Idiopathic transient hypoparathyroidism

Document Type

Conference Proceeding

Publication Date

2018

Publication Title

Endocr Rev

Abstract

Hypoparathyroidism is an 'orphan disease' with a prevalence of about 37 per 100,000 person-years in the United States. The most common etiology is post-surgical (22 per 100,000 person- years) and the rest constitutes non-surgical etiologies. We present a case of late-onset idiopathic transient hypoparathyroidism. 32 year old female was evaluated for dizziness of 2 month duration. In addition, she had nausea, headache, shortness of breath, diarrhea, and numbness of her extremities. The numbness occurred mostly upon awakening in the morning, lasted for a few seconds and often recurred multiple times during the day. During her workup, she was found to have hypocalcemia. Chart review documented normocalcemia 3 years prior. She had good dairy intake and denied symptoms of prior hypocalcemic episodes, neck surgery, radiation exposure, trauma, fractures, kidney stones, seizures, memory issues, recurrent fungal infections, familial autoimmune, infiltrative, neoplastic or calciumrelated disorders. Physical exam revealed bilateral positive Chvostek's sign. EKG showed prolonged QTc of 0.54. Serum ionized calcium was 5.1 (1.0 - 1.35 mmol/L), magnesium 1.6 (1.8 - 2.3 mg/dL), phosphorus 6.7 (2.5 - 4.5 mg/dL), PTH 9 (15 - 65 pg/mL), 25-hydroxy vitamin D 19 (> 20 ng/mL). Initial treatment included IV magnesium sulfate and calcium gluconate. She was later switched to oral magnesium oxide 400 mg twice daily, calcium carbonate 1000 mg three times daily, calcitriol 1 mcg twice daily and cholecalciferol 2000 IU daily. The ionized calcium levels were monitored at frequent intervals. Further testing showed TSH, cortisol, angiotensin converting enzyme, ferritin, transferrin, copper, ceruloplasmin to be normal. TPO antibodies and HIV were negative. ANA was positive (mixed homogenous and speckled pattern). We concluded she had primary hypoparathyroidism, though the etiology was not clear. One possibility could be autoimmune process from activating antibodies to calcium sensing receptor (CaSR). Though her blood was sent for testing, the lab was unable to process the blood sample. Over the next 2 months her calcium and PTH normalized. By month 4, she was off calcitriol. 4 weeks after stopping calcitriol, she became symptomatic and was found to be hypocalcemic with a normal PTH level. Calcitriol was restarted at 0.25 mcg daily. She is currently normocalcemic on calcitriol 0.25 mcg, calcium carbonate 500 mg daily and cholecalciferol 2000 IU daily. Late onset primary hypoparathyroidism is rare and the etiology is not often clear. Some patients have activating antibodies to CaSR. These patients may not suffer permanent hypoparathyroidism as there may be temporary alteration in CaSR function and remission is a possibility. Evaluating for these antibodies is a challenge as very few laboratories in the US offer this testing. Hence, close clinical and biochemical assessment is required in these patients.

Volume

39

Issue

2

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