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.
ABSTRACT
CASE: A 44-year-old male with past medical history of type II insulindependent diabetes mellitus (DM) and end stage liver disease (ESLD) due to alcohol use and nonalcoholic fatty liver disease (NAFLD) presented with one week of left-sided retroorbital headache and diplopia. Two weeks prior, the patient tested positive for COVID-19 and initially his severe headache was attributed to this diagnosis. On hospital presentation the patient was found to have ophthalmoplegia, ptosis and diminished sensation in the CN V1 distribution on the left. The patient was in diabetic ketoacidosis (DKA) with glucose of 686, venous blood gas of 7.32/29/15 and serum anion gap of 17. Contrasted orbital and maxillofacial CT showed complete opacification of the left sphenoid sinus and CT angiography/venography of the head were negative for venous sinus thrombosis. MRI of the brain showed left optic nerve ischemia and left frontal lobe cerebritis without abscess. Bedside nasal endoscopy with ENT showed purulent, fuzzy white debris bilaterally concerning for fungal sinusitis. He was taken urgently to the operating room and was found to have angioinvasive fungal sinusitis with cultures growing Lichthemia corymbifera, a fungus in the Mucor family. In addition to treatment with IV insulin and fluids for DKA, the patient was given amphotericin B and posaconazole;however, surgical intervention was deemed too high risk and futile in the setting of patient's comorbidities. IMPACT/DISCUSSION: Mucormycosis is a fungal infection that typically involves the sinuses, orbits and the central nervous system (CNS). Infection of the sinuses manifests with fever, sinus congestion/pain and headache, but can rapidly progress to involve the orbits, leading to vision changes, and the CNS, leading to encephalopathy. Other structures that can be involved include the cavernous sinus, leading to palsies of cranial nerves III-VI. Known risk factors for mucormycosis include DM, especially in patients with DKA, glucocorticoid treatment, immunosuppression and deferoxamine use. Urgent histopathologic diagnosis, initiation of intravenous antifungal agents (amphotericin B) and surgical intervention with ENT, ideally prior to extension beyond the sinuses, are fundamental to decreasing mortality, which is as high as 62%. There have been numerous case reports of mucormycosis in patients with COVID-19, particularly from India. Many of these patients were prescribed glucocorticoids as part of the COVID-19 treatment pathway or had underlying DM. Additional research is needed into the association between COVID-19 and invasive mucormycosis. CONCLUSION: In patients with poorly controlled DM or immunosuppression presenting with severe headache, sinus pain, and/or neurologic changes, mucormycosis must be considered, as it is a fatal entity requiring urgent surgical intervention and initiation of antifungal agents. Patients with COVID-19 infection may be at increased risk for mucormycosis, especially in those with underlying DM or on glucocorticoids.