies incorporating intense pulsed light (IPL) have shown greater MASI improvement compared with IPL alone.^28,29 However, IPL generally is limited to lighter skin phototypes due to the risk for postinflammatory hyperpigmentation in darker skin.³⁰

Lastly, long-term management requires patient education on the importance of year-round maintenance therapy, consistency, and compliance. Reinforcing adherence to photoprotection, supporting barrier repair, and setting expectations regarding prognosis are essential components to optimizing melasma treatment outcomes.¹²

Future Insights: Beyond the Current State of Melasma Research and Treatment

Future advances in melasma management likely will focus on improving disease assessment and long-term treatment durability. Tools such as the MASI and mMASI are widely used but are limited by interobserver variability and reduced sensitivity in darker skin types, highlighting the need to incorporate objective measures such as colorimetry.^10,26 There also is a need for studies that relate clinical improvement to underlying pathology. Histopathologic correlation remains limited across most therapeutic trials, and more studies should assess long-term outcomes and quality-of-life measures given the relapsing nature of melasma.²⁶

Future interventions will continue to move past the treatment of pigment alone. Increasing recognition of vascular, inflammatory, and barrier-related contributions to melasma, as well as targeting of other cell types affected by melasma, will be important considerations in future treatment innovations.^8,11 In summary, improved inclusion of patients with skin of color in clinical trials, expansion of clinical outcomes measures and objective parameters of disease evaluation, novel approaches to treatment and relapse prevention, and greater attention to patient adherence and education will be essential to achieving advancements in melasma care.¹²

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

DIAGNOSIS

Senile gluteal dermatosis (SGD). SGD is a friction- related skin injury, also known as recliner butt, chronic tissue injury, or grandfather’s disease.^1-4 The hallmarks include blanchable erythematous plaques and/or purplish discoloration of the fleshy part of the buttocks or posterior thighs, with little to no change over months to years. Additional findings may include skin erosions, lichenification, and ridging. SGD is most commonly seen in older adults with impaired mobility who spend prolonged periods in a reclined position, particularly those who slide down in a chair, “scoot,” or drag the buttocks during transfers or repositioning.

The pathogenesis of SGD is thought to involve microischemia associated with prolonged sitting.⁴ Histopathologic findings are nonspecific and may include hyperkeratosis, psoriasiform epidermal hyperplasia, vascular dilatation or proliferation in the superficial dermis, and reactive lymphohistiocytic perivascular infiltrate.⁴ The condition is poorly recognized and is likely underreported. Treatment involves reducing frictional injury by avoiding the reclined position, minimizing sliding during transfers, and frequent repositioning. Petroleum-based ointments may be applied to reduce friction and protect the skin barrier. Heat-dissipating chair cushions can be used to offload pressure and improve the local microclimate. Friction-related skin injuries need to be differentiated from pressure injuries, in which pressure and shear are the driving forces, and lesions are located over bony prominences.

Unlike SGD, chronic lichen sclerosus typically occurs in the anogenital area, including the scrotum and vulva, and is typically intensely pruritic, with white, atrophic plaques.

A stage 2 pressure injury is characterized by an area of partial-thickness skin loss with exposed dermis, usually overlying a bony prominence. Although friction-related skin injuries may contain erosions, they are often maroon or purple and are not located over a bony prominence.

Deep tissue injury (DTI) is characterized by nonblanchable dark red or purple skin discoloration, with intact or nonintact skin. While friction injuries may mimic DTIs, they lack the characteristic anatomic location over a bony prominence and the predictable evolution pattern seen in DTIs.

Incontinence-associated dermatitis (IAD) results from prolonged exposure to urine and/or feces and presents with erythema, inflammation, and epidermal erosion. Although IAD can look similar or coincide with SGD, the affected area is typically red, not purple. Skin ridging and lichenification are also not seen in IAD cases.

Sedentary behavior is prevalent among older adults, with nearly 60% spending > 4 hours per day sitting.⁵ Prolonged sitting puts them at risk for friction-related skin injuries. Even though friction-related skin injuries are typically nonprogressive, these patients are also at risk for pressure injuries that are typically acquired in a sitting position (eg, ischial and sacrococcygeal). Therefore, it is imperative that clinicians not only address SGD but also implement a pressure injury prevention plan.

DIAGNOSIS

Senile gluteal dermatosis (SGD). SGD is a friction- related skin injury, also known as recliner butt, chronic tissue injury, or grandfather’s disease.^1-4 The hallmarks include blanchable erythematous plaques and/or purplish discoloration of the fleshy part of the buttocks or posterior thighs, with little to no change over months to years. Additional findings may include skin erosions, lichenification, and ridging. SGD is most commonly seen in older adults with impaired mobility who spend prolonged periods in a reclined position, particularly those who slide down in a chair, “scoot,” or drag the buttocks during transfers or repositioning.

The pathogenesis of SGD is thought to involve microischemia associated with prolonged sitting.⁴ Histopathologic findings are nonspecific and may include hyperkeratosis, psoriasiform epidermal hyperplasia, vascular dilatation or proliferation in the superficial dermis, and reactive lymphohistiocytic perivascular infiltrate.⁴ The condition is poorly recognized and is likely underreported. Treatment involves reducing frictional injury by avoiding the reclined position, minimizing sliding during transfers, and frequent repositioning. Petroleum-based ointments may be applied to reduce friction and protect the skin barrier. Heat-dissipating chair cushions can be used to offload pressure and improve the local microclimate. Friction-related skin injuries need to be differentiated from pressure injuries, in which pressure and shear are the driving forces, and lesions are located over bony prominences.

Unlike SGD, chronic lichen sclerosus typically occurs in the anogenital area, including the scrotum and vulva, and is typically intensely pruritic, with white, atrophic plaques.

A stage 2 pressure injury is characterized by an area of partial-thickness skin loss with exposed dermis, usually overlying a bony prominence. Although friction-related skin injuries may contain erosions, they are often maroon or purple and are not located over a bony prominence.

Deep tissue injury (DTI) is characterized by nonblanchable dark red or purple skin discoloration, with intact or nonintact skin. While friction injuries may mimic DTIs, they lack the characteristic anatomic location over a bony prominence and the predictable evolution pattern seen in DTIs.

Incontinence-associated dermatitis (IAD) results from prolonged exposure to urine and/or feces and presents with erythema, inflammation, and epidermal erosion. Although IAD can look similar or coincide with SGD, the affected area is typically red, not purple. Skin ridging and lichenification are also not seen in IAD cases.

Sedentary behavior is prevalent among older adults, with nearly 60% spending > 4 hours per day sitting.⁵ Prolonged sitting puts them at risk for friction-related skin injuries. Even though friction-related skin injuries are typically nonprogressive, these patients are also at risk for pressure injuries that are typically acquired in a sitting position (eg, ischial and sacrococcygeal). Therefore, it is imperative that clinicians not only address SGD but also implement a pressure injury prevention plan.

DIAGNOSIS

Senile gluteal dermatosis (SGD). SGD is a friction- related skin injury, also known as recliner butt, chronic tissue injury, or grandfather’s disease.^1-4 The hallmarks include blanchable erythematous plaques and/or purplish discoloration of the fleshy part of the buttocks or posterior thighs, with little to no change over months to years. Additional findings may include skin erosions, lichenification, and ridging. SGD is most commonly seen in older adults with impaired mobility who spend prolonged periods in a reclined position, particularly those who slide down in a chair, “scoot,” or drag the buttocks during transfers or repositioning.

The pathogenesis of SGD is thought to involve microischemia associated with prolonged sitting.⁴ Histopathologic findings are nonspecific and may include hyperkeratosis, psoriasiform epidermal hyperplasia, vascular dilatation or proliferation in the superficial dermis, and reactive lymphohistiocytic perivascular infiltrate.⁴ The condition is poorly recognized and is likely underreported. Treatment involves reducing frictional injury by avoiding the reclined position, minimizing sliding during transfers, and frequent repositioning. Petroleum-based ointments may be applied to reduce friction and protect the skin barrier. Heat-dissipating chair cushions can be used to offload pressure and improve the local microclimate. Friction-related skin injuries need to be differentiated from pressure injuries, in which pressure and shear are the driving forces, and lesions are located over bony prominences.

Unlike SGD, chronic lichen sclerosus typically occurs in the anogenital area, including the scrotum and vulva, and is typically intensely pruritic, with white, atrophic plaques.

A stage 2 pressure injury is characterized by an area of partial-thickness skin loss with exposed dermis, usually overlying a bony prominence. Although friction-related skin injuries may contain erosions, they are often maroon or purple and are not located over a bony prominence.

Deep tissue injury (DTI) is characterized by nonblanchable dark red or purple skin discoloration, with intact or nonintact skin. While friction injuries may mimic DTIs, they lack the characteristic anatomic location over a bony prominence and the predictable evolution pattern seen in DTIs.

Incontinence-associated dermatitis (IAD) results from prolonged exposure to urine and/or feces and presents with erythema, inflammation, and epidermal erosion. Although IAD can look similar or coincide with SGD, the affected area is typically red, not purple. Skin ridging and lichenification are also not seen in IAD cases.

Sedentary behavior is prevalent among older adults, with nearly 60% spending > 4 hours per day sitting.⁵ Prolonged sitting puts them at risk for friction-related skin injuries. Even though friction-related skin injuries are typically nonprogressive, these patients are also at risk for pressure injuries that are typically acquired in a sitting position (eg, ischial and sacrococcygeal). Therefore, it is imperative that clinicians not only address SGD but also implement a pressure injury prevention plan.

Mostly it is loss that teaches us about the worth of things.
Arthur Schopenhauer¹

One of the leaders I most respected in my US Department of Veterans Affairs (VA) career was a man who had worked his way up through the ranks to become a medical center director. Usually calm, cool, and collected, he would wax poetic when discussing the hero of the VA Health Care System revolution, Ken Kizer, MD, MPH.

In this issue of Federal Practitioner, journalist Randy Dotinga interviews Kizer about the current challenges facing the VA. Though many readers will have participated in or at least know about Kizer’s unprecedented overhaul of the agency, many others, especially those new to VA, may not. It seemed a fitting time to offer an outline of the immense and positive accomplishments that occurred in the agency during his tenure, especially as, under the current administration, many of his most forward-thinking initiatives seem to be moving backward.²

When President Clinton nominated Kizer to serve as the Under Secretary for Health for the Veterans Health Administration in 1994, the poor quality care the agency delivered was castigated in popular movies like Born on the Fourth of July. Veterans who were seen in that era, and who eventually returned to a far better, kinder VA thanks to Kizer, would often tell me, “Doc, the VA was really bad then, and I was afraid to come back.” The critique of VA health care in the mid-1990s sounds like a bureaucratic déjà vu of many of the concerns Kizer raised in his interview, including fragmentation of care, access barriers, and poor coordination of treatment.³

If anyone was prepared and qualified to take on this seeming mission impossible, it was Kizer. A US Navy veteran with 6 board certifications, he came to the VA following a brave and innovative stint as the top health official in California, where he successfully took on the tobacco lobby and dramatically reduced the state’s rates of smoking and related diseases.⁴

Long before it was the subject of reality TV shows, Kizer dubbed his major renovation of the VA’s antiquated structure an “extreme makeover.”³ Though this description is an oversimplification of Kizer’s monumental efforts, the makeover can be considered in 4 to 6 buckets, depending on how various health policy experts parse the re-engineering efforts.^5-7

Decentralization. Kizer instituted the Veterans Integrated Service Network (VISN) system to coordinate the management and operations of all the hospitals, clinics, and other VA health care entities in what is roughly a region. The locus of decision-making shifted from the VA Central Office to the VISNs, intended to promote more efficient, economical, and streamlined health care delivery.

Capitation. Accompanying this restructuring was a shift to a capitated system focused on preventive care. The Veterans Equitable Resource Allocation system was designed to logically link workload and funding. This was a major shift away from VA’s previous emphasis on inpatient and specialty care and resulted in the closing of multiple hospitals.⁴

Information Systems. I can still remember the first time I sat down at a prehistoric computer to use the Computerized Patient Record System (CPRS). Though now much maligned, then it was like something out of Star Trek, at a time when almost every other health care institution was buried in paper charts. With CPRS, VA suddenly had a pioneering and much-envied electronic medical record that facilitated continuity of care, communication between professionals, and accuracy and completeness of documentation.

Data Driven Performance Improvement. The VISNs and information systems inaugurated a new era of data-driven quality improvement. The assembly and analysis of data enabled VISNs to have real-time input about comparative facility performance.

Performance Measures. The data enabled evidence-based performance measures to be developed and monitored. Though these have now become the bane of many Federal Practitioner readers’ existence, they were originally intended for VISN directors and members of the senior executive service at VA central office. These were tied to incentives that, though recently the subject of watchdog investigation, were intended to motivate and reward high-quality care.⁶

Even this cursory look at Kizer’s accomplishments is more than enough to demonstrate the magnitude of the makeover, and when the time frame of the achievements is factored in, the transformation is the equivalent of a planet changing its orbit at light speed. Rhetoric aside, there are now hundreds of research articles published in top medical and health policy journals, many of them authored by Kizer,^7,8 that have amply demonstrated that when he departed the VA in 1999, it had become “the best care anywhere.” ⁹ For example, a 2000 New England Journal of Medicine article found that from 1994 to 2000, the percentage of veterans whose care met ≥ 90% of 9 of 17 quality standards was > 70% for 13 of the measures, outperforming fee-for-service Medicare.¹⁰

There had been uncertainty about whether Kizer would seek a second term as Under Secretary when he announced that he was leaving. With concise modesty, Kizer said he had met his charge to, “re-engineer the veterans’ health care system so that it could effectively function in the 21^st century.”¹¹

Despite openly and critically discussing the many difficulties the VA currently confronts, Kizer ends his interview on a note of hope. Since he likely knows more about VA than any person alive, we need to trust his judgment that his legacy, which currently seems more in jeopardy than ever before, will somehow prevail. Perhaps I am too melancholic, but I believe it will take a professional of the stature of Dr. Kizer to take us back to that future, and I fear we will not see his likes again.

Mostly it is loss that teaches us about the worth of things.
Arthur Schopenhauer¹

One of the leaders I most respected in my US Department of Veterans Affairs (VA) career was a man who had worked his way up through the ranks to become a medical center director. Usually calm, cool, and collected, he would wax poetic when discussing the hero of the VA Health Care System revolution, Ken Kizer, MD, MPH.

In this issue of Federal Practitioner, journalist Randy Dotinga interviews Kizer about the current challenges facing the VA. Though many readers will have participated in or at least know about Kizer’s unprecedented overhaul of the agency, many others, especially those new to VA, may not. It seemed a fitting time to offer an outline of the immense and positive accomplishments that occurred in the agency during his tenure, especially as, under the current administration, many of his most forward-thinking initiatives seem to be moving backward.²

When President Clinton nominated Kizer to serve as the Under Secretary for Health for the Veterans Health Administration in 1994, the poor quality care the agency delivered was castigated in popular movies like Born on the Fourth of July. Veterans who were seen in that era, and who eventually returned to a far better, kinder VA thanks to Kizer, would often tell me, “Doc, the VA was really bad then, and I was afraid to come back.” The critique of VA health care in the mid-1990s sounds like a bureaucratic déjà vu of many of the concerns Kizer raised in his interview, including fragmentation of care, access barriers, and poor coordination of treatment.³

If anyone was prepared and qualified to take on this seeming mission impossible, it was Kizer. A US Navy veteran with 6 board certifications, he came to the VA following a brave and innovative stint as the top health official in California, where he successfully took on the tobacco lobby and dramatically reduced the state’s rates of smoking and related diseases.⁴

Long before it was the subject of reality TV shows, Kizer dubbed his major renovation of the VA’s antiquated structure an “extreme makeover.”³ Though this description is an oversimplification of Kizer’s monumental efforts, the makeover can be considered in 4 to 6 buckets, depending on how various health policy experts parse the re-engineering efforts.^5-7

Decentralization. Kizer instituted the Veterans Integrated Service Network (VISN) system to coordinate the management and operations of all the hospitals, clinics, and other VA health care entities in what is roughly a region. The locus of decision-making shifted from the VA Central Office to the VISNs, intended to promote more efficient, economical, and streamlined health care delivery.

Capitation. Accompanying this restructuring was a shift to a capitated system focused on preventive care. The Veterans Equitable Resource Allocation system was designed to logically link workload and funding. This was a major shift away from VA’s previous emphasis on inpatient and specialty care and resulted in the closing of multiple hospitals.⁴

Information Systems. I can still remember the first time I sat down at a prehistoric computer to use the Computerized Patient Record System (CPRS). Though now much maligned, then it was like something out of Star Trek, at a time when almost every other health care institution was buried in paper charts. With CPRS, VA suddenly had a pioneering and much-envied electronic medical record that facilitated continuity of care, communication between professionals, and accuracy and completeness of documentation.

Data Driven Performance Improvement. The VISNs and information systems inaugurated a new era of data-driven quality improvement. The assembly and analysis of data enabled VISNs to have real-time input about comparative facility performance.

Performance Measures. The data enabled evidence-based performance measures to be developed and monitored. Though these have now become the bane of many Federal Practitioner readers’ existence, they were originally intended for VISN directors and members of the senior executive service at VA central office. These were tied to incentives that, though recently the subject of watchdog investigation, were intended to motivate and reward high-quality care.⁶

Even this cursory look at Kizer’s accomplishments is more than enough to demonstrate the magnitude of the makeover, and when the time frame of the achievements is factored in, the transformation is the equivalent of a planet changing its orbit at light speed. Rhetoric aside, there are now hundreds of research articles published in top medical and health policy journals, many of them authored by Kizer,^7,8 that have amply demonstrated that when he departed the VA in 1999, it had become “the best care anywhere.” ⁹ For example, a 2000 New England Journal of Medicine article found that from 1994 to 2000, the percentage of veterans whose care met ≥ 90% of 9 of 17 quality standards was > 70% for 13 of the measures, outperforming fee-for-service Medicare.¹⁰

There had been uncertainty about whether Kizer would seek a second term as Under Secretary when he announced that he was leaving. With concise modesty, Kizer said he had met his charge to, “re-engineer the veterans’ health care system so that it could effectively function in the 21^st century.”¹¹

Despite openly and critically discussing the many difficulties the VA currently confronts, Kizer ends his interview on a note of hope. Since he likely knows more about VA than any person alive, we need to trust his judgment that his legacy, which currently seems more in jeopardy than ever before, will somehow prevail. Perhaps I am too melancholic, but I believe it will take a professional of the stature of Dr. Kizer to take us back to that future, and I fear we will not see his likes again.

Mostly it is loss that teaches us about the worth of things.
Arthur Schopenhauer¹

One of the leaders I most respected in my US Department of Veterans Affairs (VA) career was a man who had worked his way up through the ranks to become a medical center director. Usually calm, cool, and collected, he would wax poetic when discussing the hero of the VA Health Care System revolution, Ken Kizer, MD, MPH.

In this issue of Federal Practitioner, journalist Randy Dotinga interviews Kizer about the current challenges facing the VA. Though many readers will have participated in or at least know about Kizer’s unprecedented overhaul of the agency, many others, especially those new to VA, may not. It seemed a fitting time to offer an outline of the immense and positive accomplishments that occurred in the agency during his tenure, especially as, under the current administration, many of his most forward-thinking initiatives seem to be moving backward.²

When President Clinton nominated Kizer to serve as the Under Secretary for Health for the Veterans Health Administration in 1994, the poor quality care the agency delivered was castigated in popular movies like Born on the Fourth of July. Veterans who were seen in that era, and who eventually returned to a far better, kinder VA thanks to Kizer, would often tell me, “Doc, the VA was really bad then, and I was afraid to come back.” The critique of VA health care in the mid-1990s sounds like a bureaucratic déjà vu of many of the concerns Kizer raised in his interview, including fragmentation of care, access barriers, and poor coordination of treatment.³

If anyone was prepared and qualified to take on this seeming mission impossible, it was Kizer. A US Navy veteran with 6 board certifications, he came to the VA following a brave and innovative stint as the top health official in California, where he successfully took on the tobacco lobby and dramatically reduced the state’s rates of smoking and related diseases.⁴

Long before it was the subject of reality TV shows, Kizer dubbed his major renovation of the VA’s antiquated structure an “extreme makeover.”³ Though this description is an oversimplification of Kizer’s monumental efforts, the makeover can be considered in 4 to 6 buckets, depending on how various health policy experts parse the re-engineering efforts.^5-7

Decentralization. Kizer instituted the Veterans Integrated Service Network (VISN) system to coordinate the management and operations of all the hospitals, clinics, and other VA health care entities in what is roughly a region. The locus of decision-making shifted from the VA Central Office to the VISNs, intended to promote more efficient, economical, and streamlined health care delivery.

Capitation. Accompanying this restructuring was a shift to a capitated system focused on preventive care. The Veterans Equitable Resource Allocation system was designed to logically link workload and funding. This was a major shift away from VA’s previous emphasis on inpatient and specialty care and resulted in the closing of multiple hospitals.⁴

Information Systems. I can still remember the first time I sat down at a prehistoric computer to use the Computerized Patient Record System (CPRS). Though now much maligned, then it was like something out of Star Trek, at a time when almost every other health care institution was buried in paper charts. With CPRS, VA suddenly had a pioneering and much-envied electronic medical record that facilitated continuity of care, communication between professionals, and accuracy and completeness of documentation.

Data Driven Performance Improvement. The VISNs and information systems inaugurated a new era of data-driven quality improvement. The assembly and analysis of data enabled VISNs to have real-time input about comparative facility performance.

Performance Measures. The data enabled evidence-based performance measures to be developed and monitored. Though these have now become the bane of many Federal Practitioner readers’ existence, they were originally intended for VISN directors and members of the senior executive service at VA central office. These were tied to incentives that, though recently the subject of watchdog investigation, were intended to motivate and reward high-quality care.⁶

Even this cursory look at Kizer’s accomplishments is more than enough to demonstrate the magnitude of the makeover, and when the time frame of the achievements is factored in, the transformation is the equivalent of a planet changing its orbit at light speed. Rhetoric aside, there are now hundreds of research articles published in top medical and health policy journals, many of them authored by Kizer,^7,8 that have amply demonstrated that when he departed the VA in 1999, it had become “the best care anywhere.” ⁹ For example, a 2000 New England Journal of Medicine article found that from 1994 to 2000, the percentage of veterans whose care met ≥ 90% of 9 of 17 quality standards was > 70% for 13 of the measures, outperforming fee-for-service Medicare.¹⁰

There had been uncertainty about whether Kizer would seek a second term as Under Secretary when he announced that he was leaving. With concise modesty, Kizer said he had met his charge to, “re-engineer the veterans’ health care system so that it could effectively function in the 21^st century.”¹¹

Despite openly and critically discussing the many difficulties the VA currently confronts, Kizer ends his interview on a note of hope. Since he likely knows more about VA than any person alive, we need to trust his judgment that his legacy, which currently seems more in jeopardy than ever before, will somehow prevail. Perhaps I am too melancholic, but I believe it will take a professional of the stature of Dr. Kizer to take us back to that future, and I fear we will not see his likes again.

THE DIAGNOSIS: Coexisting Squamous Cell Carcinoma and Basal Cell Carcinoma

Dermoscopy of the plaque showed central ulceration with blood spots surrounded by branched linear vessels, which was suggestive of squamous cell carcinoma (SCC)(Figure 1A). The nodule showed shiny, white-red, structureless areas with small gray spots, bright white crystalline streaks, and short fine telangiectasias suggestive of basal cell carcinoma (BCC)(Figure 1B). Histopathology showed that the plaque had irregular nests, cords, and sheets of neoplastic keratinocytes invading the dermis (Figure 2A) and the nodule had discrete nests of basaloid cells with peripheral palisading in the dermis (Figure 2B), which confirmed the diagnosis of coexisting SCC and BCC. The patient underwent surgical excision of the lesions, which achieved clear margins. At the 2-year follow-up, there was no sign of recurrence.

Squamous cell carcinoma is the second most frequent cancer in humans. Older patients are more susceptible due to chronic UV exposure.¹ Basal cell carcinoma is the most common human cancer worldwide.² These skin cancers have different clinical manifestations, pathologic features, treatment methods, and prognoses. The coexistence of 2 types of skin cancer presents a diagnostic challenge. Possible causes of this phenomenon are not clear. It may simply be a coincidence since the lesions typically occur in sun-exposed areas such as the nose, which may be affected by photodamage.³ According to the field cancerization theory, chronically sun-exposed areas are at higher risk for development of coexisting skin cancers.⁴ A more interesting explanation is the interaction theory, which suggests that one tumor produces epidermal or stromal changes that induce the formation of a second independent tumor via the paracrine effect (ie, growth mediators from nearby cells).⁴

Dermoscopy is an important noninvasive diagnostic tool for the evaluation of skin cancer, particularly early detection. Dermoscopic findings of blood vessels, ulcers, the fiber sign, blood spots, white structureless areas, keratin, and centered vessels indicate a diagnosis of SCC.⁵ In contrast, common dermoscopic findings for BCC include arborizing vessels, ulceration, shiny white structures, and blue-gray ovoid nests or globules.⁶

Irritated seborrheic keratosis is an inflammatory variant of seborrheic keratosis, which often is challenging to identify clinically due to its similar features with SCC; however, SCC is more likely to demonstrate dotted or branched vessels, white structureless areas, white circles around follicles, irregular or peripheral vessel patterns, and central scales on dermoscopy. In contrast, irritated seborrheic keratosis is more likely to have hairpin vessels, regular vessel patterns, and white halos around vessels, which may aid in the differentiation between the two entities.⁶

Due to the higher sensitivity of dermoscopy for detecting pigmented BCC compared to nonpigmented BCC, it holds substantial diagnostic value in Asian populations, in whom pigmented BCC is the most common subtype.^6,8 However, the lack of pigmentation in the nodule in our case posed a diagnostic challenge, as the diagnosis of BCC had to rely on subtle vascular and shiny white structures rather than more obvious pigment clues. This absence of pigment, however, also helped rule out pigmented BCC as a diagnosis for the nodule. Short fine telangiectasias is the second most common vascular pattern in BCC, and bright white structures are highly suggestive of nonpigmented BCC.⁶ Therefore, dermoscopic findings of bright-white structures with fine telangiectasias should be alerted to the possibility of nonpigmented BCC.

Basosquamous carcinoma has clinical and dermoscopic features between SCC and BCC, and the presence of dermatoscopic features from both BCC and SCC should raise suspicion, but the diagnosis is particularly challenging because its presentation is nonspecific.⁹ We need to be vigilant about the possibility of coexistence of 2 types of skin cancer, and that regular physical examination and dermatoscopy are very important for early detection and diagnosis.

THE DIAGNOSIS: Coexisting Squamous Cell Carcinoma and Basal Cell Carcinoma

Dermoscopy of the plaque showed central ulceration with blood spots surrounded by branched linear vessels, which was suggestive of squamous cell carcinoma (SCC)(Figure 1A). The nodule showed shiny, white-red, structureless areas with small gray spots, bright white crystalline streaks, and short fine telangiectasias suggestive of basal cell carcinoma (BCC)(Figure 1B). Histopathology showed that the plaque had irregular nests, cords, and sheets of neoplastic keratinocytes invading the dermis (Figure 2A) and the nodule had discrete nests of basaloid cells with peripheral palisading in the dermis (Figure 2B), which confirmed the diagnosis of coexisting SCC and BCC. The patient underwent surgical excision of the lesions, which achieved clear margins. At the 2-year follow-up, there was no sign of recurrence.

Squamous cell carcinoma is the second most frequent cancer in humans. Older patients are more susceptible due to chronic UV exposure.¹ Basal cell carcinoma is the most common human cancer worldwide.² These skin cancers have different clinical manifestations, pathologic features, treatment methods, and prognoses. The coexistence of 2 types of skin cancer presents a diagnostic challenge. Possible causes of this phenomenon are not clear. It may simply be a coincidence since the lesions typically occur in sun-exposed areas such as the nose, which may be affected by photodamage.³ According to the field cancerization theory, chronically sun-exposed areas are at higher risk for development of coexisting skin cancers.⁴ A more interesting explanation is the interaction theory, which suggests that one tumor produces epidermal or stromal changes that induce the formation of a second independent tumor via the paracrine effect (ie, growth mediators from nearby cells).⁴

Dermoscopy is an important noninvasive diagnostic tool for the evaluation of skin cancer, particularly early detection. Dermoscopic findings of blood vessels, ulcers, the fiber sign, blood spots, white structureless areas, keratin, and centered vessels indicate a diagnosis of SCC.⁵ In contrast, common dermoscopic findings for BCC include arborizing vessels, ulceration, shiny white structures, and blue-gray ovoid nests or globules.⁶

Irritated seborrheic keratosis is an inflammatory variant of seborrheic keratosis, which often is challenging to identify clinically due to its similar features with SCC; however, SCC is more likely to demonstrate dotted or branched vessels, white structureless areas, white circles around follicles, irregular or peripheral vessel patterns, and central scales on dermoscopy. In contrast, irritated seborrheic keratosis is more likely to have hairpin vessels, regular vessel patterns, and white halos around vessels, which may aid in the differentiation between the two entities.⁶

Due to the higher sensitivity of dermoscopy for detecting pigmented BCC compared to nonpigmented BCC, it holds substantial diagnostic value in Asian populations, in whom pigmented BCC is the most common subtype.^6,8 However, the lack of pigmentation in the nodule in our case posed a diagnostic challenge, as the diagnosis of BCC had to rely on subtle vascular and shiny white structures rather than more obvious pigment clues. This absence of pigment, however, also helped rule out pigmented BCC as a diagnosis for the nodule. Short fine telangiectasias is the second most common vascular pattern in BCC, and bright white structures are highly suggestive of nonpigmented BCC.⁶ Therefore, dermoscopic findings of bright-white structures with fine telangiectasias should be alerted to the possibility of nonpigmented BCC.

Basosquamous carcinoma has clinical and dermoscopic features between SCC and BCC, and the presence of dermatoscopic features from both BCC and SCC should raise suspicion, but the diagnosis is particularly challenging because its presentation is nonspecific.⁹ We need to be vigilant about the possibility of coexistence of 2 types of skin cancer, and that regular physical examination and dermatoscopy are very important for early detection and diagnosis.

THE DIAGNOSIS: Coexisting Squamous Cell Carcinoma and Basal Cell Carcinoma

Dermoscopy of the plaque showed central ulceration with blood spots surrounded by branched linear vessels, which was suggestive of squamous cell carcinoma (SCC)(Figure 1A). The nodule showed shiny, white-red, structureless areas with small gray spots, bright white crystalline streaks, and short fine telangiectasias suggestive of basal cell carcinoma (BCC)(Figure 1B). Histopathology showed that the plaque had irregular nests, cords, and sheets of neoplastic keratinocytes invading the dermis (Figure 2A) and the nodule had discrete nests of basaloid cells with peripheral palisading in the dermis (Figure 2B), which confirmed the diagnosis of coexisting SCC and BCC. The patient underwent surgical excision of the lesions, which achieved clear margins. At the 2-year follow-up, there was no sign of recurrence.

Squamous cell carcinoma is the second most frequent cancer in humans. Older patients are more susceptible due to chronic UV exposure.¹ Basal cell carcinoma is the most common human cancer worldwide.² These skin cancers have different clinical manifestations, pathologic features, treatment methods, and prognoses. The coexistence of 2 types of skin cancer presents a diagnostic challenge. Possible causes of this phenomenon are not clear. It may simply be a coincidence since the lesions typically occur in sun-exposed areas such as the nose, which may be affected by photodamage.³ According to the field cancerization theory, chronically sun-exposed areas are at higher risk for development of coexisting skin cancers.⁴ A more interesting explanation is the interaction theory, which suggests that one tumor produces epidermal or stromal changes that induce the formation of a second independent tumor via the paracrine effect (ie, growth mediators from nearby cells).⁴

Dermoscopy is an important noninvasive diagnostic tool for the evaluation of skin cancer, particularly early detection. Dermoscopic findings of blood vessels, ulcers, the fiber sign, blood spots, white structureless areas, keratin, and centered vessels indicate a diagnosis of SCC.⁵ In contrast, common dermoscopic findings for BCC include arborizing vessels, ulceration, shiny white structures, and blue-gray ovoid nests or globules.⁶

Irritated seborrheic keratosis is an inflammatory variant of seborrheic keratosis, which often is challenging to identify clinically due to its similar features with SCC; however, SCC is more likely to demonstrate dotted or branched vessels, white structureless areas, white circles around follicles, irregular or peripheral vessel patterns, and central scales on dermoscopy. In contrast, irritated seborrheic keratosis is more likely to have hairpin vessels, regular vessel patterns, and white halos around vessels, which may aid in the differentiation between the two entities.⁶

Due to the higher sensitivity of dermoscopy for detecting pigmented BCC compared to nonpigmented BCC, it holds substantial diagnostic value in Asian populations, in whom pigmented BCC is the most common subtype.^6,8 However, the lack of pigmentation in the nodule in our case posed a diagnostic challenge, as the diagnosis of BCC had to rely on subtle vascular and shiny white structures rather than more obvious pigment clues. This absence of pigment, however, also helped rule out pigmented BCC as a diagnosis for the nodule. Short fine telangiectasias is the second most common vascular pattern in BCC, and bright white structures are highly suggestive of nonpigmented BCC.⁶ Therefore, dermoscopic findings of bright-white structures with fine telangiectasias should be alerted to the possibility of nonpigmented BCC.

Basosquamous carcinoma has clinical and dermoscopic features between SCC and BCC, and the presence of dermatoscopic features from both BCC and SCC should raise suspicion, but the diagnosis is particularly challenging because its presentation is nonspecific.⁹ We need to be vigilant about the possibility of coexistence of 2 types of skin cancer, and that regular physical examination and dermatoscopy are very important for early detection and diagnosis.