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Herpes zoster infection followed by Henoch-Schönlein purpura in a girl receiving infliximab for ulcerative colitis.

To the Editor: We read with great interest the article by Lee et al on the development of Henoch-Schönlein purpura (HSP) after tumor necrosis factor(TNF) antagonist–etanercept therapy for psoriasis. To our knowledge, there is only another report of HSP in adults treated with etanercept for rheumatoid arthritis (RA), and a few reports of herpes zoster infections and vasculitides in patients receiving TNFantagonists (TA) (either etanercept or infliximab) for various diseases, such as RA, inflammatory bowel disease (IBD), Behçet disease, and amiloidosis. We report a case of herpes zoster followed by HSP in a 12-year-old girl receiving infliximab for treatment of left-sided ulcerative colitis. She was on mesalamine for 17 months, azathioprine for 15 months, and infliximab (5 mg/kg every 8 weeks after induction) for 6 months, because of steroid dependency. Until then, she had a good response to infliximab with no side-effects. Herpes zoster was diagnosed because of the development of a painful, vesicular rash in the left suprascapular and subclavicular regions; she was given acyclovir for 1 week with good response. Ten days after herpes zoster resolution, she was referred for the onset of right ankle painful swelling associated with an erythematous, purpuric rash on the lower extremities and buttocks. Laboratory values showed erythrocyte sedimentation rate, 91 mm/Hg; IgG, 2220 mg/dL; IgA, 195 mg/dL; IgM, 16 mg/dL; fecal occult blood, positive; and complete blood count, blood urea nitrogen, creatinine, transaminases, clotting tests, C-reactive protein (CRP), amylase, and urinalysis were normal . A clinical diagnosis of HSP was made. Within 1 week, cutanous and articular lesions disappeared; they relapsed with a milder extent after 1 month. Infliximab was discontinued; she was followed with mesalamine and azathioprine therapy, and so far she had no colitis or herpes zoster and HSP relapse. Infliximab is a chimeric monoclonal antibody used for the treatment of rheumatoid arthritis and inflammatory bowel disease. Most case reports of cutanous vasculitides and herpes zoster describe onset of symptoms within 3 months of infliximab initiation. Pathogenic theories for the development of vasculitides include autoantibody production; binding of the TNF antagonist to target cells inducing apoptosis and release of nuclear antigens; down-regulation of CRP, a molecule that clears apoptotic debris, with subsequent higher immunogenic load. Herpes zoster is caused by reactivation of the latent varicella zoster virus after a primary infection, more frequently in immunocompromised adults. In vitro studies have shown that TNFinhibits replication of the virus and expression of viral antigens; this antiviral activity may be blocked by the TNF antagonist. Herpes zoster infection is more common in patients receiving both immunosuppressive agents and the TNF antagonist. HSP is a systemic vasculitis characterized by deposition of IgA immune complexes in small vessels. It occurs more frequently in children than in adults, and is often preceded by a respiratory tract infection. The classic tetrad consisting of rash, arthralgias, abdominal pain, and renal involvement may occur in any order, over a period of days to weeks. Rare complications include intestinal perforations, involvement of central nervous system, heart, eyes, pancreas, and lungs. Skin biopsy with immunofluorescence investigation may confirm the diagnosis. The pathogenic role of TNFin HSP remains controversial. To our knowledge, this is the first report on these associated side-effects in a patient receiving infliximab. Although we cannot ascribe our patient’s herpes zoster and HSP pathogenesis solely to infliximab therapy, we think clinicians should be aware of these possible manifestations in patients with IBD receiving immunosuppressing drugs.