Hypomagnesemia following thyroidectomy: Prospective observational - Pilot study

Abstract

Background: Magnesium plays a role in the active transport of calcium (Ca+2) and potassium ions across cell membranes. Most of Mg+2 is intracellular or in the bone <1% is in the blood serum. Post thyroidectomy, hypoparathyroidism leads to acute hypocalcemia that leads to hypomagnesemia. The relation of Ca+2 and magnesium (Mg+2) metabolism is complex and mainly related to the interaction of these cations with parathyroid hormone (PTH) post thyroidectomy. Magnesium is an essential regulator of Ca+2 flux and intracellular action of Ca+2. Hypomagnesemia impairs hypocalcaemia-induced PTH release, which is corrected rapidly after magnesium replacement. Attempting to correct only hypocalcemia may prolong symptoms. It is important to monitor both Ca+2 and Mg+2 levels following thyroidectomy to facilitate prompt resolution of symptoms. The aim: is to highlight the prevalence of hypomagnesemia following thyroidectomy and its association with hypocalcemia which mandate early recognition and treatment to prevent prolongation of hypocalcemia and permanent hypoparathyroidism. Methods: Institutional review board was obtained (E20-4615) and posted in ClinicalTrials.gov NCT04351451. Informed consent taken from all patients. This is a prospective open Label observational pilot study in patients who underwent thyroidectomy. The study period was from January 2019 to January 2020. A total of 74 patients with normal renal function. Serum Ca+2, magnesium, phosphate level, and Vitamin D level are all checked preoperatively and in the first postoperative day. Results: Post thyroidectomy 56.8% of patients had hypomagnesemia. 59.5.1% had hypocalcemia and 41.9% of had combined low level of Ca+2 and Mg+2 (P = 0.004). Conclusions: Causes of hypocalcemia and hypomagnesemia following thyroidectomy is of multi factorial related mainly to Ca+2, Mg+2 interaction in relation to PTH level.