Department of Endocrinology and Metabolism, Aristotle University of Thessaloniki, AHEPA University Hospital, 1 Stilponos Kyriakidi Street, 54636 Thessaloniki, Greece.
J Clin Endocrinol Metab. 2012 Jul;97(7):2341-6. doi: 10.1210/jc.2012-1170. Epub 2012 Apr 17.
Hypocalcemia, transient or permanent, represents a common complication after total thyroidectomy, but data on the secretory capacity of the parathyroid glands in thyroidectomized patients without clinical or biochemical hypocalcemia are limited.
To address this issue, we studied the parathyroid response to acute hypocalcemia induced by iv infusion of sodium bicarbonate in normocalcemic patients submitted to total thyroidectomy at the early postoperative period and 3 months later.
Sixty patients who underwent total thyroidectomy for benign thyroid disease and did not develop clinical or biochemical hypocalcemia and hypoparathyroidism postoperatively and 50 healthy volunteers were included in the study. Patients (at 48 h and 3 months after surgery) and controls (after overnight fast) were subjected to a sodium bicarbonate infusion test.
In healthy volunteers plasma intact PTH increased significantly at 3 min after infusion (4.42 ± 0.15 ng/ml vs. 11.22 ± 0.5 ng/ml, P < 0.001) and gradually returned to baseline values. In the thyroidectomized patients, mean PTH levels were also increased after sodium bicarbonate infusion but to a significantly lesser degree compared with healthy controls (1.77 mean fold increase vs. 2.57 mean fold increase, respectively, P < 0.001). Using as criterion the lowest fold increase of plasma PTH levels at 3 min after infusion observed in healthy volunteers, 38% of the thyroidectomized patients at 48 h after surgery and 6.6% of the patients at 3 months after surgery demonstrated a diminished PTH response to acute hypocalcemia induced by sodium bicarbonate infusion.
In thyroidectomized patients, normal postoperative calcium and PTH values do not exclude a reduced secretory response of the parathyroids to hypocalcemic stimuli.
低钙血症,无论是短暂性还是永久性的,是甲状腺全切除术后常见的并发症。但在甲状腺全切除术后无临床或生化低钙血症的患者中,关于甲状旁腺分泌能力的资料有限。
为了解决这个问题,我们研究了在甲状腺全切除术后早期和 3 个月后,接受静脉输注碳酸氢钠诱导的急性低钙血症时甲状旁腺的反应。
60 例因良性甲状腺疾病接受甲状腺全切除术的患者,术后无临床或生化低钙血症和甲状旁腺功能减退症,50 例健康志愿者纳入研究。患者(术后 48 小时和 3 个月)和对照组(空腹过夜后)接受碳酸氢钠输注试验。
在健康志愿者中,输注后 3 分钟时,血浆完整 PTH 显著升高(4.42 ± 0.15ng/ml 比 11.22 ± 0.5ng/ml,P<0.001),并逐渐恢复至基线值。在甲状腺切除患者中,尽管在碳酸氢钠输注后 PTH 水平也有所增加,但与健康对照组相比,增加程度明显较低(分别为 1.77 倍平均增加和 2.57 倍平均增加,P<0.001)。使用健康志愿者输注后 3 分钟时观察到的血浆 PTH 水平最低倍数增加作为标准,术后 48 小时的 38%甲状腺切除患者和术后 3 个月的 6.6%患者表现出对碳酸氢钠诱导的急性低钙血症的 PTH 反应降低。
在甲状腺切除术后的患者中,正常的术后钙和 PTH 值不能排除甲状旁腺对低钙刺激的分泌反应降低。