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Radiation Medicine Centre, Bio-Medical Group, Bhabha Atomic Research Centre, Tata Memorial Hospital, Parel, Bombay-12, India
(Received 25 March 1974)
Pendred's syndrome is characterized by familial goitre, nerve deafness and a partial release of radio-iodine from the thyroid on perchlorate administration. This last was thought to be due to impaired activity of peroxidase enzymes or to some abnormality of receptor proteins where iodination occurs. Burrow, Spaulding, Alexander & Bower (1973) reported that peroxidase activity in such patients is normal but studies on thyroidal iodoproteins have shown variable results (Medeiros-Neto, Nicolau, Kieffer & Ulhoa-Cintra, 1968; Milutinovic et al. 1969).
A 22-year-old deaf-mute woman (N.G.) with a goitre which had progressively increased in size from infancy was euthyroid in all respects: basal metabolic rate, 10·0%; serum cholesterol concn, 174·3 mg/100 ml; tri-iodothyronine (T3) red blood cell uptake, 14·6%; stable protein-bound iodine levels, 5·7 μg/100 ml. Radioactive iodine uptake by the thyroid was 65·7%
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Abstract
Administration of a goitrogen (methimazole) and a low iodine diet to rats over a two-week period resulted in hypothyroidism and thyroid hyperplasia compared with controls (control: total serum thyroxine (T4) 66 ± 4 nmol/l, thyroid weight 5±1 mg/100 g body weight; experimental: T4 undetectable, thyroid weight 27 ± 4 mg/100 g body weight after 2 weeks of treatment; mean ± s.d., n=10). Immunohistochemistry carried out using a specific endothelial cell marker, CD31, and morphometric analysis (point counting of immunopositive cells) revealed that the progression of goitre in the rat thyroid is accompanied by an increase in capillary endothelial cell growth (neovascularisation). Fibroblast growth factor-2 (FGF-2) immunohistochemistry revealed widespread staining for the protein in the follicular cells of control glands. Less intense staining was found in the stroma and follicular cell nuclei. During hyperplasia and subsequent neovascularisation there was a progressive increase in the FGF-2 immunoreactivity at all locations during the two-week treatment period. Thrombospondin-1 (TSP1) immunoreactivity in the control rat thyroid was found in the stroma and in the endothelial cells, while weak follicular cell staining was also present. In the goitrous rat thyroid the TSP1 immunoreactivity was present after 1 week of treatment in the endothelial cells and most follicular cells, whilst stromal localisation was weak. After week 2 of treatment the endothelial cell and stromal localisation was no longer apparent, although a follicular localisation was still present. Transforming growth factor-β1 (TGFβ1) immunoreactivity was present in the cytoplasm of a minority of the follicular cells in control rat thyroids, while their nuclei were unstained. In the goitrous rat thyroid an increased intensity of staining for TGFβ1 was seen in all follicular cells, many of which now also demonstrated immunopositive nuclei, within one week of goitrogen administration. These results show that in the hyperplastic thyroid increases in FGF-2 and TGFβ1, and decreases in TSP1, accompany angiogenesis. These factors may interact in an autocrine/paracrine relationship to stimulate the neovascularisation that occurs during goitre formation.
Journal of Endocrinology (1996) 148, 485–499
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SUMMARY
Two siblings, a brother (H. B.) and a sister (R. B.) with long standing goitres were investigated. Radioactive iodine uptake by the thyroid was increased and a significant portion of the plasma radioactive iodine was not extractable with butanol. Chromatography of butanol extracts of serum after radioactive iodine administration showed distinct peaks of triiodothyronine and thyroxine. Microscopic examination of the surgical specimens of the goitres showed Hürthle cell carcinoma with follicles devoid of colloid in both specimens. Sucrose density gradient centrifugation, gel filtration on Sephadex G-200, salting out procedures, starch gel electrophoresis and immunological tests of the supernatant soluble fraction of thyroid homogenates showed a lack of thyroglobulin. Further fractionation of the soluble proteins showed that albumin was apparently involved in the synthesis of thyroid hormones in the absence of thyroglobulin.
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Pharmacological doses of glucocorticoids inhibit thyroid function in man and laboratory animals due to suppression of thyrotrophin (TSH) secretion (Wilber & Utiger, 1969). Administration of prednisolone or dexamethasone for 1–2 days results in a suppression of basal serum TSH levels in normal subjects and in patients with primary hypothyroidism, whilst the pituitary TSH reserve capacity, as assessed by the response to synthetic thyrotrophin releasing hormone (TRH), remains unaltered (Wilber & Utiger, 1969; Besser, Ratcliffe, Kilborn, Ormston & Hall, 1971; Haigler, Pittman & Hershman, 1971). However, impairment of serum TSH response to administered TRH does occur in patients treated with glucocorticoids for 1 or more months (Otsuki, Dakoda & Baba, 1973). These studies suggest that glucocorticoids may inhibit TSH secretion at both hypothalamic and pituitary levels but the main effect of the short-term treatment is suppression of TRH production.
Nicoloff, Fisher & Appleman (1970) found that the circadian rhythm of thyroidal
