Endocrine Abstracts

JOINT3823

Introduction: Hypocalcemia can occur as a complication of total thyroidectomy. In this context, postoperative hypoparathyroidism is due to accidental removal, damage or devascularization of the parathyroid glands. Hypocalcemia can also occur as part of hungry bone syndrome (HBS) in patients who have previously had long-standing hyperthyroidism, as it causes increased bone turnover with overall bone resorption, which then transitions to osteoblastic activity once the excess hormone is eliminated.

Case report: A 26-year-old woman underwent total thyroidectomy for long-standing Graves’ disease with concomitant orbitopathy. Postoperatively, she developed hypocalcemia. She was discharged from the ENT department with calcium carbonate 6 g daily and calcitriol 3 mg daily. She did not show up for endocrinology follow-up as scheduled. One month after surgery, she was hospitalized because of severe symptomatic hypocalcemia (paresthesias, abdominal cramps, positive Trousseau’s and Chvostek’s signs). Laboratory findings revealed an unmeasurably low PTH level, severe hypocalcemia (total calcium 1.3 mmol/l, ionized 0.47 mmol/l), hypomagnesemia (0.54 mmol/l) and hyperphosphatemia (2.4 mmol/l). These findings were primarily suggestive of iatrogenic (postoperative) hypoparathyroidism, but likely with concomitant HBS aggravating hypocalcemia, as the patient had severe long-standing hyperthyroidism prior to surgery. Persistent symptomatic hypocalcemia despite treatment necessitated transfer to the ICU, where she received intravenous calcium chloride as a continuous infusion, magnesium sulfate, and further dose adjustments of calcitriol, calcium carbonate and cholecalciferol were made. The targeted calcium levels could not be achieved, so teriparatide was initiated in two daily doses together with other medications. A short time later she was switched to palopegteriparatide 18 mg subcutaneously daily. Satisfactory calcium levels were maintained and the patient was discharged on the following daily doses: calcitriol 3 mg, calcium carbonate 12 g and palopegteriparatide 18 mg. Over the next few months, calcium levels were maintained with only minor adjustments to the above therapy. The patient stopped coming for regular check-ups and stopped taking the medications regularly. Inadequate adherence to therapy led to severe hypocalcemia (this time asymptomatic) and she was hospitalized. Satisfactory calcium levels were achieved and maintained by adjusting calcium and vitamin D supplementation alone, without PTH replacement therapy.

Conclusion: Palopegteriparatide can serve as a bridging therapy in patients with severe hypocalcemia due to hypoparathyroidism and HBS after total thyroidectomy for Graves’ disease in the period when satisfactory serum calcium levels cannot be maintained with high doses of calcium and vitamin D supplementation.