We found HLA‐DR5 to be present among 53% of 40 patients with goitrous autoimmune (Hashimoto's) thyroiditis compared to 26% of 80 controls. No deviations from those expected in the incidences of HLA‐A, B, C antigens were seen. In contrast HLA‐DR3 was increased among 50 patients with atrophic thyroiditis (65%) compared to controls (24%). These findings stress the immunogenetic heterogeneity between the goitrous and atrophic varieties of thyroiditis.
One‐hundred‐and‐forty‐seven patients with autoimmune thyroiditis were studied with respect to HLA antigens as they related to various clinical features. HLA‐B8 was found to be significantly increased among 59 patients with atrophic thyroiditis (57% vs. 26% for controls) but was identical to controls in 88 patients with goitrous thyroiditis (26%). No relation was found in either group between B8 and thyroid autoantibody titer or, in the case of goitrous thyroiditis, the rate of progression of the disease. Thus a link seems to be established between Graves' disease and atrophic thyroiditis in that both are significantly associated with HLA‐B8. This study stresses the need to take clinical features into consideration when examining for HLA/disease associations.
In order to further elucidate the genetics of Graves’disease, we studied two families with several affected members, as well as tested the degree to which HLA haplotypes were shared in affected sibpairs. Further, we sought to identify the disease related haplotypes by determining the haplotypes shared among affected parent‐child combinations. In one family, two affected sibs differed at four possible parental HLA haplotypes; no evidence of recombination was observed which could account for the result. In the other family, five siblings were affected. Four out of the five affected sibs shared the maternal haplotype HLA‐A11, Bw51, Cw5, Cw‐, DRw5, Bfs, GLO1, whereas three shared the paternal haplotype HLA‐Al, B8, Cw‐, DRw3, Bf and GLO1. Looking at haplotype sharing, two pairs of sibs were found to be HLA identical, whereas the fifth sib shared one haplotype with one of these pairs but not with the other. Out of 14 (eight of our own and six from the literature) affected sibpairs examined, nine were found to be HLA identical and four shared one haplotype, suggesting that the contribution of both paternal haplotypes may be necessary for the susceptibility to the disease. Fourteen parent‐child combinations were studied; in only three out of 13 in which the shared haplotype could be ascertained was the haplotype B8 positive; this distribution is similar to controls. However, of the remaining 10 combinations which did not share a B8 positive haplotype, five were B8 positive at one or the other of the nonshared haplotypes.
LettersAnaemia in rheumatoid arthritis SIR, The unreferenced assertion by Farah, Sturrock, and Russell that iron deficiency anaemia is a common feature of rheumatoid arthritis and is often caused by an asymptomatic peptic ulcer' should not go unchallenged. The diagnosis of iron deficiency in patients with inflammatory disease is difficult, unless bone marrow estimations of iron stores are performed. Perhaps the authors would care to support the statement regarding the prevalence of iron deficiency in rheumatoid arthritis with a suitable reference.In our experience upper gastrointestinal lesions, including asymptomatic peptic ulceration, are common in patients taking non-steroidal anti-inflammatory drugs and are found no more frequently in patients whose anaemia is microcytic, or those with positive faecal occult bloods, than in those with a normocytic anaemia or negative faecal occult bloods.2 This observation together with other evidence3 strongly suggests that upper gastrointestinal lesions are not the cause of iron deficiency when it does occur in rheumatoid arthritis. The mere coincidence of two abnormalities does not imply any causal association.
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