S Halevy1, A D Cohen, E Livni. 1. Department of Dermatology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Abstract
BACKGROUND: Drug-related T-cell activity in cutaneous drug reactions may be assessed by in vitro cytokine release tests. The diagnostic role of in vitro drug-induced interferon-gamma (IFN-gamma) release was evaluated in a patient with Stevens-Johnson syndrome. CASE REPORT: Stevens-Johnson syndrome was diagnosed in a 58-year-old man, treated with colchicine (1 mg daily for 39 days) and allopurinol (300 mg daily for 13 days). Based on a clinical-epidemiologic score, allopurinol was more likely to be the causative agent. In vitro drug-induced IFN-gamma release test was conducted on this patient and on two controls, using an enzyme-linked immunoabsorbent assay (ELISA) technique. Increased IFN-gamma release was observed following an in vitro challenge of the patient's lymphocytes with allopurinol, but not following in vitro challenge with colchicine. An in vitro challenge with allopurinol in two control patients, treated with allopurinol without adverse drug reactions, did not induce a significant increase in IFN-gamma release. CONCLUSIONS: The role of allopurinol as the drug responsible for the induction of Stevens-Johnson syndrome in our patient was confirmed by in vitro allopurinol-induced IFN-gamma release, which may indicate a drug-specific immune response.
BACKGROUND: Drug-related T-cell activity in cutaneous drug reactions may be assessed by in vitro cytokine release tests. The diagnostic role of in vitro drug-induced interferon-gamma (IFN-gamma) release was evaluated in a patient with Stevens-Johnson syndrome. CASE REPORT: Stevens-Johnson syndrome was diagnosed in a 58-year-old man, treated with colchicine (1 mg daily for 39 days) and allopurinol (300 mg daily for 13 days). Based on a clinical-epidemiologic score, allopurinol was more likely to be the causative agent. In vitro drug-induced IFN-gamma release test was conducted on this patient and on two controls, using an enzyme-linked immunoabsorbent assay (ELISA) technique. Increased IFN-gamma release was observed following an in vitro challenge of the patient's lymphocytes with allopurinol, but not following in vitro challenge with colchicine. An in vitro challenge with allopurinol in two control patients, treated with allopurinol without adverse drug reactions, did not induce a significant increase in IFN-gamma release. CONCLUSIONS: The role of allopurinol as the drug responsible for the induction of Stevens-Johnson syndrome in our patient was confirmed by in vitro allopurinol-induced IFN-gamma release, which may indicate a drug-specific immune response.