Rituximab and thyroid function.

摘要

Report of a Case. In August 2006, a 39-year-old woman with rheumatoid arthritis (RA) was seen at the outpatient clinic for exacerbation of RA. In the previous few months, she had progressively swollen and painful joints, notably her wrists, knees, and feet. A review of her medi- cal history revealed that in addition to an erosive, rheumatoid factor anticitrullinated protein antibody-positive RA since 1995 she had autoimmune hypothyroidism and diabetes mellitus type 1 since 1986. For these conditions she used long-acting (24 U/d) and short-acting (50 U/d) insulin and L-thyroxine (262.5 ug/d). Findings from physical examination were unremarkable except for polyarthritis (shoulders, elbows, wrists, knees, ankles, hands, and feet). Her RA disease activity score of 28 joints (DAS28) was 8.3 (low disease status, DAS28<3.2). Type 1 diabetes mellitus and hypothyroidism were in a well-controlled condition (hemoglobin A_(1c) level of 6.8% [reference range, 4.0%-6.0%] [to convert to proportion, multiply by 0.01], thyrotropin (TSH) level of 1.18 mU/L [reference range, 0.35-4.70 mU/L], and free thyroxine [FT_4] level of 20 pmol/L [to convert to nanograms per deciliter, divide by 12.871] [reference range, 10-23 pmol/L]). Because this patient was refractory to tumor necrosis factor-blocking agents (etanercept and infliximab) and disease-modifying antirheumatic drugs (sulfasalazine and metho-trexate), B-lymphocyte depletion therapy (rituximab) was started in a 2-week cycle of 1000 mg intravenously, with the addition of 100 mg of methylprednisolone to prevent infusion-related adverse events.