Primary Adrenal Insufficiency After COVID-19 Infection

• Published in: AACE clinical case reports Vol. 8; no. 2; pp. 51 - 53
• Main Authors: Sánchez, Julienne, Cohen, Melissa, Zapater, Joseph L., Eisenberg, Yuval
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2022; American Association of Clinical Endocrinology; Elsevier
• Subjects: Addison disease; adrenal insufficiency; Case Report; COVID-19; SARS-CoV-2; COVID-19; CT; SARS-CoV-2; adrenal insufficiency; Addison disease; AI; AAI; AAI, autoimmune adrenal insufficiency; AI, adrenal insufficiency; CT, computed tomography
• ISSN: 2376-0605; 2376-0605
• DOI: 10.1016/j.aace.2021.11.001

The multisystemic effects of COVID-19 are becoming evident. In the adrenal gland, adrenal hemorrhage and infarction after COVID-19 infection have been reported. Our objective is to present a case of autoimmune adrenal insufficiency diagnosed after COVID-19 infection, without the evidence of a hemorrhage or an infarction. A 64-year-old woman with hypothyroidism and type 2 diabetes presented with a 1-week history of abdominal pain, nausea, and vomiting. She had experienced asymptomatic COVID-19 infection 5 months prior and reported an unintentional 30-lb weight loss. The home medications included enalapril, atorvastatin, and levothyroxine. A physical examination was notable for hypotension, epigastric tenderness, and mucocutaneous hyperpigmentation. Laboratory tests revealed a serum sodium level of 117 mmol/L (range, <20 mmol/L), thyroid-stimulating hormone level of 0.33 μIU/mL (range, 0.35-4.00 μIU/mL), free thyroxine level of 1.4 ng/dL (range, 0.6-1.7 ng/dL), serum osmoles of 253 mOsm/kg (range, 279-300 mOsm/kg), urine osmoles of 324 mOsm/kg (range, 300-900 mOsm/kg), and urine sodium level of 104 mmol/L. The morning cortisol level was 2.6 μg/dL (reference [ref], >18 μg/dL). This was followed by a high-dose, 250-μg adrenocorticotropic hormone (ACTH) stimulation test, which revealed that the cortisol level was 2.3, 2.9, and 2.6 μg/dL (ref, >18 μg/dL) at baseline, 30 minutes, and 60 minutes, respectively. The ACTH level was 1944 pg/mL (range, 7.2-63.3 pg/mL), the aldosterone level was <3.0 ng/dL (range, 4.0-31.0 ng/dL), and anti-21-hydroxylase antibody was present (ref, negative). A computed tomography scan of the adrenals was unremarkable. Hypotension and hyponatremia resolved after initiation of intravenous hydrocortisone, and she was discharged on hydrocortisone and fludrocortisone. The patient’s symptoms, elevated ACTH level, low cortisol level, and presence of 21-hydroxylase antibodies were consistent with Addison disease. COVID-19 might have contributed to rapid, clinically relevant disease progression after the infection. The development of autoimmune Addison disease in the patient might be related to the prior COVID-19 infection.