Case Reports

IgA Vasculitis in the Setting of Biologic Therapy for Psoriasis and Recurrent Cutaneous Methicillin-Resistant Staphylococcus aureus Colonization

Author and Disclosure Information

IgA vasculitis is a form of cutaneous small-vessel leukocytoclastic vasculitis (LCV) that has various triggers, including anti–tumor necrosis factor (TNF) α therapy. As the use of more targeted biologic therapies such as the IL-17 inhibitor secukinumab increases, so do reports of associated adverse events. Herein, we describe an uncommon case of IgA vasculitis in a man undergoing biologic therapy with adalimumab and secukinumab for psoriasis with recurrent cutaneous methicillin-resistant Staphylococcus aureus (MRSA) colonization. A review of the current literature also is provided.

Practice Points

  • Biologic medications including adalimumab and more rarely secukinumab may be associated with leukocytoclastic vasculitis; a smaller subset of patients may experience IgA vasculitis.
  • The IL-23 blocker ustekinumab may represent an ideal therapeutic agent when secukinumabassociated vasculitis is suspected. Because IL-23 is the main driver and sustainer of TH17 cell differentiation, it may cease the main causative cytokine cascades “upstream.”


 

References

Case Report

A 47-year-old man presented with a sudden-onset rash consisting of red bumps on the abdomen and legs that had been ongoing for several days. He had known psoriasis and psoriatic arthritis that had been well controlled with adalimumab for the last 18 months. He reported concurrent onset of nausea but denied fevers, chills, night sweats, unintentional weight loss, abdominal pain, and pruritus. He endorsed prior cutaneous infections of methicillin-resistant Staphylococcus aureus (MRSA). His medical history also included diabetes mellitus, hypertension, and obesity. His other medications included oral losartan-hydrochlorothiazide, amlodipine, naproxen, and atorvastatin.

Physical examination revealed numerous thin purpuric papules—some with adherent scale—distributed on the lower legs, extensor forearms, and abdomen. Abdominal lesions were confined to weight-related striae (Figure 1). The palms, soles, oral mucosa, and face were spared. Three punch biopsies were performed, including 1 for direct immunofluorescence (DIF), and the patient was instructed to apply clobetasol to the affected areas twice daily until further notice.

A and B, Numerous thin purpuric papules distributed on the left lower leg and abdomen, where the lesions were confined to weight-related striae.

FIGURE 1. A and B, Numerous thin purpuric papules distributed on the left lower leg and abdomen, where the lesions were confined to weight-related striae.

Pathology showed perivascular extravasation of erythrocytes, neutrophils, eosinophils, and leukocytoclasis surrounding blood vessels associated with fibrin (Figure 2). Direct immunofluorescence showed granular deposition of IgA, complement component 3, and fibrinogen in a superficial dermal vascular pattern (Figure 3). These results were consistent with IgA small-vessel vasculitis. One specimen was consistent with the patient’s known psoriasis.

A biopsy from the left dorsal forearm showed superficial dermal perivascular extravasation of erythrocytes, neutrophils, eosinophils, and leukocytoclasis surrounding blood vessels associated with fibrin (H&E, original magnification ×10).

FIGURE 2. A biopsy from the left dorsal forearm showed superficial dermal perivascular extravasation of erythrocytes, neutrophils, eosinophils, and leukocytoclasis surrounding blood vessels associated with fibrin (H&E, original magnification ×10).

Urinalysis revealed moderate hemoglobinuria, and urine microscopy showed 174 red blood cells per high-power field. Creatinine was high at 1.87 mg/dL (reference range, <1.34 mg/dL; patient’s baseline, 0.81 mg/dL) and glomerular filtration rate was low (42 mL/min, patient’s baseline, >60 mL/min [reference range, 90–120 mL/min]). Erythrocyte sedimentation rate (21 mm/h [reference range, 0–22 mm/h]) and C-reactive protein were elevated (2.2 mg/dL [reference range, 0.3–1.0 mg/dL]). Given his history of cutaneous MRSA infections, a bacterial culture swab was collected from the skin surface to check for colonization, which showed moderate growth of MRSA. Naproxen was discontinued over concern of worsening the patient’s renal status. The patient was instructed to rest at home with his legs elevated, wear compression socks when ambulatory, use chlorhexidine antiseptic daily as a body wash when showering, and apply mupirocin three times daily to the biopsy sites. He was referred to urology for his microhematuria, where cystoscopy revealed no abnormalities.A month passed with no improvement of the patient’s cutaneous vasculitis, and his psoriatic arthritis worsened without his usual use of naproxen. He developed abdominal pain and loss of appetite. A prednisone taper was ordered starting at 40 mg/d (28.8 mg/kg), which provided relief of the skin and joint symptoms only until the course was completed 12 days later.

Direct immunofluorescence obtained from perilesional skin of the left forearm showed granular deposition of IgA, complement component 3, and fibrinogen in a superficial dermal vascular pattern (IgA, original magnification ×40).

FIGURE 3. Direct immunofluorescence obtained from perilesional skin of the left forearm showed granular deposition of IgA, complement component 3, and fibrinogen in a superficial dermal vascular pattern (IgA, original magnification ×40).

Five weeks after the initial presentation, the patient returned with a more severe eruption consisting of innumerable purpuric papules that coalesced in plaques on the abdomen, arms, and legs. He also had erythematous facial pustules and mild palmar petechiae (Figure 4). Three biopsies were performed, including 1 for DIF and 1 from a pustule on the forehead. Histology and DIF were again consistent with IgA small-vessel vasculitis. The forehead biopsy was compatible with steroid acne (attributed to recent prednisone use) and psoriasis.

A and B, Numerous purpuric thin papules coalescing in plaques on the dorsal hands and left medial thigh.

FIGURE 4. A and B, Numerous purpuric thin papules coalescing in plaques on the dorsal hands and left medial thigh.

Rheumatology was consulted, and adalimumab was discontinued 6 weeks after the initial presentation out of concern for drug-induced cutaneous vasculitis. Vasculitis work-up was unremarkable, including antineutrophil cytoplasmic antibodies, rheumatoid factor, cyclic citrullinated peptide, and serum protein electrophoresis. Oral dapsone was started at 100 mg/d, with the tentative plan of starting secukinumab if cutaneous symptoms improved. For 3 weeks, the patient’s cutaneous symptoms steadily improved.

Nine weeks after initial presentation to dermatology (3 weeks after discontinuing adalimumab) the patient self-administered his first dose of secukinumab at home. Several hours later, he reported sudden reappearance of vasculitis. He denied diarrhea, abdominal pain, bowel movement urgency, fevers, fatigue, and unintentional weight loss. Antistreptolysin O and hepatitis A antibodies were negative. He was instructed to hold secukinumab indefinitely.

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