PMON82 SARS-CoV-2 Associated Hypophysitis and Central Diabetes Insipidus
Authors: Engel Ashley , Maas Diana 
Published: November 2022

Abstract

Background
The SARS-CoV-2 infection, known for severe respiratory complications, has also been found to cause multiple endocrinopathies. SARS-CoV-2 enters pneumocytes through the angiotensin-converting enzyme 2 receptor. The adrenal, thyroid, testes, ovaries, hypothalamic, and pituitary tissues express ACE2 receptors, making them putative targets.2,4 Hypothalamic and pituitary involvement was first reported in 2005 and cases continue to be reported during the newest pandemic.1,3 We present a case of central DI following positive RT-PCR testing for SARS-CoV-2.

Clinical Case
A 44-year-old man presented with headache, multiple neurologic symptoms, polyuria, and polydipsia approximately three weeks following a positive SARS-CoV-2 test. A pituitary MRI showed thickening of the infundibular stalk and inhomogeneity of the pituitary gland, suggestive of hypophysitis. A water deprivation study demonstrated undetectable ADH and inability to concentrate urine spontaneously, but increased urine osmolality in response to DDAVP consistent with central DI. He was started on oral DDAVP with improvement of polyuria and polydipsia. Additional hormone testing showed normal thyroid function and Cosyntropin stimulation, mild hypogonadotropic hypogonadism, and mild elevation in IGF-1. Pituitary hormone abnormalities were transient and DDAVP was discontinued three months later. However, neurologic symptoms persisted. Repeat pituitary MRI three months later was unchanged. Due to spontaneous resolution of pituitary hormone abnormalities, no biopsy of the hypothalamic pituitary area was performed.

Conclusion
We present a case of central DI following known SARS-CoV-2 infection. The patient presented with sudden onset polyuria and polydipsia prompting need for pituitary evaluation. Testing confirmed central DI which resolved within three months. Involvement of the HPA was first noted in 2005 by Leow et al. who reported SARS causing reversible hypophysitis.1 We found three similar cases of patients developing DI approximately four weeks following SARS-CoV-2 infection; however only one case with evidence of infundibular hypophysitis.2,5,6 Two contributing mechanisms of HPA dysfunction are thought to be the result of direct hypothalamic damage or reversible hypophysitis.4 The worldwide presence of SARS-CoV-2 and myriad of complications following infection prompts need for further research and follow-up to better determine clinical recovery for SARS-CoV-2. Reference: 1. Leow MK, et al. Hypocortisolism in survivors of severe acute respiratory syndrome (SARS). Clin Endocrinol (Oxf). 2005;63(2): 197-202. 2. Misgar RA, et al. Central diabetes insipidus (Infundibuloneuro hypophysitis): A late complication of COVID-19 infection. J Endocrinol Invest. 2021;44(12): 2855-2856. 3. Nonglait PL, et al. Hypophysitis after COVID-19 Infection. Indian J Endocrinol Metab. 2021;25(3): 255-256. 4. Pal R. COVID-19, hypothalamo-pituitary-adrenal axis and clinical implications. Endocrine. 2020;68(2): 251-252. 5. Rajevac H, et al. DIABETES INSIPIDUS AS A SYMPTOM OF COVID-19 INFECTION: CASE REPORT. Chest. 2020;158(4): A2576. 6. Sheikh AB, et al. Diabetes Insipidus and Concomitant Myocarditis: A Late Sequelae of COVID-19 Infection. Journal of Investigative Medicine High Impact Case Reports. January 2021.
Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.