Digital vasculitis in a patient with rheumatoid arthritis: good response on anti-TNF blockade
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KeywordsRheumatoid Arthritis Vasculitis Immunosuppressive Drug Swell Joint Count Active Vasculitis
Rheumatoid arthritis (RA) may be complicated by vasculitis. Vasculitis usually affects small vessels of the skin causing nailfold infarcts, but may also affect larger vessels and cause severe damage to internal organs. In such cases, treatment with high doses of corticosteroids or other immunosuppressive drugs may be necessary. TNF-alpha blockade has been shown to be an effective and safe treatment for RA, but thus far no reports have addressed the effect of TNF-alpha blockade on extra-articular manifestations of RA, such as vasculitis. We report a patient with RA and nailfold infarcts which repeatedly disappeared for several weeks following monthly i.v. injections with an anti-TNF alpha receptor fusion protein.
A 46 year old woman was diagnosed as having rheumatoid factor positive, erosive RA in 1982. Due to the uncontrollable disease she was included in 1994 in a study with Ro 45-2081, a fusion protein combining two p55 TNF receptors with the Fc component of an IgG human antibody (Roche, Basel, Switzerland, sTNFR:Fc). After a three months placebo controlled phase she was treated with 50 mg sTNFR:Fc every four weeks. Clinical response was impressive with swollen joint counts decreasing from 32 to 5 and C-reactive protein CRP levels declining from 95 at baseline to 20 after the first injection. Low disease activity was sustained for the following years. Besides sTNFR:Fc her medication consisted of oral prednisone 5 mg a day and occasionally paracetamol 500 mg. In the spring of 1999 she first noticed nailfold infarcts on the fingers of both hands. These lesions disappeared after every injection of sTNFR:Fc and reappeared three weeks thereafter when the clinical effects of sTNFR:Fc were decreasing. This effect on the digital vasculitis has been well documented during several cycles of sTNFR:Fc administration.
The prompt disappearance of nailfold infarcts after sTNFR:Fc administration observed in our patient strongly suggests a therapeutic effect of sTNFR:Fc on active vasculitis. This observation raises the question whether blocking of TNF-alpha might also be effective in more severe forms of vasculitis and possibly other extra-articular manifestations of RA, some of which are life threatening and are currently treated with high doses of corticosteroids and immunosuppressive drugs.