No abstract

The fasting serum phosphate level, the tubular maximal (Tm) phosphate reabsorption and the mean renal phosphate threshold were measured in 18 hyper-and six hypothyroid patients in comparison with 11 euthyroid control subjects. A significant increase of serum inorganic phosphate, phosphate Tm and of the mean renal phosphate threshold were found in hyperthyroidism. These findings suggest an increased tubular reabsorption of phosphate in hyperthyroidism. Four main possible mechanisms of such a renal handling of phosphate in thyroid disease are briefly mentioned although their acceptance needs more direct proof.

No abstract

In 17 goitrous persons in an iodine-deficient area, in 23 nongoitrous inhabitants of the same village, in 10 goitrous persons in Athens, and 8 normal controls the perchlorate discharge test was performed, either in the simple standard form or after pretreatment with either 0.5 or 2.0 mg potassium iodide or 2.5 mg carbimazole. With the simple test or with 0.5 mg potassium iodide, there was no significant discharge in any group studied. With 2.5 mg carbimazole, there was a profound discharge of the trapped iodide in both groups in the iodine-deficient area. With 2.0 mg potassium iodide, however, there was a clear discharge in the two goitrous groups (i.e. the one in the endemic area and the second in Athens), a less pronounced discharge in the controls studied in Athens, and no discharge at all in the nongoitrous inhabitants of the iodine-deficient endemic area. These findings provide evidence for an abnormality present in the patients with endemic goiter, most probably faulty iodine utilization due to impaired organic binding. The nongoitrous persons in the endemic areas, on the other hand, seem to be even more efficient in handling the trapped iodide than the controls studied in Athens. These findings may provide an explanation for previous observations that in endemic areas only part of the population develop a goiter, whereas the others adapt successfully to iodine deficiency without significantly enlarging their glands.

F ollowing an I. V. calcium injection, there was a delayed return of the serum calcium to the basal levels in 17 patients with Graves' disease, 14 patients with simple goiter, and to patients totally thyroidectomized compared to 17 controIs. 111e results in 12 cases of toxic adenoma of the thyroid and seven persons after partial thyroidectomy (mainly lobectomy) did not differ significantly from the normals. F ollowing an I. V. injection of radioactive 47 Ca, the slope of the disappearance curve was faster in seven thyrotoxic patients compared to seven controIs. An I. V. injection of stable calcium chloride a<> celerated the slope in the normals but was without effect in the thyrotoxics. It is concluded that in cases with a diffuse disease process in the thyroid, such as Graves' disease or simple goiter, there is a deficient calcitonin release in response to provoked hypercalcaemia. Such a deficiency can not be proved in patients with a localized thyroid disease or fOllowing the surgical removal of a single thyroid lobe.