SARS-CoV-2 Induced Autoimmune Polyglandular Syndrome Type 2: A Case Report

Document Type

Conference Proceeding

Publication Date

10-22-2025

Publication Title

J Endocr Soc

Keywords

aldosterone, antihypertensive agent, fludrocortisone, glucose, glutamate decarboxylase 65 antibody, hemoglobin A1c, hydrocortisone, levothyroxine, potassium, renin, sodium, sodium chloride, steroid, steroid 21 monooxygenase, thyroid peroxidase antibody, thyrotropin, Addison disease, adult, autoimmune hypothyroidism, autoimmune polyendocrinopathy candidiasis ectodermal dystrophy, autoimmunity, body weight loss, case report, clinical article, conference abstract, coronavirus disease 2019, diagnosis, distress syndrome, dizziness, drug therapy, exertional dyspnea, family history, gastroesophageal reflux, human, hyperpigmentation, hyponatremia, hypotension, insulin dependent diabetes mellitus, latent autoimmune diabetes in adults, male, pediatrician, Raynaud phenomenon, scleroderma, Severe acute respiratory syndrome coronavirus 2, tachycardia, thyroid disease

Abstract

Background: Autoimmune polyglandular syndrome type 2 (APS-2) is a rare condition characterized by the coexistence of autoimmune adrenal insufficiency (Addison's disease), autoimmune thyroid disease, and often type 1 diabetes mellitus. Viral infections are known to trigger autoimmune diseases, with some studies suggesting an increased risk of autoimmune conditions following infections, including SARS-CoV-2. However, the direct association between COVID-19 and APS-2 remains underexplored. Case Description: A 47-year-old male with a history of gastroesophageal reflux disease (GERD) and Raynaud's disease presented with dizziness, hypotension, unintentional weight loss, increased salt cravings, and dyspnea on exertion. His daughter's pediatrician observed skin hyperpigmentation, prompting further evaluation. He had a history of SARS-CoV-2 infection six months prior and had received a 5-day course of steroids. Family history was notable for scleroderma and possible thyroid disease in his mother.The primary care providermeasured an 8amcortisol, which was low (4.1 μg/dL), alongside an elevated TSH (13.48 uIU/L) and lowfree T4 (0.91 ng/dL), prompting referral to endocrinology. On exam, he was hypotensive (90/60 mmHg), tachycardic (pulse 112), and had diffuse skin hyperpigmentation but was not in acute distress.Laboratory findings showed hyponatremia (sodium 133 mmol/L), highnormal potassium (4.7 mmol/L), suppressed aldosterone (<3 ng/dL), elevated renin (701.1 pg/mL), elevated ACTH (1,370 pg/mL), and low morning cortisol (2.1 μg/dL), suggestive of Addison's disease. Testing for 21-hydroxylase antibodies was positive. Thyroid tests revealed elevated TSH (17.62 uIU/mL), lowfree T4 (0.49 ng/dL), and positive thyroid peroxidase antibodies (92 IU/mL), confirming autoimmune hypothyroidism. Screening for type 1 diabetes was positive for GAD65 antibodies (120 IU/mL) and a hemoglobin A1c of 5.6%, indicating latent autoimmune diabetes (LADA). Diagnosis and Management: The patient was diagnosed with Autoimmune Polyglandular Syndrome Type 2, consisting of Addison's disease, autoimmune hypothyroidism, and stage 1 LADA. He was started on hydrocortisone, fludrocortisone, and levothyroxine. His glucose and hemoglobin A1c are being monitored. Discussion and Conclusion: This case suggests a possible link between SARS-CoV-2 and APS-2. Viral infections, including COVID-19, may trigger autoimmune responses in genetically predisposed individuals. The patient's history of COVID-19, followed bymultiple autoimmune conditions, supports this hypothesis. This case contributes to the growing literature on post-viral autoimmune diseases and highlights the need for further research into SARS-CoV-2 as an autoimmune trigger. Clinicians should be vigilant in recognizing and managing post-COVID autoimmune endocrinopathies.

Volume

9

First Page

A210

Last Page

A211

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