CASE REPORT
A 25-year-old previously healthy female presented to dermatology with a 1.5-year history of steroid-unresponsive PG diagnosed by a previous dermatologist on her lower extremities. Previous treatment included multiple oral prednisone tapers, perilesional Kenalog injections, and topical clobetasol cream with limited to no improvement. On review of systems, the patient reported increased fatigue, easy bruisability, striae, facial redness, hip pain, and hair loss over the past six years; past laboratory testing was unremarkable. The patient denied any past medical history, including inflammatory bowel disease (IBD), arthritis, hematologic abnormalities, and HIV. She reported no relevant family or social history.
Physical examination revealed facial plethora, moon facies, supraclavicular fat pads, macular purpura on the bilateral upper extremities, truncal wide, purple striae, increased fine hair without terminal hair growth along her upper back, anterior clavicle, and neck (Figures 1a, b). Her left, distal, anteromedial lower leg had two cribriform scars from previous ulcers and her right distal anterior lower leg had two active ulcerations (Figure 2). Given the prior lack of response to systemic steroids, the patient started on cyclosporine 4 mg/kg daily for one month with limited to no improvement on wound closure no improvement on wound closure, at which time it was discontinued as a re- sult of new onset hypertension, and changed to mycophenolate mofetil (1000mg twice daily). Prior to taking cyclosporine, she never had a history of hypertension. Her active wounds were treated with local wound management, which included Santyl, dapsone, and bandaging with xeroform, non-adherent dressing, and Coban wrap.
Physical examination revealed facial plethora, moon facies, supraclavicular fat pads, macular purpura on the bilateral upper extremities, truncal wide, purple striae, increased fine hair without terminal hair growth along her upper back, anterior clavicle, and neck (Figures 1a, b). Her left, distal, anteromedial lower leg had two cribriform scars from previous ulcers and her right distal anterior lower leg had two active ulcerations (Figure 2). Given the prior lack of response to systemic steroids, the patient started on cyclosporine 4 mg/kg daily for one month with limited to no improvement on wound closure no improvement on wound closure, at which time it was discontinued as a re- sult of new onset hypertension, and changed to mycophenolate mofetil (1000mg twice daily). Prior to taking cyclosporine, she never had a history of hypertension. Her active wounds were treated with local wound management, which included Santyl, dapsone, and bandaging with xeroform, non-adherent dressing, and Coban wrap.
