ODP100 Hypoparathyroidism in the Setting of COVID-19: Increasingly Common Phenomenon

Abstract

Abstract Background Acquired hypoparathyroidism (HPT) in adults is most commonly caused by post-surgical or autoimmune damage to the parathyroid glands. Genetic defects causing abnormal gland development, impaired parathyroid hormone (PTH) production or action are rare and typically diagnosed in childhood. Recent literature suggests surprisingly high prevalence of hypocalcemia in patients with SARS-CoV-2 infection and this finding is associated with poor outcomes. [1] We present a case of new onset HPT in a patient admitted with respiratory failure due to COVID-19. Case presentation A 63-year-old woman with history of obesity, GERD, asthma, presented to the ED with fever, cough, dyspnea, and diarrhea. She was found to have low O2 saturation, CXR revealed multifocal interstitial and airspace opacities. Her PCR SARS-CoV-2 test was positive and she was admitted to ICU. She was incidentally found to have severe hypocalcemia Ca 5.2 mg/dL (8.5 - 10.3 mg/dL), ionized Ca 2.46 mg/dL (4.50 - 5.10 mg/dL), albumin 3.7 g/dL (3.5 - 5. 0 g/dL). She denied any history of neck surgery, radiation or trauma and personal or family history of autoimmune or calcium disorders. Her calcium levels were normal over the past 4 years. She denied symptoms of hypocalcemia prior to presentation and reported leg cramps and finger numbness in the ED. Further work-up revealed PTH 13 pg/mL (15 - 65 pg/mL), 25-OH vitamin D 16 ng/mL (30 - 80 ng/mL), Mg 1.2 mg/dL (1.4 - 2.5 mg/dL), phosphorus 4.9 mg/dL (2.3 - 4.5 mg/dL), bicarbonate 26 mmol/L (22 - 32 mmol/L). Patient was started on Ca (IV and PO), Mg, and vitamin D replacement. PTH reassessment on days 6, 14, and 19 showed persistently low/inappropriately normal PTH (22, 14, and 8 pg/mL respectively) despite normalization of magnesium levels. Patient was discharged on Ca, Mg, and vitamin D supplementation with follow-up in Endocrinology clinic for further evaluation of her hypoparathyroidism progression. Conclusion SARS-CoV-2 infection causes a hypersensitive immune reaction and widespread inflammation. Emerging evidence suggests that this cytokine-mediated reaction and hypoxia associated with COVID-19 can affect the parathyroid glands, resulting in impaired PTH secretion. Furthermore, direct parathyroid tissue invasion and destruction by means of entry via angiotensin-converting enzyme 2 receptors has also been proposed [2]. Hypocalcemia in our patient could be multifactorial, however we believe that COVID-19 induced HPT was the leading mechanism. We hope that further research explores this hypothesis and elucidates the underlying pathophysiology.