A Case of Primary Adrenal Insufficiency Due to Disseminated Histoplasmosis

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Journal of the Endocrine Society

Abstract

Introduction: Histoplasmosis is a fungal infection caused by Histoplasma capsulatum. Disseminated histoplasmosis is mostly seen in immunocompromised hosts, and adrenal involvement is common. Despite common adrenal involvement, adrenal insufficiency is exceedingly rare, especially in immunocompetent patients. Clinical Case: A 75-year-old male with a past medical history of histoplasmosis two decades ago presented with unintentional weight loss, fatigue, and orthostatic hypotension. Computed tomography of the chest and abdomen showed calcified thoracic lymph nodes, pulmonary and splenic granulomas, and lobulated thickening of bilateral adrenal glands. Laboratory results were significant for sodium of 125 mEq/L (n: 135-145 mEq/L), morning cortisol of 2 mcg/dL (n: 3.7-19.4 mcg/dL), ACTH of 642 pg/mL (n: 6-46 pg/mL), negative 21-hydroxylase antibody, positive mycelial and histoplasma antibodies, and elevated histoplasma serum antigens. The patient was diagnosed with adrenal insufficiency and disseminated histoplasmosis. Treatment with intravenous hydrocortisone and itraconazole started and resulted in significant improvement of blood pressure and symptoms. The patient completed the itraconazole course and was put on oral hydrocortisone. Clinical Lessons: Histoplasmosis-induced adrenal insufficiency is a rare complication believed to occur in less than 10% of cases with disseminated disease. Although autoimmune adrenalitis is the most common cause of primary adrenal insufficiency in developed countries, histoplasmosis plays a significant role in North America, particularly in endemic areas such as the Ohio and Mississippi River Valleys. Disseminated histoplasmosis most commonly occurs in an immunocompromised host. Even though our patient was immunocompetent, his advanced age increased his risk for disseminated histoplasmosis due to the decline in the immune system that occurs with aging. Clinical differentiation of infectious causes of Addison’s disease from an autoimmune etiology may be challenging. As seen in our case, imaging tests can be useful in differentiation since the radiographic appearance of glands destroyed by histoplasmosis or other infections is large (>4.5 cm), while in autoimmune adrenalitis the glands are often atrophic and reduced in size. Our patient still requires daily hydrocortisone replacement. However, partial recovery of the adrenal gland was reported by clinical studies with early diagnosis and antifungal therapy. Our case adds to the limited body of literature on Addison’s disease due to disseminated histoplasmosis in immunocompetent hosts. We recommend considering the diagnosis of histoplasmosis in patients presenting with adrenal insufficiency, especially in endemic areas.

Volume

9

Issue

Suppl 1

First Page

A159

Comments

ENDO 2025 Endocrine Society Annual Meeting, July 12-15, 2025, San Francisco, CA

Last Page

A159

DOI

10.1210/jendso/bvaf149.294

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