Scaly rash

Scaly plaques on sun-exposed skin with hyperpigmentation and dyspigmentation are classic signs of cutaneous lupus erythematosus (CLE). (The dyspigmentation seen in this case signaled that she likely had chronic cutaneous lupus erythematosus [CCLE]—a subtype of CLE.) At the patient’s follow-up primary care visit, her antinuclear antibodies titer was 1:1280 (≥ 1:160 is considered a positive test) and her 24-hour urine protein was 1188 mg (normal levels in adults, < 150 mg/d). In light of the patient’s joint pain, lab findings, and skin manifestations, she was also given a diagnosis of systemic lupus erythematosus (SLE).

Lupus erythematosus has an increased prevalence in women and typically occurs between the ages of 20 to 50 years.¹ The incidence and prevalence of this condition is also greater in Black patients. CLE can either occur with SLE or independently. Patients with CLE should be monitored for the development of SLE. A diagnosis of CLE is based mainly on clinical features; biopsy is only indicated if there is a high degree of uncertainty.

Patients with CLE may suffer from a lower quality of life compared to patients with other dermatologic conditions due to the often disfiguring and disabling nature of the condition.^1,2 Additionally, Black patients have an even higher chance of developing depressive symptoms associated with CCLE.²

Therapeutic management for CLE involves photoprotection by wearing sun-protective clothing, sunscreen, and limiting sun exposure.¹ Initial treatment includes topical or intralesional corticosteroids, or topical calcineurin inhibitors. Systemic therapy is similar to that used for SLE. Oral glucocorticoids, and antimalarial agents are considered first-line systemic therapy.¹ Second-line treatment includes methotrexate, mycophenolate mofetil, systemic retinoids, and azathioprine. Other immunosuppressive agents that are less commonly used include clofazimine, cyclophosphamide, and rituximab.¹

The patient was treated sequentially with trials of oral azathioprine 50 mg bid, then prednisone 10 mg once daily, and then hydroxychloroquine 400 mg daily, without significant change in her condition. Additionally, topical steroids did not improve the patient’s symptoms. She was subsequently started on rituximab 1000 mg intravenously with a second dose repeated 2 weeks later, and another treatment 6 months after that. One year after her visit to the ED, the patient was experiencing marked improvement in her lesions.

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Photo courtesy of Christy Nwankwo BA. Text courtesy of Christy Nwankwo, BA, University of Missouri-Kansas City School of Medicine and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque

Scaly plaques on sun-exposed skin with hyperpigmentation and dyspigmentation are classic signs of cutaneous lupus erythematosus (CLE). (The dyspigmentation seen in this case signaled that she likely had chronic cutaneous lupus erythematosus [CCLE]—a subtype of CLE.) At the patient’s follow-up primary care visit, her antinuclear antibodies titer was 1:1280 (≥ 1:160 is considered a positive test) and her 24-hour urine protein was 1188 mg (normal levels in adults, < 150 mg/d). In light of the patient’s joint pain, lab findings, and skin manifestations, she was also given a diagnosis of systemic lupus erythematosus (SLE).

Lupus erythematosus has an increased prevalence in women and typically occurs between the ages of 20 to 50 years.¹ The incidence and prevalence of this condition is also greater in Black patients. CLE can either occur with SLE or independently. Patients with CLE should be monitored for the development of SLE. A diagnosis of CLE is based mainly on clinical features; biopsy is only indicated if there is a high degree of uncertainty.

Patients with CLE may suffer from a lower quality of life compared to patients with other dermatologic conditions due to the often disfiguring and disabling nature of the condition.^1,2 Additionally, Black patients have an even higher chance of developing depressive symptoms associated with CCLE.²

Therapeutic management for CLE involves photoprotection by wearing sun-protective clothing, sunscreen, and limiting sun exposure.¹ Initial treatment includes topical or intralesional corticosteroids, or topical calcineurin inhibitors. Systemic therapy is similar to that used for SLE. Oral glucocorticoids, and antimalarial agents are considered first-line systemic therapy.¹ Second-line treatment includes methotrexate, mycophenolate mofetil, systemic retinoids, and azathioprine. Other immunosuppressive agents that are less commonly used include clofazimine, cyclophosphamide, and rituximab.¹

The patient was treated sequentially with trials of oral azathioprine 50 mg bid, then prednisone 10 mg once daily, and then hydroxychloroquine 400 mg daily, without significant change in her condition. Additionally, topical steroids did not improve the patient’s symptoms. She was subsequently started on rituximab 1000 mg intravenously with a second dose repeated 2 weeks later, and another treatment 6 months after that. One year after her visit to the ED, the patient was experiencing marked improvement in her lesions.

‌

Photo courtesy of Christy Nwankwo BA. Text courtesy of Christy Nwankwo, BA, University of Missouri-Kansas City School of Medicine and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque

Scaly plaques on sun-exposed skin with hyperpigmentation and dyspigmentation are classic signs of cutaneous lupus erythematosus (CLE). (The dyspigmentation seen in this case signaled that she likely had chronic cutaneous lupus erythematosus [CCLE]—a subtype of CLE.) At the patient’s follow-up primary care visit, her antinuclear antibodies titer was 1:1280 (≥ 1:160 is considered a positive test) and her 24-hour urine protein was 1188 mg (normal levels in adults, < 150 mg/d). In light of the patient’s joint pain, lab findings, and skin manifestations, she was also given a diagnosis of systemic lupus erythematosus (SLE).

Lupus erythematosus has an increased prevalence in women and typically occurs between the ages of 20 to 50 years.¹ The incidence and prevalence of this condition is also greater in Black patients. CLE can either occur with SLE or independently. Patients with CLE should be monitored for the development of SLE. A diagnosis of CLE is based mainly on clinical features; biopsy is only indicated if there is a high degree of uncertainty.

Patients with CLE may suffer from a lower quality of life compared to patients with other dermatologic conditions due to the often disfiguring and disabling nature of the condition.^1,2 Additionally, Black patients have an even higher chance of developing depressive symptoms associated with CCLE.²

Therapeutic management for CLE involves photoprotection by wearing sun-protective clothing, sunscreen, and limiting sun exposure.¹ Initial treatment includes topical or intralesional corticosteroids, or topical calcineurin inhibitors. Systemic therapy is similar to that used for SLE. Oral glucocorticoids, and antimalarial agents are considered first-line systemic therapy.¹ Second-line treatment includes methotrexate, mycophenolate mofetil, systemic retinoids, and azathioprine. Other immunosuppressive agents that are less commonly used include clofazimine, cyclophosphamide, and rituximab.¹

The patient was treated sequentially with trials of oral azathioprine 50 mg bid, then prednisone 10 mg once daily, and then hydroxychloroquine 400 mg daily, without significant change in her condition. Additionally, topical steroids did not improve the patient’s symptoms. She was subsequently started on rituximab 1000 mg intravenously with a second dose repeated 2 weeks later, and another treatment 6 months after that. One year after her visit to the ED, the patient was experiencing marked improvement in her lesions.

‌

Photo courtesy of Christy Nwankwo BA. Text courtesy of Christy Nwankwo, BA, University of Missouri-Kansas City School of Medicine and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque