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- Author: W. J. IRVINE x
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SUMMARY
Human thyroid cells were grown in tissue culture in media containing normal human serum, Hashimoto serum, and rabbit sera containing antibodies to purified human thyroglobulin and to crude thyroid extract, respectively. The thyroid cells grew equally well in all media, with the exception of the rabbit serum containing antibodies to crude thyroid extract.
Intact thyroid cells obtained from tissue culture failed to fix Hashimoto antibodies in the presence of complement, whereas the constituents of disrupted thyroid cells gave a strongly positive complement-fixation test with Hashimoto serum. It is therefore suggested that the intact thyroid cell is impermeable to complement-fixing Hashimoto antibody.
The evidence afforded by the present work adds further weight to the belief that Hashimoto's disease may not be due to a simple auto-immunizing process consequent upon the interaction of thyroid antigen and the known circulating auto-antibodies. Evidence in support of an alternative hypothesis involving 'cell-bound' antibodies with disruption of the follicular basement membrane is discussed.
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It has been established in animals that anterior pituitary hormones control their own secretion by regulating at a hypothalamic level the release of their hypothalamic factors (Motta, Fraschini & Martini, 1969). If a negative 'short-feedback' of thyroid-stimulating hormone (TSH) on the hypothalamus exists in man, the high plasma TSH levels of untreated primary hypothyroidism should fall markedly after the administration of bovine TSH which shares the biological, but not the immunological, properties of human TSH. This report describes the effects of bovine TSH on human plasma TSH (H-TSH) levels in patients with primary hypothyroidism.
Twenty-seven patients with untreated primary hypothyroidism were studied, of whom 20 had been treated with 131I and four by subtotal thyroidectomy for thyrotoxicosis. The remaining three patients had spontaneous primary hypothyroidism. The diagnosis of primary hypothyroidism was made on clinical grounds and on the basis of a low serum protein-bound iodine (< 3·8 μg/100 ml),
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Thyrotrophin releasing hormone (TRH) is a potent stimulus of the release of thyrotrophin (TSH) and prolactin from the anterior pituitary gland of man (Bowers, Friesen, Hwang, Guyda & Folkers, 1971; Jacobs, Snyder, Wilber, Utiger & Daughaday, 1971; L'Hermite, Vanhaelst, Copinschi, Leclercq, Golstein, Bruno & Robyn, 1972; Toft, Boyns, Cole, Groom, Hunter & Irvine, 1973). Whereas the plasma TSH response to intravenous TRH is enhanced in patients with primary hypothyroidism, and abolished in patients with thyrotoxicosis, the relationship between thyroid status and prolactin release by TRH is not clear. Although there is a small increase in plasma prolactin in hypothyroidism (Jacobs et al. 1971; Toft et al. 1973) the response to TRH is not significantly different from that seen in normal subjects (Toft et al. 1973). Recently, Snyder, Jacobs, Utiger & Daughaday (1973) found that when patients with thyroid disease were studied before and after treatment, the prolactin response to TRH
