Abstract #1004257: Primary Adrenal Insufficiency after COVID-19 Infection

Abstract

1004257 Primary Adrenal Insufficiency after COVID-19 Infection Author Block: Julienne Sanchez Perez University of Illinois Hospital; Melissa Cohen, MD Co-author, University of Illinois Hospital; Joseph L. Zapater, MD Co-author, University of Illinois Hospital; Yuval Eisenberg, MD Co-author, Endocrinology, Diabetes and Metabolism, University of Illinois Hospital Introduction: The clinical presentation of SARS-CoV-2 ranges greatly from asymptomatic disease to critical illness. The multisystemic effect of COVID-19 is becoming increasingly apparent, but its impact on the endocrine system, in particular, the hypothalamic adrenal axis has yet to be defined. Case Description: A 64-year-old woman with hypothyroidism and type 2 diabetesmellitus presented to the emergency roomwith a 1week history of abdominal pain, nausea, and vomiting. The patient experienced an asymptomatic COVID-19 infection 5 months prior and reported an unintentional 30-lb weight loss since. She had been admitted several times at an outside hospital for hyponatremiawhere she never received exogenous steroids. Physical exam was notable for hypotension, epigastric tenderness, and hyperpigmentation of oral mucosa. Chemistry was significant for hyponatremia 117 mmol/L (135-145). Hyponatremia workup revealed a TSH of 0.33 mcIU/ml (0.35-4.00), free T4 1.4 ng/dl (0.6-1.7), serum osmoles 253 mOsm/kg (279-300), urine osmoles 324 mOsm/kg (300-900) and urine sodium 104 mmol/l consistent with hypotonic hyponatremia. Fluid restriction and salt tablets were initiated. Morning 8 AM cortisol returned low (2.6 mg/dl (ref: >18). A highdose 250 mcg ACTH stimulation test followed; cortisol levels returned 2.3, 2.9, and 2.6 mg/dl (ref: >18) at baseline, 30, and 60 minutes, respectively. ACTH level was elevated to 1944 pg/ml (7.263.3), aldosterone was undetectable < 3.0 ng/dl (upright: 4.0-31.0), anti-21-hydroxylase antibody were positive (ref: neg). CT scan of the abdomen returned unremarkable for any adrenal pathologies. S19 Fluid restriction and salt tablets were discontinued. Hypotension and hyponatremia resolved after initiation of Hydrocortisone IV 25 mg q8h. She was discharged on Hydrocortisone 30 mg daily and Fludrocortisone 0.05 mg daily. Discussion: This patient presented with hyponatremia and biochemical evidence of adrenal insufficiency confirmed by an abnormal stress cortisol response to a high-dose ACTH stimulation test. The markedly elevated ACTH level, inappropriately low aldosterone level, and the presence of anti-21-hydroxylase antibodies support the diagnosis of Addison s disease. Primary adrenal insufficiency (AI) after COVID-19 due to adrenal infarcts and hemorrhage have been documented, but the normal CT suggested that the etiology of AI, in this case, was not due to the aforementioned. This case is the first to suggest the onset of Addison’s disease in the COVID-19 sequelae. https://doi.org/10.1016/j.eprac.2021.04.509