We report a 29-year-old Japanese woman with disseminated intravascular coagulation (DIC) and adult onset Still's disease (AOSD). Her disease was refractory to high-dose glucocorticoids, two courses of steroid pulse therapy, and addition of cyclosporine (3.5 mg/kg/day). The serum interleukin-6 level was markedly elevated. Therefore, we administered an anti-interleukin-6 receptor antibody (tocilizumab, 8 mg/kg fortnightly), which dramatically improved her symptoms and the levels of acute-phase proteins. In addition, rapid tapering of the glucocorticoid dose was possible. Four months later, she was maintained on tocilizumab infusion once a month with low-dose steroid therapy. Cyclosporine is one of the first-line immunosuppressants for AOSD, especially when associated with DIC, hepatic failure, or hemophagocytic syndrome. In patients with cyclosporine-resistant AOSD, tocilizumab may be another useful option.
Aim: The tuberculin skin test (TST) is used to diagnose tuberculosis; however, the influence of tumor necrosis factor (TNF) inhibitors on the test is unclear. This study investigated whether therapy with TNF inhibitors suppresses the TST reaction due to immunosuppression or whether the TST reaction increases due to reactivation of latent Mycobacterium tuberculosis infection.Method: Ninety-one patients with rheumatoid arthritis receiving TNF inhibitors (40 using infliximab and 51 using etanercept) were studied. The TST was performed before starting TNF inhibitors (T1) and more than 1 year after starting them (T2).Results: At T1, the reaction was negative in 45 patients, weakly positive in 21 patients, moderately positive in 18 patients and strongly positive in seven patients, while the numbers at T2 were 44, 20, 16 and 11, respectively. There were no significant differences of the TST reaction between T1 and T2 in all patients (P = 0.657), patients using infliximab (P = 0.462) or patients using etanercept (P = 1.00). No patients with a strongly positive TST reaction at T1 became negative at T2. However, two patients who were negative at T1 became strongly positive at T2. Although they had no signs of M. tuberculosis infection, isoniazid prophylaxis was given.
Conclusion:The TST reaction was not suppressed after more than 1 year of therapy with TNF inhibitors. Patients in whom the TST reaction changes from negative to strongly positive may need appropriate prophylaxis.
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