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The authors followed up the incidence of permanent hypothyroidism in 35 patients with subacute thyroiditis (SAT) in their past history. The investigations were made one to four years after the acute episode. Ten of these presented repeated recurrences despite the therapy with glucocorticoids. The investigations included serum determination by RIA of T4, T3, TSH and thyroglobulin as well as of circulating thyroid antibodies. Permanent hypothyroidism subsequent to SAT occurred in two patients. In one of them it occurred following thyroid surgery performed for repeated recurrences. Both patients presented high levels of circulating thyroglobulin antibodies suggesting a possible transition to autoimmune thyroiditis. In the authors' opinion permanent hypothyroidism is likely to develop after SAT only in association with an autoimmune process or after thyroid surgery.

Calcium ions are of irnportance for the function of every cell in the organism, and this applies also for the fat eells. In incubated slices of rabbit adipose tissue, ACTH-or epinephrine-stirnulated Iipolysis was accompanied by an increase in.tissue calcium (A/cgün and Rudman 1969). Werner and Löw (1973, 1974) investigated the effects of the hormones of calcium homeostasis, parathyroid hormone and calcitonin, upon lipolysis of incubated rat adipose tissue pieces and demonstrated that parathyroid hormone induced a 3 to 5 fold inerease in glycerol release, which was aecompanied by enhanced calcium aeeumulation in the tissue, whereas calcitonin exerted opposite effeets. As the question remained open whether these meehanisms were instrumental in the human organism, too, the influences of parathyroid hormone and of calcitonin upon incubated slices of human adipose tissue were studied.

The expression of thyroid hormones receptors in osteoblasts and osteoclasts has involved these cells as direct targets for triiodothyronine (T3), but thyroid hormones may also interact with other hormones or local growth factors to exert their actions on bone cells. Among these, growth hormone (GH) is recognised as participating in the acquisition and maintenance of bone mass and exerting stimulatory effects on human osteoblastic cells. The aim of this study was to investigate T3 effects on primary human adult osteoblast-like cells (HOB) as well as to test for possible interactions between T3 and GH on bone cell metabolism. Primary human bone cell cultures were obtained by outgrowth from trabecular bone fragments from the hip and knee. Dose-response studies demonstrated enhanced [3H]-thymidine incorporation for T3 at 10(-9), 10(-8), 10(-7) and 20(-7) M, with a maximal response of 162.81 +/- 12.97 % with T3 10(-8) M, compared to vehicle (p < 0.001). Time-course studies showed an increased osteoblast-like cell proliferation after 24 h, followed by a decrease of cell proliferation by 48 h and 72 h of culture, respectively, when compared to control cells, with a maximal response after 72 h (T3 10(-10) M: 45.21 +/- 6.97 %, p < 0.01). In addition, T3 markedly increased specific alkaline phosphatase (AP) activity in HOB (10(-10) M: 169.86 +/- 12.14 % vs. control, p < 0.001), but no significant influence on type I procollagen propeptide (PICP) production was observed. At 10(-9) - 10(-7) g/ml, GH significantly enhanced HOB proliferation (p < 0.001) however, GH effects were not dose-dependent. Triiodothyronine, at a high concentration (10(-7) M), stimulated GH-receptor (GHR) mRNA levels by 165.20 +/- 16.54 % after 24 h (p < 0.05). Correspondingly, a synergistic effect of T 3 with the same concentration and GH on cell proliferation in human adult osteoblast-like cells was found.

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