甲状旁腺功能减退需要同时补充钙和活性维生素D以避免低钙血症状态。在妊娠后期和产后期间(特别是哺乳期),有一个被低估的,然而,明显的“假性甲状旁腺功能亢进”的发生令人着迷,因此,补充剂量可能需要减少或停止,预防高钙血症.对甲状旁腺状态改善的这种明显现象(“缓解”或“解决”)的解释尚不完全理解;本综述的目的是分析医学(和灰色)文献中有关该谜团的病例报告,为此类患者的治疗提供全面的病理生理解释和建议。通过PubMed/Medline进行了文献检索,CINAHL,Cochrane图书馆数据库,Scopus,UpToDate,谷歌学者,以及没有时间限制的灰色文献,分析文献中所有可用的文章,描述妊娠晚期和产后(哺乳期)女性甲状旁腺状态的明显改善。还包括非甲状旁腺低的病例报告,以进一步分析和综合总体可能的病理生理解释。通过文献检索,确定了24篇论文,涵盖了甲状旁腺功能减退患者的这种现象,在没有潜在甲状旁腺功能减退症的患者中,还有多例类似发生的报告。病理生理学被认为是由于妊娠期间胎盘产生甲状旁腺激素相关肽(PTHrP)而发生的,产后期间泌乳乳腺进一步生产。观察到一个典型的模式,在整个妊娠和泌乳期间,PTHrP升高和PTH抑制(存在于正常和甲状旁腺功能减退的受试者中)。PTHrP诱导的高钙血症的概念在没有甲状旁腺功能减退症的患者中得到进一步证实。包括胎盘分泌过多和乳腺肿大的受试者。显然,甲状旁腺功能减退症患者可能需要在妊娠晚期和哺乳期减少剂量,由于高钙血症的风险。除了甲状旁腺功能减退症患者,这种病理生理现象发生在毫无戒心的患者中,证明所有与孕妇接触的临床医生都需要意识到这种罕见但危险的发生。
Hypoparathyroidism requires management with both calcium supplementation and active vitamin D to avert a state of hypocalcemia. During late gestation and the postpartum period (specifically lactation), there is an under-recognized, yet intriguing occurrence of apparent \'pseudohyperparathyroidism\', whereby supplementation dosages may need to either be reduced or discontinued, to prevent hypercalcemia. The explanation for this apparent phenomenon of improved parathyroid status (\'remission\' or \'resolution\') is incompletely understood; the purpose of this review is to analyze the case reports of this enigma within the medical (and grey) literature, providing an overall pathophysiological explanation and recommendation for the management of such patients. A literature search was conducted through PubMed/Medline, CINAHL, Cochrane Library Database, Scopus, UpToDate, Google Scholar, and the grey literature without a time-restricted period, analyzing all available articles within the literature describing an apparent improvement in parathyroid status in late-gestation and postpartum (lactating) females. Non-hypoparathyroid case reports were also included to further analyze and synthesize an overall likely pathophysiological explanation. Through the literature search, 24 papers were identified covering such a phenomenon in patients with hypoparathyroidism, alongside multiple additional reports of a similar occurrence in patients without underlying hypoparathyroidism. The pathophysiology is believed to occur due to the placental production of parathyroid hormone-related peptide (PTHrP) during gestation, with further production from the lactating mammary glands during the postpartum period. A typical pattern is observed, with increased PTHrP and suppressed PTH throughout both gestation and lactation (present in both normal and hypoparathyroid subjects). The concept of PTHrP-induced hypercalcemia is further demonstrated in patients without hypoparathyroidism, including subjects with placental hypersecretion and mammary gland enlargement. It is evident that patients with hypoparathyroidism may require a dosage reduction during late gestation and lactation, due to the risk for hypercalcemia. In addition to patients with hypoparathyroidism, this pathophysiological phenomenon occurs in unsuspecting patients, demonstrating the need for all clinicians in contact with pregnant females to be aware of this uncommon - yet perilous - occurrence.