INTRODUCTION
Vasculitis refers to a group of multiorgan diseases that frequently present with cutaneous manifestations. Vasculitis may be medication-induced, however, confirming
the diagnosis of drug-induced vasculitis is challenging given the lack of a gold standard for confirmatory testing and significant contraindications to medication re-challenge. We report a case of possible medication-induced cutaneous vasculitis
associated with ustekinumab, complicated by a positive
immunoassay for antineutrophil cytoplasmic antibodies (ANCA).
REPORT OF CASE
A 55 year-old woman with a history of psoriasis, type II diabetes mellitus, coronary artery disease, depression, heart failure, hemorrhoids, hypothyroidism, hyperlipidemia, and obesity presented with multiple, painful bilateral lower extremity
ulcers. For her psoriasis she had been treated with oral methotrexate 25 milligrams weekly for three years with persistently active skin lesions, and she had been recently
started on ustekinumab 90 milligrams administered subcutaneously eight and four weeks prior to presentation.
The patient presented with a new, painful, purpuric, and ulcerative eruption on her lower legs. She also reported
recent-onset intermittent epistaxis, gross hematuria, and scant hematochezia. Her other medications included carvedilol, fluoxetine, furosemide, insulin, isosorbide mononitrate,
levothyroxine, losartan, metolazone, pravastatin, and spironolactone, all of which she had been taking for at least 22 months, except fluoxetine, which had been started five months prior to presentation.
Physical examination was remarkable for BMI 48.8 kg/m2 and bullous purpuric plaques with central erosions with crusts and eschars and surrounding erythema involving the bilateral lower extremities (Figure 1), with a background of diffuse psoriatic plaques.
Skin punch biopsy of the left leg (Figure 2) demonstrated epidermal
necrosis with blister formation, and a perivascular and interstitial neutrophil-rich infiltrate in the dermis. Multiple superficial
and deep vessels demonstrated vascular injury and fibrinoid necrosis of the vessel walls, associated with leukocytoclasis
and hemorrhage, consistent with vasculitis. Skin culture was positive for methicillin-sensitive Staphylococcus aureus. Blood cultures for bacteria and mycobacteria were negative.
Given the patient’s presentation of epistaxis, hematuria, and hematochezia, and considering the depth and extent of the vascular inflammation, she was evaluated for possible multi-system vasculitis. Laboratory test results included a Westergren erythrocyte sedimentation rate of 72 mm/hour, a C-reactive protein of 26.2 mg/L, and negative tests for anti-nuclear antibodies, rheumatoid factor, serum cryoglobulins, serum protein electrophoresis, Hepatitis B virus surface antigen,
Hepatitis B virus surface antibody, Hepatitis B virus core antibody, Hepatitis C antibody, and interferon-gamma release assay (QuantiFERON®â€“TB Gold). Transthoracic echocardiogram was negative for vegetation.
Testing ANCA by indirect immunofluorescence (IIF) proved negative.
Concomitantly measured enzyme-linked immunosorbent
