Hypoparathyroidism Manifesting a Decade After Thyroidectomy

Postoperative hypocalcemia usually occurs in the first days after surgery and can be the result of dynamic changes in electrolytes after interventions. When accompanied by a low parathyroid hormone (PTH) level, it is considered hypoparathyroidism.

Case Description:

41-year-old female with history of hypertension and multinodular goiter status post total thyroidectomy (16 years prior) presented with full body and jaw stiffness of 1-hour duration. She reported perioral tingling for the last 5 years and bilateral forearm tingling in the past week. She recalled taking calcium supplements for a brief period after surgery and then again 5 years after surgery. She had not taken any supplements for the last 9 years. Examination shows no neck masses or lymphadenopathy, no limb deformities, and positive Chvostek sign. Laboratory showed serum calcium of 5.1mg/dL (8.9-10.7), ionized calcium 0.92mmol/L (1.16-1.32), albumin 3.7g/dL (3.7-4.9), phosphorus 6.0mg/dL (2.5-4.6), magnesium 1.2mg/dL (1.8-2.8), intact PTH 15.9pg/mL (8.7-77.1), and 25-OH vitamin D of 6.5ng/mL (30.0-100.0). Pathology report confirmed removal of only 1 parathyroid gland. She was started on intravenous calcium gluconate; followed by calcium carbonate, calcitriol, magnesium, and ergocalciferol. Two months after, while taking only calcium carbonate, she showed persistent hypocalcemia with serum calcium of 7.4mg/dL, PTH of 14pg/mL. Calcium decreased to 5.9mg/dL when supplements were stopped; increased to 9.5mg/dL after resuming calcium carbonate and calcitriol.

Discussion:

The literature describes an incidence of 0% to 6% of permanent hypoparathyroidism following complete thyroid resection. The fragile nature of the parathyroid glands leaves them susceptible to injuries after manipulation. The short half-life of the PTH allows for prompt clinical manifestations of hypocalcemia after thyroidectomy. Rarely, the manifestations can take several years to present, which is known as “late-onset” or “delayed” hypoparathyroidism. It has been hypothesized that this phenomenon is the result of progressive atrophy of the parathyroid glands; others suggest that scar tissue in the glands leads to hypo-vascularization and slowly progressive ischemia.

There are 5 case reports of delayed presentation of post-surgical hypoparathyroidism described in the literature. Four out of five cases were reported in women; three of these cases underwent thyroidectomy for thyroid cancer and two of them for multinodular goiter. Most of the cases presented 12-14 years after surgery; symptoms range from muscle cramps and paresthesia to seizures.

Our patient may have had parathyroid insufficiency since her thyroidectomy with intermittent manifestations of hypocalcemia with unclear triggers. It is possible this admission was exacerbated by severely low vitamin D levels. She requires long term treatment for hypocalcemia now as parathyroid glands have completely failed. This case also illustrates that patients with permanent hypoparathyroidism should be followed on a yearly basis to ensure medication adherence and they should be warned about ominous manifestations of hypocalcemia in the long term.