AS SEEN ON TV: A CAUTIONARY TALE OF VITAMIN D SUPPLEMENTATION FOR COVID-19 PREVENTION

ABSTRACT

CASE An 80-year-old woman with untreated osteoporosis and suspected primary hyperparathyroidism presents to establish care. Review of systems and physical examination are normal. She has mild hypercalcemia (11.2), and normal albumin and phosphorous. Parathyroid hormone (PTH) is elevated (71). Bone density testing demonstrates osteoporosis at the hip and spine (Tscore -2.9 and -3.0). She reports self-medicating with 12,000 IU of vitamin D daily to prevent COVID-19 infection, which she learned about from a popular news source;she is unvaccinated for COVID-19. Her vitamin D 25-OH level is 172 (normal 30-100). The patient was instructed to stop vitamin D supplementation. Additional work up for hyperparathyroidism was initiated, including 24-hour urine collection for calcium, and she was referred for a parathyroidectomy. IMPACT/DISCUSSION: Adequate vitamin D supplementation has been postulated to reduce the risk and severity of the COVID-19 infection through its immunomodulatory effects that augment the immune cell response, decrease inflammation, and prevent RAAS system dysregulation, which is associated with more severe coronavirus infection. However, trials and metaanalyses have yielded inconclusive data, with most reporting no associations between adequate or high-dose vitamin D supplementation and COVID-19 morbidity and mortality. Nonetheless, popular news sources and social media have called for high-dose vitamin D supplementation, which can result in hypervitaminosis D through patient self-medication. Both hypervitaminosis D and primary hyperparathyroidism present with signs and symptoms of hypercalcemia, including nephrolithiasis, osteoporosis, bone pain, weakness, and neuropsychiatric changes. Hypervitaminosis D is caused by ingestion of too much exogenous vitamin D (normally more than 10,000 IU/day), dysregulation of the vitamin D pathway, or overproduction of vitamin D. Primary hyperparathyroidism is caused by parathyroid adenomas, hyperplasia, and carcinomas. Distinguishing between the two conditions involves a thorough history and physical, laboratory measurements, and occasionally imaging. Hypervitaminosis D patients have suppressed PTH levels, serum 25(OH)D > 150ng/mL, and hyperphosphatemia while primary hyperparathyroidism patients have normal/elevated PTH levels, low/normal 25(OH)D levels, and hypophosphatemia. Primary hyperparathyroidism is the most common cause of hypercalcemia, but this case highlights the importance of screening for and identifying other etiologies of hypercalcemia. This patient's vitamin D toxicity can be treated by stopping vitamin D supplementation. Her primary hyperparathyroidism meets criteria for a parathyroidectomy due to the presence of osteoporosis. CONCLUSION: 1. High dose vitamin D supplementation is ineffective as prophylaxis against the COVID-19 infection. 2. Hypercalcemia secondary to vitamin D toxicity is distinguished from primary hyperparathyroidism by PTH, 25(OH)D, and phosphorus levels.