Abstract
Adult primary myxoedema is usually due to an autoimmune thryoiditis characterized by progressive shrinking of the thyroid gland, loss of epithelium, dense infiltration by sensitized lymphocytes and plasma cells with final replacement of the gland by a fibrous scar1. Antibodies directed against thyroglobulin (TgHA) and microsomal antibodies (McHA), detectable years before the onset of hormonal failure, and cell-mediated immune mechanisms contribute to the pathogenesis2. When 90% of the gland is destroyed, the secretion of thyroid hormones (T3/T4) falls below normal needs and pituitary thyrotrophs react by producing over 100 times the normal amount of thyroid-stimulating hormone (TSH)3 which should normally lead to regrowth of the gland as happens in goitrous Hashimoto thyroiditis4. The inability of the thyroid in primary myxoedema to respond to the trophic action of TSH suggested that blocking antibodies exist in this disease which compete with TSH for its receptors5,6. The trophic effect of TSH can be assayed in vitro by measuring DNA-synthesis by Feulgen cytophotometry7; elevated pentose-shunt oxidative activity correlates with DNA synthesis8. Here we report that immunoglobulins from patients with adult, primary myxoedema block the trophic effect of TSH, as assessed by this in vitro system. This is in marked contrast to the growth stimulation induced by immunoglobulins from patients with thyrotoxic Graves' disease with prominent goitres7.
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Drexhage, H., Bottazzo, G., Bitensky, L. et al. Thyroid growth-blocking antibodies in primary myxoedema. Nature 289, 594–596 (1981). https://doi.org/10.1038/289594a0
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DOI: https://doi.org/10.1038/289594a0
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