儿茶酚胺可导致嗜铬细胞瘤和甲状腺功能亢进症中的高钙尿症和高钙血症。

Catecholamines cause the hypercalciuria and hypercalcaemia in phaeochromocytoma and in hyperthyroidism.

作者信息

Skrabanek P

出版信息

Med Hypotheses. 1977 Mar-Apr;3(2):59-62. doi: 10.1016/0306-9877(77)90055-x.

Abstract

Catecholamines induce bone resorption and hypercalcaemia by the beta-adrenergic effect in bone and hypercalciuria by the alpha adrenergic effect in kidney. The interplay between the alpha-adrenergic hypercalciuria and beta-adrenergic hypercalcaemia explains why in some, but not all, phaeochromocytomas hypercalcaemia occurs. The hypothesis predicts hypercalciuria in both phaeochromocytoma and neuroblastoma. In hyperthyroidism, negative calcium balance and hypercalcaemia cannot be attributed to the direct effect of thyroid hormones on the bone but can be explained by augmentation of the catecholamine effects on bone and kidney by thyroid hormones. The hypothesis offers a solution for an apparent paradox in hyperthyroidism of increased urinary cAMP while nephrogenous cAMP is decreased. It also explains why propranolol corrects hypercalcaemia without influencing renal calcium loss.

摘要

儿茶酚胺通过对骨骼的β-肾上腺素能效应诱导骨吸收和高钙血症，并通过对肾脏的α-肾上腺素能效应导致高钙尿症。α-肾上腺素能高钙尿症和β-肾上腺素能高钙血症之间的相互作用解释了为什么在一些（但不是所有）嗜铬细胞瘤中会出现高钙血症。该假说预测嗜铬细胞瘤和神经母细胞瘤都会出现高钙尿症。在甲状腺功能亢进症中，负钙平衡和高钙血症不能归因于甲状腺激素对骨骼的直接作用，而是可以通过甲状腺激素增强儿茶酚胺对骨骼和肾脏的作用来解释。该假说为甲状腺功能亢进症中出现的一个明显矛盾提供了解决方案，即尿中环磷酸腺苷（cAMP）增加而肾源性cAMP减少。它还解释了为什么普萘洛尔能纠正高钙血症而不影响肾钙流失。