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The frequency of polyglandular autoimmune syndrome Type II, (idiopathic or autoimmune Addison's disease associated with autoimmune thyroid disease, and/or insulin-dependent diabetes mellitus), was retrospectively investigated in 44 patients (26 females and 18 males) with idiopathic Addison's disease (median age at onset 32.5 years, range 8-62; median observation time 17 years, range 0.5-41) evaluated between 1966 and 1988 in the Department of Endocrinology, General Hospital, Malmö. Twenty-two patients (16 females and 6 males) fulfilled the criteria for polyglandular autoimmune syndrome Type II and of these 16 had autoimmune thyroid disease and 9 insulin-dependent diabetes mellitus. In 7 of 9 patients insulin-dependent diabetes mellitus developed prior to Addison's disease, whereas autoimmune thyroid disease was diagnosed before as well as after Addison's disease and with a similar age distribution as Addison's disease. In conclusion, the present study indicates that polyglandular autoimmune syndrome Type II occurs in about 50% of patients with idiopathic Addison's disease and that autoimmune thyroid disease is more common than insulin-dependent diabetes mellitus in these patients. The present study also indicates that insulin-dependent diabetes mellitus precedes Addison's disease in a majority of these patients and usually develops at a young age, whereas autoimmune thyroid disease precedes as well as succeeds Addison's disease and occurs at all ages in these patients.

Propylthiouracil (PTU) and propranolol can suppress, while methimazole (MMI) can enhance, mitogenic activation of lymphocytes. The present study investigated whether this effect of PTU, as has been shown for propranolol, relates to local anaesthetic activity. MMI (1 mM) but not PTU (1 mM) reduced the action potential in rat skeletal muscle. Thus, PTU seems to lack local anaesthetic activity. Moreover, the recorded local anaesthetic capacity of MMI hardly explains the stimulatory influence of MMI on lymphocyte activation. Apparently, the interference of MMI and PTU with lymphocyte activation seems to be due to another mechanism than local anaesthetic activity.

Biological growth activity (bioassayable GH) was determined in blood from healthy individuals and from patients with acromegaly using the rate of longitudinal bone growth in hypophysectomized rats with tetracycline as intravital marker. Also radioimmunoassayable GH and somatomedin A activity were determined. In pooled plasma or serum from normal subjects no bioassayable growth activity was demonstrated. In the clinically active acromegalic patients as a group as well as in one individual patient there was a significant (P less than 0.05) bioassayable growth activity in serum as compared to serum from normal subjects. The bioassay determination of GH in plasma/serum from normal subjects and acromegalic patients was hampered by the toxicity and the problems connected with the administration of large volumes.

In this prospective study, 25 consecutive patients with untreated primary hypothyroidism were tested with a highly sensitive perimetric technique, since a high prevalence of visual field defects has been described in this condition. All patients had clinical hypothyroidism, a serum TSH value greater than 20 mU/l (reference range 0.4-4.0) and decreased/low normal serum total T4 concentration. Visual fields were tested with fully automated threshold-measuring computerized perimetry of the central 30 degrees field. Interpretation of fields included computer-assisted analysis provided by a perimetric statistical programme package. In 23 patients, conventional inspection and computer-assisted analysis showed no visual field defects. Two patients were excluded from the latter analysis: one patient who did not respond adequately at computerized perimetry and in whom manual field tests were entirely normal: one patient who had low sensitivity values in the uppermost parts of both visual fields owing to markedly swollen upper eye lids. In conclusion, although pituitary hyperplasia has been well documented in primary hypothyroidism, the present prospective study clearly indicates that visual field defects are not a common finding in patients with this disease.

3,4-Dihydroxypyridine (3,4-DHP), a goitrogenic derivative of the plant amino acid mimosine, has no SH-group, in contrast to conventional antithyroid agents such as methimazole (MMI) and propylthiouracil (PTU). The current in vitro study shows that 3,4-DHP, like MMI and PTU, inhibits iodination of human thyroglobulin and interferes with mitogenic activation of human lymphocytes. This, together with a very low murine bone marrow toxicity, probably related to the absence of an SH-group, makes 3,4-DHP a potential antithyroid drug.

To explore suppressor T lymphocyte function in Graves' disease, studies were performed in one group of patients in the hyperthyroid state and in another group in the euthyroid state after treatment. Peripheral blood lymphocytes were cultured for 1-7 days. Pokeweed mitogen (PWM; 1.25 micrograms/ml) was added at the initiation of the cultures or after 24 h. The degree of lymphocyte activation was assessed by measurements of the cellular uptake of [3H]thymidine and expressed in counts per minute (CPM). The suppressor lymphocyte function was estimated by a quotient between the maximum CPM values from cultures with and without preincubation. For the hyperthyroid group (n = 15) the quotient was 1.00 +/- 0.07 (mean +/- SEM), for the euthyroid patient group (n = 21) 1.12 +/- 0.05 and for the healthy control group (n = 21) 1.37 +/- 0.08. There was a significant difference between the quotients for the control group and the hyperthyroid (P less than 0.01) as well as the euthyroid (P less than 0.05) patient group. The quotients for the two groups of patients did not differ significantly. In conclusion, the present study supports the view of a defect in suppressor T lymphocyte function in patients with Graves' disease in the hyperthyroid state and indicates that this defect can persist in the euthyroid state after treatment.

The metabolism of vitamin D is essential in the control of bone and mineral metabolism. Hyperthyroidism as well as hypothyroidism effect the metabolism of bone tissue and vitamin D. We present a dihydrotachysterol-calcium treated patient with post-operative hypothyroidism, who developed hypercalcaemia, when the thyroxine dosage was increased.