Thyroid storm revealing suspected evolving autoimmune polyglandular syndrome type 2 with steroid-limited assessment of autoimmune adrenal insufficiency: a case report.

Background: Autoimmune polyglandular syndrome type 2 (APS-2) is a rare autoimmune disorder characterized by the coexistence of autoimmune adrenal insufficiency with autoimmune thyroid disease and/or type 1 diabetes mellitus. Its heterogeneous and progressive presentation frequently delays diagnosis, particularly during acute endocrine emergencies where one dominant manifestation may obscure concurrent glandular dysfunction. Recognition of evolving autoimmune disease before overt adrenal insufficiency develops remains particularly challenging, especially when emergency corticosteroid therapy is initiated before endocrine evaluation. Case Description: We report the case of a 53-year-old woman admitted with severe thyrotoxicosis presenting with marked weight loss, persistent vomiting, generalized weakness, and sinus tachycardia. Laboratory evaluation demonstrated suppressed thyroid-stimulating hormone and markedly elevated free thyroxine levels, fulfilling the clinical criteria for suspected thyroid storm, prompting immediate treatment with hydrocortisone, propranolol, thiamazole, and intravenous fluids resulted in rapid clinical improvement. Further investigation confirmed Graves' disease with positive anti-thyroid antibodies and diffuse uptake on thyroid scintigraphy. Additional studies revealed hypercalcemia with suppressed parathyroid hormone levels, vitamin B12 deficiency, positive anti-parietal cell antibodies, and autoimmune atrophic gastritis compatible with pernicious anemia. Biochemical confirmation of primary adrenal insufficiency was not possible because glucocorticoid therapy had been initiated before adrenal function testing. Nevertheless, the presence of anti-21-hydroxylase antibodies strongly supported autoimmune adrenalitis and raised suspicion for evolving APS-2. Extended autoimmune testing also demonstrated positivity for anti-gp210 antibodies and anti-triple tissue antibodies, suggesting latent autoimmune hepatobiliary involvement. Although these findings were not diagnostic of hepatobiliary or additional gastrointestinal autoimmune disease, they supported a broader autoimmune phenotype and highlighted the need for long-term multidisciplinary surveillance. Conclusions: This case highlights the diagnostic challenge of recognizing evolving APS-2 during an acute endocrine emergency, when severe thyrotoxicosis predominates and early corticosteroid therapy appropriately prioritized patient stabilization but limited definitive biochemical assessment of adrenal function. Compared with previously reported cases, this report emphasizes the value of identifying autoimmune adrenalitis before overt Addison's disease becomes clinically apparent and illustrates the importance of comprehensive autoimmune evaluation in patients presenting with severe thyrotoxicosis and multiple autoimmune manifestations. Early recognition, comprehensive autoimmune investigation, and multidisciplinary longitudinal follow-up are essential to prevent potentially life-threatening endocrine complications.