| Spitzweg et al., Rochester, MN, USA, and Marburg, Germany, used both monoclonal and polyclonal antibodies against the human iodide sodium symporter (hNIS) protein, to investigate NIS immunoreactivity in different organs. Human salivary glands showed immunoreactivity in ductal cells, acinar cells, and interlobal ductal cells. Gastric and colonic mucosa showed intense protein staining in chief and parietal cells in gastric mucosa, and in epithelial cells of colonic mucosa. In normal human pancreas, NIS protein was found in ductal cells, exocrine parenchymal cells and Langerhans islets. From this spread expression of hNIS, the authors hypothesize that hNIS may serve as a common antigen in the pathogenesis of polyglandular autoimmune diseases. (Comment: NIS antibodies have already shown to be circulating in patients with autoimmune thyroid disease.) Sanders et al., Cardiff, UK, and Poznan, Poland, tested whether the region of the TSHR to which TSHR autoantibodies (TRAB) bind, are different when TRAB act as TSH agonists or as antagonists. The interaction between TRAB and TSHR was studied using porcine TSHR that was labelled with a monoclonal antibody to the TSHR C terminus. The authors analyzed sera from 20 patients with Hashimoto's disease, 10 patients with systemic lupus erythematodes and 50 patients with Graves' disease. They found that irrespective if TRAB acted as agonists or antagonists, they principally bound to the same region of the TSH receptor. (This work is now published in full in J Clin Endocrinol Metab 84:3797,1999). (Comment: From the results of this study the following question emerges: If the binding site is (exactly?) the same, how is the opposite effect of the agonists and antagonists being explained?) Benvenga et al., Messina, Italy, measured thyroid hormone antibodies in 20 patients with Sjögren syndrome, 23 with rheumatoid arthritis, and 88 with Hashimoto's disease. IgG thyroid hormone antibodies occurred in 50%, 26%, and 20% of the groups respectively, while these figures were for IgM thyroid antibodies, 26%, 23%, and 10% respectively. The antibodies included those against T3 or T4, or both. There was a preference for T3 antibodies. (Comment: It is noteworthy that in Hashimoto's disease the prevalence of thyroid hormone antibodies is lowest, while TG- and TPO-antibody titers are probably highest.) Brix et al., Odense, Denmark, evaluated the genetic contribution in the etiology of Hashimoto's disease/atrophic thyroiditis in a Danish twin pair study, based on a population sample of 2.945 Danish female-female twin pairs, born between 1953 and 1972. The overall prevalence of (individual) autoimmune hypothyroidism was 0.41% (24/5.890). There was no difference in prevalence between monozygotic (n = 11) and dizygotic (n = 13) twin individuals (0.42% and 0.40% respectively). The concordance rate for monozygotic pairs was 0.55 but 0 for dizygotic pairs (p = 0.01). This difference suggests that genetics play a role in the pathogenesis of autoimmune thyroid disease in humans. However, the fact that the concordance rate in monozygotic twins was below 1 suggests an additional role for environmental factors in the etiology. Innociencio et al., Campinas, SP, Brazil, measured TgAb and TPOAb in 25 patients with systemic sclerosis (SS), 25 with rheumatoid arthritis (RA), and 13 with antiphospholipid syndrome (APL). In the total group of patients, 8% had subclinical hypothyroidism, and 6% subclinical hyperthyroidism. TgAb and/or TPOAb were present in 13/25 SS patients, 8/25 RA patients, and 0/13 APL patients. The prevalence of thyroid antibodies was significantly above normal in SS and RA patients (p < 0.02), Kurtev et al., Sofia, Bulgary, found in a group of 71 children and adolescents with insulin dependent diabetes mellitus, goiter formation in 43/71 and TgAb and/or TPOAb in 40/71 of patients. Ultrasound pictures were suspected for autoimmune thyroiditis in 15/24 patients. The authors conclude an increase prevalence of autoimmune thyroid disease in this group of subjects. (Comment: It was not mentioned if these subjects were living in an area of iodine deficiency.) Hollowell et al., Boston, MA, and Los Angeles, CA, USA, evaluated 31.000 U.S. men, women and children of = 6 yr., sampled to represent the geographic and ethnic distribution of the US population (NHANES III, 1988-1994), for thyroid function and circulating thyroid antibodies. TgAb and TPOAb were positive in 11.5% and 12.6% respectively. The proportion increased significantly with age and was less among blacks than among whites. TgAb and urine iodide excretion > 1000 ug/g creatinine, were associated with (elevated) TSH > 4.5 µU/ml. A TSH > 4.5 µU/ml, between 40 and 80+years, increased from 5.7 to 14.4% in females and from 3.7 to 10.2% in males. The authors conclude that TSH and thyroid antibody values should be interpreted in the context of age, sex, and race. (Comment: This study shows (again) that also in men an elevated serum TSH after middle age is a common feature. I think that routine determination of serum TSH in middle aged and older subjects of both sexes, will not only be of benefit to potential patients, but also economical on a cost-effective basis. Furthermore a high iodine promotes thyroid failure, as has been reported also from Denmark.) |
