What is the pathophysiology of hypercalcemia due to thyroid surgery?

Updated: Jan 25, 2018
  • Author: Pramod K Sharma, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Answer

Answer

The parathyroid glands produce parathyroid hormone (PTH), which is intimately involved in the regulation of serum calcium. PTH increases serum calcium levels by causing bone resorption, increasing renal absorption of calcium, and stimulating the synthesis of the biologically active form of vitamin D (1,25-dihydroxy vitamin D).

1,25-Dihydroxy vitamin D increases serum calcium levels by means of a number of mechanisms, including increasing the intestinal absorption of calcium. PTH also increases renal excretion of phosphorus. Therefore, low PTH levels result in high serum phosphorus levels.

Inadequate production of PTH leads to hypocalcemia. Hypoparathyroidism, and the resulting hypocalcemia, may be permanent or transient. The rate of permanent hypoparathyroidism is 0.4-13.8%. The condition may be due to direct trauma to the parathyroid glands, devascularization of the glands, or removal of the glands during surgery.

The rate of temporary hypocalcemia is reportedly 2-53%. The cause of transient hypocalcemia after surgery is not clearly understood. It may be attributable to temporary hypoparathyroidism caused by reversible ischemia to the parathyroid glands, hypothermia to the glands, or release of endothelin-1. Endothelin-1 is an acute-phase reactant known to suppress PTH production, and levels have been elevated in patients with transient hypoparathyroidism.

Other hypotheses have been put forth to account for transient hypocalcemia not caused by hypoparathyroidism. These include calcitonin release and hungry-bone syndrome. Calcitonin is produced by the thyroid and inhibits bone breakdown while stimulating renal excretion of calcium. Its effects on calcium metabolism oppose those of PTH. Hungry-bone syndrome occurs in patients with preoperative hyperthyroidism. These patients have increased bone breakdown in their hyperthyroid state. When a patient's thyroid hormone level drops acutely after surgery, his or her stimulus to break down bone is removed. The bones, now "hungry" for calcium, remove calcium from the plasma, decreasing serum calcium levels.


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