کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4280096 | 1611543 | 2011 | 7 صفحه PDF | دانلود رایگان |

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.
Journal: The American Journal of Surgery - Volume 201, Issue 5, May 2011, Pages 685–691