Lalau J D, Sebert J L, Quichaud J
Presse Med. 1985 Nov 23;14(40):2053-7.
The abnormalities of calcium-phosphorum metabolism observed in hyperthyroidism (tendency to hypercalcaemia with subsequent functional hypoparathyroidism, increase in serum alkaline phosphatase and in hydroxyprolinuria) essentially result from excessive mobilization of bone calcium and phosphates by the thyroid hormones themselves. Histomorphometric studies have shown that the skeletal repercussions of hyperthyroidism are almost constant. There is, in particular, excessive bone remodelling due to increased bone-forming and bone-resorbing cellular activities. However, since bone resorption is quantitatively more stimulated than bone formation, the physiological bone loss is accelerated and is only partly repaired by re-establishment of the normal thyroid function.
甲状腺功能亢进症中观察到的钙磷代谢异常（倾向于高钙血症并随后出现功能性甲状旁腺功能减退、血清碱性磷酸酶升高和羟脯氨酸尿增加）本质上是由甲状腺激素自身过度动员骨钙和磷酸盐所致。组织形态计量学研究表明，甲状腺功能亢进症对骨骼的影响几乎是恒定的。特别是，由于成骨细胞和破骨细胞活性增加，导致骨重塑过度。然而，由于骨吸收在数量上比骨形成受到的刺激更大，生理性骨质流失加速，只有通过恢复正常甲状腺功能才能部分修复。
