The prevalence of mitral valve prolapse was investigated in 126 patients with hyperthyroidism due to Graves' disease or toxic nodular goitre and that of hyperthyroidism in 64 patients with mitral valve prolapse. One hundred and eleven asymptomatic healthy subjects comprised a control group. The patients with hyperthyroidism were divided into those with Graves' disease and those with toxic nodular goitre. Of the group as whole, 12 (9.5%) patients had mitral valve prolapse compared with six (5.4%) in the control group, but the difference was not statistically significant. The prevalence of mitral valve prolapse in the patients with toxic goitre was also not significantly different from that in the controls. When the prevalence in the group with Graves' disease was compared with that in the control group (16.3% vs 5.4%) the difference was significant. Only one patient with mitral valve prolapse had hyperthyroidism.

An increased prevalence of mitral valve prolapse has been found in Graves’ disease and a common autoimmune etiology has been suggested for both disorders. We investigated the prevalence of mitral valve prolapse in 87 patients with autoimmune chronic lymphocytic thyroiditis, 50 patients with nongoitrous hypothyroidism and 111 healthy control subjects. Mitral valve prolapse was found in 16.09% of patients with chronic lymphocytic thyroiditis compared to 6 and 5.4% in nongoitrous hypothyroidism and normal controls, respectively. The result is statistically significant, p < 0.02, and confirms that the prevalence of mitral valve prolapse is significantly increased in patients with autoimmune disorders of the thyroid gland, when compared to normals and nonautoimmune conditions.

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It has been recently shown that acute hypercalcemia increases the release of growth hormone in man. We investigated the effect of intravenous administration of calcium gluconate on the levels of growth hormone, during OGTT, in 8 non-obese subjects. When an OGTT was performed with the addition of Lv. normal saline, no significant increase of serum growth hormone concentration was seen. However i.v. administration of calcium gluconate with OGTT induced a significant increase of growth hormone at 120 and 180 minutes (from 1.4 ± 0.8 ng/ml to 13.4 ± 5.7 ng/ml and 9.3 ± 2.1 ng/ml respectively). The growth hormone response to acute hypercalcemia was not abolished by a simultaneous OGTT, showing that the stimulatory effect of high levels of plasma calcium overcomes the inhibitory action of glucose.

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