Acute inflammatory polyarthritis following streptokinase.
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Biomedical subjects
Publications and source records attributed to R Clague.
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Properdin factor B (Bf) phenotyping was carried out in 392 patients with rheumatoid arthritis (RA) and in 360 controls. In RA there were increased frequencies of both the Bf*S gene (83 vs 78%; pc = 0.0003) and the BfSS genotype 73 vs 61%; pc = 0.0002) and reduced frequencies of the Bf*F1 gene (0.5 vs 2.2%; pc = 0.03) and the BfFS genotype (20 vs 29%; pc = 0.0007). The frequencies of Bf*S in DR4 positive and DR4 negative RA were similar so that the findings were not accounted for by linkage disequilibrium between DR4 and Bf*S.
We have studied HLA haplotypes, autoimmune diseases and circulating autoantibodies in 23 families with multiple cases of rheumatoid arthritis; 76 per cent of rheumatoid arthritis and 70 per cent of non-rheumatoid individuals were positive for HLA-DR4. The haplotypes Bw44-Bf*S-DR4; B40-Bf*S-DR4; and B15-Bf*S-DR4 were found in 13, 9 and 7 per cent of probands respectively and the B15-Bf*S-DR4 haplotype was found between four and five times more frequently in DR4-positive rheumatoid arthritis than in DR4 positive, non-rheumatoid arthritis families. Rheumatoid arthritis segregated with a DR4 positive haplotype in 13 families and with a DR4 negative haplotype in seven. Analysis of HLA haplotype sharing showed greater than random sharing by affected siblings which is in keeping with genes within the MHS influencing susceptibility to rheumatoid arthritis. Autoimmune thyroid disorders were seen in 8 per cent of family members investigated. They were significantly more frequent in those families in which rheumatoid arthritis segregated with a non-DR4 bearing HLA haplotype. This suggests that genes for autoimmune thyroid disease might predispose to rheumatoid arthritis independently of DR4. These genes are probably not HLA-linked, as there was no trend for HLA haplotype sharing to be increased in sibling pairs with either rheumatoid arthritis and thyroid disease or rheumatoid arthritis and thyroid autoantibodies respectively.
The segregation of HLA haplotypes with rheumatoid arthritis (RA) was studied in 13 selected, multicase families. HLA-DR4 was present in 77% of RA probands (32% controls). No single haplotype was associated with RA in different families. Analysis of HLA haplotype sharing in affected relatives showed no significant difference to the expected distribution. It seems likely therefore that the HLA-DR4 antigen itself rather than a linked susceptibility gene predisposes to RA. In 2 of 3 HLA-DR4 negative families, there were members with autoimmune thyroid disease. It is suggested that genetic susceptibility to RA may be associated with both HLA-DR4 and genes for autoimmune thyroid disease.
Triiodothyronine (T3) suppression and thyrotropin-releasing hormone (TRH) tests were used to study thyroid function in 50 patients with thyroid disease. The results of the thyroid function tests were compared with the levels of serum thyroid-stimulating immunoglobulins (TSI) measured by a radio-receptor assay. In euthyroid and hyperthyroid patients, the presence of TSI corresponded with the absence of TSH control of thyroid function. However, in two hypothyroid patients with serum TSI levels readily detectable in the receptor assay, T3 suppression and TRH tests indicated that thyroid function was under TSH control.