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A 41-year-old woman presented for evaluation of a pruritic eruption with an abrupt onset, starting on her flanks and then spreading to her arms and legs. She had 2 weeks of fever, chills, malaise, migratory joint pain, nausea, and mental confusion. An antistreptolysin O titer was positive. Upon hospital admission, bilateral lower-extremity chorea movements were observed, and her C-reactive protein level was elevated (3.7 mg/dL). Biopsy results supported erythema marginatum. Based on these clinical and laboratory findings, the diagnosis of acute rheumatic fever was established.

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Dermatologic manifestations can be the initial signs of a systemic disease, and a thorough investigation may be warranted to rule out a life-altering diagnosis. We present a case of an 11-year-old boy with a concurrent presentation of eruptive syringomas and juxtaclavicular beaded lines on his neck. While a biopsy confirmed the benign diagnosis, the initial presentation led to a concerning differential including pseudoxanthoma elasticum and warranted a complete investigation.

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Vemurafenib is a selected BRAF kinase inhibitor approved for treating metastatic or unresectable melanoma, which has numerous cutaneous side effects unfortunately, including three previously reported cases of asymptomatic areola and/or nipple hyperkeratosis. We present the first case of painful bilateral nipple hyperkeratosis secondary to vemurafenib in an 84-year-old woman. She was successfully treated with tretinoin 0.05% cream that allowed her to comfortably continue treatment. With increased awareness of this condition, we found a second case of asymptomatic nipple hyperkeratosis secondary to vemurafenib in our clinic. As this medication gains acceptance for treatment of metastatic melanoma, it is imperative that dermatologists are aware of this potentially uncomfortable side effect that can result in decreased compliance and impaired quality of life.

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Chondrodermatitis nodularis helicis (CNH) is characterized by a tender nodule located on the helix or antihelix. Age groups impacted by CNH vary from study to study, but the majority of studies report an average age range from 50 to 80 years. Various treatment options have been described in the literature, including surgical techniques, laser therapy, curettage, topical and intralesional corticosteroids, and pressure relieving techniques. The main goal of therapy is to reduce pain and improve clinical appearance. In recent years, new therapies have been described for CNH with great results and lower recurrence rates. It is our hope that this review can serve as a reference for both practitioners and patients looking to treat CNH.

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An elderly patient presented with two clusters of asymptomatic fleshy and pedunculated papules. Biopsy of the papules was consistent with neurofibromas. Decades prior she had undergone a surgery for the excision of a large schwannoma. Given her lack of other neurofibromatosis findings, the patient was diagnosed with multisegmental neurofibromatosis (multi-SN) with deep schwannoma, a possible new phenotype of SN. Because this entity may be associated with internal malignancy, it is important to screen and educate these patients as well as to provide regular follow-up.

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Pityriasis rubra pilaris is a rare inflammatory disorder characterized by follicular papules on an erythematous base often exhibiting islands of unaffected skin, follicular plugging, and palmoplantar hyperkeratosis. While vitamin A deficiency and autoimmune reactions have been hypothesized as possible etiologies of this condition, pityriasis rubra pilaris-like eruptions secondary to medications are extremely rare. To our knowledge, only three other cases have been reported, and pityriasis rubra pilaris has never been reported in association with bevacizumab. We present a 70-year-old man who developed erythroderma both clinically and histologically consistent with pityriasis rubra pilaris 10 days after intravitreal injection of bevacizumab for age-related macular degeneration. As immune-modulating drugs grow in their application for a host of diseases, recognition of associated medication complications is important.

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A 69-year-old man from Texas with an unremarkable past medical history presented with a 2-year history of a diffuse, spreading annular eruption involving most of his trunk. He noticed progressive numbness of his hands and feet but no other systemic symptoms. He had never traveled outside of the United States. Skin biopsy confirmed a diagnosis of leprosy, and he was initiated on appropriate therapy.

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We describe a 2-year-old African-American boy with a 4-month history of gradually worsening unilateral edema that was initially noted on his left hand and then approximately 2 weeks later on his left lower extremity. In addition, linear hypopigmented patches were noted along the left forearm and leg, with no appreciable scarring or induration. The edema on the left-hand side of his body progressed so that he developed tense bullae on his left hand. Two months later, the hypopigmented patches were indurated and bound-down, especially over the left groin and thigh. A biopsy specimen from this area showed features characteristic of morphea. In this patient, dilated lymphatic channels secondary to the sclerosis of the morphea caused the bullae. Bullous morphea is a rare condition. We were unable to find any reports its occurrence in children under 18 with associated lymphedema. This entity should be included in the differential for acquired unilateral edema in children.

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Levodopa is the major drug used in the treatment of patients with Parkinson's disease. However, levodopa continues to be 'contra-indicated' for patients with Parkinson's disease associated with malignant melanoma. Case reports have suggested that levodopa has a causal relationship with malignant melanoma due to their shared dopamine biochemical pathway. Clinical characteristics of 54 patients with both Parkinson's disease and melanoma were analyzed (43 cases from the literature and 11 from our institution). The results suggest that the occurrence of both Parkinson's disease and melanoma in these patients is coincidental rather than causal. It did not appear that the Parkinson's disease patients on levodopa therapy were predisposed to melanoma, nor did levodopa therapy appear to exaggerate melanoma if it were previously present.

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