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World journal of surgery · Feb 2013
Excessive decrease in serum magnesium after total thyroidectomy for Graves' disease is related to development of permanent hypocalcemia.
- Sara Salehi Hammerstad, Ingrid Norheim, Trond Paulsen, Lise Marit Amlie, and Erik Fink Eriksen.
- The Hormone Laboratory, Oslo University Hospital-Aker, Postbox 4959, Nydalen, 0424 Oslo, Norway. sara.hammerstad@medisin.uio.no
- World J Surg. 2013 Feb 1; 37 (2): 369-75.
BackgroundTransient postoperative hypocalcemia is one of the most common complications after thyroidectomy. Permanent hypocalcemia, however, is rare, but usually requires life-long treatment and follow-up. The risk of permanent hypocalcemia has been shown to be significantly higher in patients with Graves' disease. In the present study we evaluated short-term and long-term changes in serum calcium, phosphate, magnesium, and parathyroid hormone (PTH) levels in order to characterize subjects at risk of postoperative hypoparathyroidism.MethodsForty patients who underwent total thyroidectomy for Graves' disease were included in the study. Calcium, phosphate, magnesium, and PTH were measured before surgery and regularly during the year that followed.ResultsPostoperative hypocalcemia was seen in 21/40 (53 %) patients. Undetectable PTH (<0.6 pmol/L) was registered in 11/40 (27 %) patients. All patients with measurable PTH 6-48 h after operation regained normal calcium. Of those with undetectable PTH after 6-48 h, four developed permanent hypocalcemia. We found a significantly lower serum calcium level before operation in patients who developed permanent hypocalcemia compared to those who did not (p < 0.001). We also found a significant correlation between the decrease in serum magnesium from time 0 to 48 h after operation and permanent hypocalcemia (p = 0.015).ConclusionsSerum calcium prior to operation, serum PTH, and degree of decrease in magnesium levels in serum 48 h after operation may predict development of permanent hypocalcemia. Magnesium plays an important role in calcium homeostasis via stimulation of PTH secretion and modulation of PTH receptor sensitivity. Both mechanisms may have played a role for the findings reported in this article.
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