• Yeşim Erbil, Nese Colak Ozbey, Serkan Sari, Haluk Recai Unalp, Orhan Agcaoglu, Feyzullah Ersöz, Halim Issever, and Selçuk Ozarmagan.
• Department of General Surgery, Istanbul University, 34093 Capa, Istanbul, Turkey. yerbil2003@yahoo.com
• Am. J. Surg. 2011 May 1; 201 (5): 685-91.

BackgroundThe etiology of postoperative hypocalcemia after total thyroidectomy appears to be multifactorial, that is, postoperative transient hypoparathyroidism, low 25-hydroxy vitamin D (25-OHD) concentrations, aging, and hyperthyroidism with increased bone turnover. Our aim was to evaluate the factors responsible for postoperative hypocalcemia in euthyroid vitamin D-deficient/insufficient Graves patients who underwent total thyroidectomy at our institution.MethodsThirty-five consecutive patients with Graves disease treated by total thyroidectomy were included in the present study. All patients were vitamin D deficient/insufficient (ie, 25-OHD concentrations of <20/<30 ng/mL, respectively). Patients were divided into 2 groups according to postoperative serum albumin corrected calcium concentrations: group 1 (n = 13) patients had postoperative serum calcium concentrations of 8 mg/dL or less; group 2 (n = 22) patients had serum calcium concentrations greater than 8 mg/dL. Bone turnover markers (deoxypiridinoline, bone-specific alkaline phosphatase) and 25-OHD were determined the day before surgery.ResultsIn group 1 patients, disease duration was significantly longer, 25-OHD and postoperative parathyroid hormone concentrations were significantly lower, and bone turnover markers were significantly higher. Logistic regression analysis revealed that a postoperative parathyroid hormone concentration less than 10 pg/mL was the most powerful parameter to predict postoperative hypocalcemia (odds ratio, 23; 95% confidence interval, 3.3-156).ConclusionsIn Graves patients with vitamin D deficiency/insufficiency, postoperative (transient) hypoparathyroidism is the most significant parameter to determine the development of postoperative hypocalcemia.Copyright © 2011 Elsevier Inc. All rights reserved.

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