McMaster University, 1101-75 Bold St, Hamilton, Ontario L8P 1T7, Canada.
Best Pract Res Clin Endocrinol Metab. 2012 Aug;26(4):517-22. doi: 10.1016/j.beem.2012.01.004. Epub 2012 May 31.
Hypoparathyroidism is characterized by hypocalcemia, hyperphosphatemia and low or inappropriately normal levels of parathyroid hormone (PTH). Pseudohypoparathyroidism is characterized by similar findings however PTH is elevated due to PTH resistance. PTH is a key calcium regulating hormone essential for calcium homeostasis, vitamin D-dependant calcium absorption, renal calcium reabsorption and renal phosphate clearance. The most common cause of hypoparathyroidism is iatrogenic in the setting of anterior neck surgery. Hypoparathyroidism may be due to congenital or acquired disorders. Causes include autoimmune diseases, genetic abnormalities, destruction or infiltrative disorders of the parathyroids. Impaired secretion of PTH may be seen with hypomagnesemia or hypermagnesemia Work-up includes a comprehensive history, physical examination, and a relevant biochemical investigation. Treatment of symptomatic or profound asymptomatic hypocalcemia (Corrected Calcium (Ca) < 1.9 mmol/L) is aimed at rapid intravenous administration of calcium and oral supplementation of vitamin D metabolites. Oral calcium and vitamin D analogs are critical in the treatment of hypocalcemia. In the long-term management of hypoparathyroidism thiazide diuretics are of value as they enhance renal calcium reabsorption and increase serum calcium and are of particular benefit in those with activating mutations of the calcium-sensing receptor. Parathyroid hormone replacement is of great value in improving serum calcium and lowering serum phosphate as well as the doses of calcium and calcitriol supplementation required. It has been shown to lower urinary calcium losses. Careful monitoring of vitamin D, phosphorous, and calcium is necessary during acute and long-term therapy. Although hypocalcemic patients commonly present with symptoms of neuromuscular irritability with perioral numbers paresthesias, tingling, seizures and, bronchospasm; hypocalcemia may be identified on the biochemical profile of an asymptomatic patient.
甲状旁腺功能减退症的特征是低钙血症、高磷血症和甲状旁腺激素 (PTH) 水平降低或不适当正常。假性甲状旁腺功能减退症的特征是类似的发现，但由于 PTH 抵抗，PTH 升高。PTH 是一种关键的钙调节激素，对钙稳态、维生素 D 依赖性钙吸收、肾钙重吸收和肾磷酸盐清除至关重要。甲状旁腺功能减退症最常见的原因是颈部前手术中的医源性。甲状旁腺功能减退症可能是由于先天性或后天性疾病引起的。病因包括自身免疫性疾病、遗传异常、甲状旁腺破坏或浸润性疾病。低镁血症或高镁血症可导致 PTH 分泌受损。检查包括全面的病史、体格检查和相关的生化检查。有症状或严重无症状低钙血症（校正钙 (Ca) < 1.9 mmol/L）的治疗旨在快速静脉内给予钙和口服补充维生素 D 代谢物。口服钙和维生素 D 类似物在治疗低钙血症中至关重要。在甲状旁腺功能减退症的长期管理中，噻嗪类利尿剂具有价值，因为它们增强了肾钙重吸收，增加了血清钙，并且对钙敏感受体激活突变的患者特别有益。甲状旁腺激素替代疗法在改善血清钙和降低血清磷以及降低钙和骨化三醇补充剂的剂量方面具有重要价值。它已被证明可以降低尿钙丢失。在急性和长期治疗期间，需要仔细监测维生素 D、磷和钙。尽管低钙血症患者常出现神经肌肉激惹的症状，如口周麻木、刺痛、抽搐和支气管痉挛；但在无症状患者的生化特征中也可以发现低钙血症。
