SAT196 COVID-19 Pneumonia And Primary Hyperparathyroidism Exacerbation

Abstract

Abstract Disclosure: A. Khan: None. P. Rimal: None. M. Biggs: None. A. Ahmed: None. C. Musurakis: None. J.L. Gilden: None. A. Moid: None. Introduction: It is well known that COVID-19 virus damages the body by either inflicting the injury directly, or by initiating a systemic immune response, resulting in inflammation. Our case report explores how parathyroid glandular dysfunction and calcium levels (Ca) can be affected in a patient with active COVID-19 pneumonia. Clinical Case: A 58-year-old male, unvaccinated for COVID-19, with COPD, primary hyperparathyroidism (PHPT), chronic kidney disease, and ethanol use presented to the emergency room with confusion, vomiting, and lethargy. Preadmission medications included hydrochlorothiazide. Following a positive COVID-19 test, he was diagnosed with acute hypoxic respiratory failure secondary to COVID-19 pneumonia. After emergent treatment with BiPAP and IV steroids, he was transferred to the ICU, where he completed treatment with remdesivir, dexamethasone, and baricitinib. He was also treated for ethanol withdrawal. Notably, this patient had a history of chronic asymptomatic hypercalcemia secondary to PHPT with Ca prior to admission ranging from 10.9-13.6 mg/dl (nl=8.5-10.1mg/dl), PTH range 145-345 pg/ml (nl=14-65 pg/ml), creatinine (Cr) 1.2-1.4 mg/dl (nl= 0.67-1.17 mg/dl). On this admission, Ca was 12.2mg/dl, albumin 2.4 g/dl (3.4-5.0 g/dl), PTH 531 pg/ml, Cr 3.4 mg/dl, 25OH vitamin D 29.3 ng/mL (nl= 30-100 ng/mL). After fluids, Ca initially improved to 10.9mg/dl and Cr soon after normalized. Mental status also improved after hydration. However, Ca then rose significantly to 14.1mg/dl with mental status decline. IV zoledronic acid was administered, resulting in lowering serum calcium and improvement of mental status. Conclusion: This patient’s clinical course was notable for the improvement of Ca initially with hydration. However, a significant rise in Ca approaching parathyroid crisis range was seen shortly thereafter, despite normalization of Cr. Whereas hypocalcemia has been noted in most cases of Ca dysfunction associated with COVID-19 infection, in this case, we postulate that the COVID-19 infection may have triggered parathyroiditis, thus exacerbating the underlying PHPT. One such mechanism is the use of receptors like angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) by COVID-19 virus, which are found on endocrine glands including the parathyroid. Similarly, COVID-19 virus exerts its inflammatory effects using IL-6, which is also a key cytokine that causes hypercalcemia by stimulating bone resorption. Furthermore, COVID-19 infection is notorious for causing nausea/vomiting, and diarrhea, culminating in dehydration which worsens hypercalcemia. It is therefore necessary that physicians foresee impending complications of COVID-19 infection with concurrent parathyroid disease and take early steps to prevent and treat them. Presentation: Saturday, June 17, 2023