The determination of serum TMA in middle-aged women can identify an important group of women at risk of developing an elevated serum TSH. TMA measurement is of potential use in the prevention of cardiovascular disease. An elevated serum TSH, however, in our study-group does not seem to be accompanied by an abnormal lipid profile, as reported by others.

Studies in hypothyroid rats show that, when infused with a combination of thyroxine (T4) plus triiodothyronine (T3) to normalize thyrotropin (TSH), euthyroidism in all organs is only ensured when T(4) and T(3) are administered in a ratio as normally secreted by the rat thyroid. As substitution with T(4)-only results in an abnormal serum T(4)/T(3) ratio, it is also possible that in humans, euthyroidism does not exist at the tissue level in many organs, considering that iodothyronine metabolism in the human and the rat share many similar mechanisms. Recent reports in which cognitive function and well-being are compared in patients with primary hypothyroidism substituted with T(4)-only versus substitution with T(4) plus T(3) result in controversial findings in that either positive or no effects were found. In all these studies T(3) was used in the plain form that results in nonphysiologic serum T(3) peaks. In these studies it is suggested that substitution with T(3 )should preferably be performed with a preparation that slowly releases T(3) to avoid these peaks. In the study reported here we show that treatment of hypothyroid subjects with a combination of T(4) plus slow-release T(3) leads to a considerable improvement of serum T(4) and T(3) values, the T(4)/T(3) ratio and serum TSH as compared to treatment with T(4)- only. Serum T(3) administration with slow-release T(3) did not show serum peaks, in contrast to plain T(3).

8 patients with papillary cancer (4 with metastases, 4 in remission), 7 follicular cancer patients (6 with metastases), 2 patients with anaplastic thyroid cancer, and 4 other non-medullary thyroid cancer patients all received an intravenous bolus injection of 220 MBq [¹¹¹In-DTPA-D-Phe¹]octreotide. Planar anterior and posterior n camera images of head-neck, chest and abdomen were obtained 24 and 48 h after injection. All primary cancers showed [¹¹¹ln-DTPA-D-Phe¹]octreotide uptake; none occurred in patients in remission. The results were compared with conventional radio-iodine scintigraphy in patients with metastasised, differentiated thyroid cancer.

Thyrotrophin binding inhibiting immunoglublins (TBII) were measured in twenty-five patients with unequivocal hyperthyroid Graves' disease with a radioreceptor assay for TSH before, during and the end of treatment with antihyroid drugs and triiodothyronine. To assess the outcome of this therapy patients were followed for 10--90 months (mean 63 months). Before treatment there was significant correlation between TBII activity and serum thyroxine (r = -0.48, P less 0.05) and between TBII activated and 24 hour 131I thyroid uptake (r = -0.57, P less than 0.01). No relationship was found between TBII activated and 20 min, 4 hour and 48 hour 131I thyroid uptakes before institution of therapy. During treatment a significant correlation between TBII index and 20 min 131I thyroid uptake was found (r = -0.55, P less than 0.001). Both before and during treatment there was a significant correlation between TBII and LATS activity (r = -0.65, P less than 0.001). From the magnitude of this correlation coefficient it can be concluded that related, although not the same immunoglobulins, are measured with the two assay techniques. It is not possible to predict the occurrence of a relapse from the presence or absence of TBII activity at the end of treatment in this group of patients. The relapse rate was four out of eight for patients without TBII activity in their serum at the end of treatment and five out of nine for patients with TBII activity. From the data presented it can be concluded that although there is a significant relation between TBII activity and some indices of thyroid function before and during treatment, the correlation coefficients are too small to conclude that TBII alone is responsible for the hyperfunction of the thyroid. The same conclusion can be drawn from the fact that TBII activity has no prognostic value in relation to a possible relapse.