Recombinant human epidermal growth factor enhances wound healing of pyoderma gangrenosum in a patient with ulcerative colitis.

摘要

To the Editor:A 38-year-old woman was admitted to our department because of a progressive, painful ulceration on the left heel pad. Fifteen years ago she had been diagnosed with ulcerative colitis (UC) involving the entire colon. She has maintained disease remission with 5-aminosalicylic acid treatment the onset of symptoms is rapid, somemonths or years after continuous therapy. Lupus-like syndrome occasionally develops as a side effect of long-term medication with several drugs, including infliximab. An immuno-logic characteristic of drug-induced lupus is the presence of auto-antibodies. Specifically, ANAs have been detected in patients treated with infliximab for Crohn's disease (CD), rheumatoid arthritis (RA), and psoriasis. Anti-double-stranded DNA antibodies are associated with drug-induced lupus and this autoimmune syndrome has been reported in clinical trials as well as in individual patients after infliximab therapy. In a large series of patients with CD treated with infliximab, Colombel et al identified 3 patients with clinical symptoms consistent with drug-induced lupus after 5, 10, and 19 infusions. All patients had ANA, 2 had anti-double-stranded DNA antibodies, and 2 had anti-his-tone antibodies. Positivity for double-stranded DNA antibodies was suggested to be a feature of infliximab-related systemic lupus erythematosus cases. Anti-histone antibodies, albeit more prevalent, are not specific of drug-induced lupus. The precise cause of this autoimmune phenomenon has not been elucidated yet. Four main mechanisms were hypothesized: hap-ten hypothesis, direct cytotoxicity (drug metabolites alter degradation and clearance of apoptotic cells, which eventually leads to loss of tolerance to self-antigens), lymphocyte activation, and disruption of central immune tolerance.9 In infliximab-treated patients, increased cell lysis may lead to exposure to self-antigens. Alternatively, inhibition of TNF signaling per se may lead to autoimmune reactions. Treatment with biologic agents should be discontinued inpatients who develop symptoms consistent with lupus-like syndrome.