Evidence map›Paper›PMID 42568851›Full record

ArticleIDCases2026

An unusual cause of chronic recurrent vomiting and life-threatening hyperkalemia: primary adrenal insufficiency due to probable bilateral adrenal tuberculosis.

Malegna Temesgen Garuma, Nuredin Ahmed Hassen, Yaarosan Zawde Kibrat, Gadisa Fikadu Asefa, Wondimu Bekele Nega

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Article in IDCases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 authors.

Malegna Temesgen GarumaDepartment of Internal Medicine, St. Paul's Hospital Millennium Medical College, Addis Ababa, Ethiopia.
Nuredin Ahmed HassenDepartment of General Surgery, Hamdi Hospital, Harar, Ethiopia.
Yaarosan Zawde KibratDepartment of Internal Medicine, St. Paul's Hospital Millennium Medical College, Addis Ababa, Ethiopia.
Gadisa Fikadu AsefaDepartment of Emergency and Critical Care, Haramaya University, Harar, Ethiopia.
Wondimu Bekele NegaDepartment of Clinical radiology, Hamdi Hospital, Harar, Ethiopia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Adrenal tuberculosis remains a leading cause of primary adrenal insufficiency in tuberculosis-endemic regions. Its clinical presentation is often insidious and non-specific, leading to significant diagnostic delays. Gastrointestinal symptoms, though common in adrenal insufficiency, may dominate the clinical picture and direct attention away from the underlying endocrine disorder. Case Summary: A 40-year-old Ethiopian woman presented with a five-month history of intermittent abdominal pain and recurrent non-bloody vomiting. Associated symptoms included myalgia, arthralgia, intermittent low-grade fever, night sweats, and significant unintentional weight loss. She had multiple outpatient and emergency department visits and was repeatedly treated with proton pump inhibitors and different medications for an unspecified rheumatologic condition, with no definitive diagnosis established. On admission, she was hypotensive with laboratory evaluation revealing hyponatremia and severe hyperkalemia. Morning serum cortisol was markedly reduced along with elevated ACTH, supporting the diagnosis of adrenal insufficiency. HIV serology was negative. Pre and post contrast computed tomography demonstrated bilateral enlarged heterogeneously hypo-attenuating adrenal glands with internal punctate calcifications and thin peripheral rim-like enhancement. The patient was initiated on anti-tuberculous therapy with glucocorticoid and mineralocorticoid replacement. At one-month follow-up, the patient reported marked clinical improvement with complete resolution of vomiting, improved appetite, decreased fatigue, and ability to resume usual daily activities. Conclusion: This case highlights the importance of considering adrenal tuberculosis in patients from endemic regions presenting with unexplained chronic gastrointestinal symptoms, constitutional features, and electrolyte abnormalities. A high index of suspicion is essential for timely diagnosis and treatment.

Indexed as

Addison diseaseAdrenal tuberculosisBilateral adrenal calcificationCase reportHyperkalemiaPrimary adrenal insufficiency

Identifiers

PMID42568851
PMCPMC13448186

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