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Original Research

Mechanisms behind Post-Thyroidectomy Hypocalcemia: Interplay of Calcitonin, Parathormone, and Albumin—A Prospective Study

, MS, , MD, , MS & , MS
Pages 217-225 | Received 31 May 2016, Accepted 07 Sep 2016, Published online: 07 Oct 2016
 

ABSTRACT

Purpose of study: Hypocalcemia after thyroidectomy is attributed to injury or ischemia to parathyroid glands. Transient hypocalcemia in thyroidectomy when parathyroids are preserved is not adequately explained. Release of calcitonin and hypoalbuminemia are two proposed reasons. Primary objective of this study was to find the change in calcitonin in the postoperative period after total thyroidectomy. Secondarily, hypocalcemia and its correlation with calcitonin, albumin, and parathormone were also studied. Materials and methods: This Cohort study was carried out at the general surgical department of a tertiary level teaching institution from April 2015 to December 2015. One hundred adult patients undergoing total thyroidectomy, with at least three parathyroids being preserved were included. Changes in calcium, calcitonin, albumin, and parathormone were studied based on preoperative levels and the values at 1, 6, 24, and 48 hr after surgery. Results: Calcitonin increased at one hour after thyroidectomy and fell below preoperative levels subsequently. Parathormone showed a mild rise at one hour and normalized subsequently. Total calcium, corrected calcium, and albumin showed decline at one hour and recovered gradually over the next two days. At preoperative level, calcium had significant correlation with parathormone alone. Calcium levels at one hour had significant correlation with calcitonin. All post-operative calcium levels had significant correlation with parathormone and the number of parathyroids preserved in situ without auto-transplantation. Conclusions: There is significant hypocalcemia within the first 24 hr after thyroidectomy, caused by calcitonin release and hypoalbuminemia. Preservation of maximum number of parathyroids in-situ can counter and normalize this hypocalcemia.

ACKNOWLEDGMENTS

The authors would like to thank Dr. Aravind Reghukumar, MBBS, MD, assistant professor, department of infectious diseases, for helping with the design of the study. We also thank Dr. Arun C Das, MBBS, junior resident, department of general surgery for helping with the data collection. We thank Dr. Jayageetha, PhD, associate professor, department of statistics and epidemiology, for providing help with the statistical analysis of data. None of these contributors received any financial compensation for their work.

Declaration of interest: None of the authors report any conflicts of interest. The authors alone are responsible for the content and writing of the paper.

FUNDING

This study was funded by the State Board for Medical Research, Government Medical College, Trivandrum, India, vide order No. A2-SBMR (2013–2014)/15790/2013/MCT, dated 19-02-2015.

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