Serum protein binding of thyroxine and diphenylhydantoin.
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Biomedical subjects
Publications and source records attributed to R W Lightfoot.
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The significance of abnormal serum anti-DNA and complement levels persisting in SLE patients on treatment has been explored. Instances when serologic abnormalities returned to normal were followed by a significantly longer mean duration of remission. When anti-DNA persisted at abnormal levels, a more severe exacerbation was likely to follow, although this result was not the case for persisting hypocomplementemia. These data did not result from two variants of SLE, one mild and one severe, because druation of remission correlated directly with dosage of steroid. Randomly discovered abnormalities in anti-DNA and complement levels were of limited predictive value, because they frequently persisted for over 1 year before exacerbations occurred. Hypocomplementemia resolved spontaneously without recognizable exacerbation in nearly half the observed instances.
HLA-B27 is frequently, but not invariably, found in patients with spondylarthritic diseases. Recently it has been shown that HLA-C-locus antigens w1 and w2 (w1/2) are in linkage disequilibrium with B27. A group of 139 patients with seronegative arthritis or spondylitis has been studied to determine the clinical and radiographic features associated with these antigens. An increased frequency of spondylarthritis was present in HLA-B27-negative, Cw1/2-positive patients when compared with B27- and Cw1/2-negative patients (P less than 0.01). In addition, a large group of patients who did not fulfill accepted criteria for a specific spondylarthritic syndrome were identified; the frequency of both HLA-B27 and Cw1/2 was greater in these individuals than in healthy blood donors. Thus HLA-Cw1/2 are spondylitis-associated antigens. These findings suggest that the critical genetic locus is neither B27 nor Cw1/2 but is a closely linked gene.
The presentation of SLE in one member of a twin pair has provided the background for discussion of genetic and environmental variables involved in the pathogenesis of the syndrome. There are promising leads (developing in parallel with studies in man and in NZB mice) suggesting that SLE results from the interaction of genetic factors with an etiologic stimulus provided by type-C RNA viruses. The principles of management of SLE have been reviewed briefly.
This double-blind multicenter study compares the effect of adding auranofin (AF) 3 mg bid or placebo to patients already taking nonsteroidal antiinflammatory drugs for rheumatoid arthritis. The 242 patients who completed 3 months of therapy demonstrated that the group receiving AF responded better than those receiving placebo. Of the 144 patients who completed 6 months coded medication, the efficacy in the AF group was superior to the placebo group in several parameters including a reduction in the number of painful or swollen joints, grip strength, dropout rate, and global efficacy as judged by the evaluating physician. A significant lowering of the Westergren erythrocyte sedimentation rate and immunoglobulin levels was noted in the AF treated patients. This study includes data summarizing the difference between both groups with respect to on-therapy conditions and toxicity.