Serum calcium, sodium, potassium, chloride, magnesium, phosphorus, osmolarity, total protein, albumin, parathyroid hormone, and calcitonin values were systematically surveyed in 135 patients who underwent thyroidectomy and in 104 control surgical patients. A transient and moderate hypocalcemia developed after operation in thyroidectomized and control patients. Concentrations of other electrolytes, osmolarity, proteins, and albumin followed the same pattern of evolution. After thyroidectomy, the degree and duration of hypocalcemia increased with the extent of thyroid resection. A profound hypocalcemia (less than 2.0 mmol/L) and a marked reduction of the parathyroid hormone concentration (below normal) were present in 12% and 8% of cases after subtotal thyroidectomy and in 22% after total thyroidectomy. Calcitonin values did not increase after thyroidectomy. A slight correlation was observed between the preoperative serum alkaline phosphatase level and the minimal postoperative serum calcium level. It is concluded that post-thyroidectomy hypocalcemia is a multifactorial phenomenon. It is due, at least in part, to hemodilution. A temporary parathyroid insufficiency after subtotal and total thyroidectomy, and an avidity of the skeleton for calcium in hyperthyroid patients, may aggravate the hypocalcemia.

Overt hypothyroidism is known to be associated with increased serum creatine kinase (CK) levels. However, there is little information on CK levels in subclinical hypothyroidism. The aim of the study was to assess the relationship between CK levels and thyroid function in overt and subclinical hypothyroidism. Thyroid function tests (thyrotropin [TSH], free thyroxine [FT4], free triiodothyronine [FT3]) and the serum levels of CK were obtained from 23 patients admitted to a general hospital for illnesses other than thyroid or muscular diseases, myocardial ischemia, or brain damage. Overt hypothyroidism, based on thyroid function tests, was present in 10 patients, whereas hypothyroidism could be classified as subclinical in the other 13. A positive correlation was observed between CK and thyrotropin, and to a lesser extent between CK and thyroid hormones. Moreover, the correlation between CK and TSH and between CK and FT4 was detectable in subclinical hypothyroidism. Our data suggest that even in subclinical hypothyroidism there is some degree of dysfunction in skeletal muscle metabolism.

Calcitonin (CT) deficiency and its possible repercussions on bone mass were studied in a group of 9 adult patients (7 females, 2 males) with congenital hypothyroidism of dysgenetic origin. Using a new extraction method (exCT) which considerably improves the sensitivity and the specificity of the assay for CT-monomer, we measured CT levels before and after a short calcium (Ca) stimulation test (2 mg Ca/kg over 5 minutes) to evaluate C-cell secretory reserve. Mean basal plasma CT concentrations were lower in the hypothyroid women (mean +/- SEM: 0.6 +/- 0.1 pg/ml) than in 30 normal female controls (1.7 +/- 0.2 pg/ml, P less than 0.001). Serum calcium increased similarly in the two groups, but postinfusion CT levels were lower in the hypothyroid women, (1.7 +/- 0.2 pg/ml) than in normal women (16.8 +/- 2.9 pg/ml), P less than 0.001. Hypothyroid women showed a 10% reduction in bone mineral content at the diaphyseal site in the radius, 0.840 +/- 0.037 g/cm, compared with normal age-matched controls, 0.930 +/- 0.020 g/cm, (P less than 0.05). Our study demonstrates the existence of a profound CT-monomer deficiency in adult patients with thyroid agenesis or dysgenesis. Both calcitonin deficiency and thyroid hormone treatment could play a role in the observed bone loss. Attention should therefore be paid to bone metabolism during treatment of congenital hypothyroidism to avoid further bone loss.

The present study concerns eighteen chronic alcoholics with minimal liver damage. A significant reduction in total serum T4 with an accompanying drop in circulating TBG was observed in these otherwise euthyroid patients. During alcohol withdrawal, we observed a rapid increase in T4 and TBG into the normal range. We suggest that the fall in the level of circulating thyroxine-binding globulin is related to a defect in its synthesis or secretion by the liver due to ethanol consumption. Caution is recommended in the interpretation of thyroid function tests in chronic alcoholics.

Mineral metabolism is frequently disturbed in hyperthyroidism. In a group of seventy-two patients with hyperthyroidism, we observed an increase in serum diffusible calcium in 50% of the cases, elevated inorganic phosphorus in 30% and elevated alkaline phosphatase in 44% of the cases. Correlations existed between the values of diffusible calcium, inorganic phosphorus, alkaline phosphatase and certain indices of thyroid function (T4, FT41, T3, FT3I), of which that with T3 was the best (P less than 0.001). Our results suggest that the magnitude of the disturbances of mineral metabolism depends on the severity of the hyperthyroidism and that it is the T3 level that constitutes the best index of that severity.