Acute adrenal insufficiency revealed by pulmonary tuberculosis: A rare association, a case report

Aims: Acute adrenal insufficiency (AAI) is a rare but potentially life-threatening complication of pulmonary tuberculosis (TB). We report a case highlighting the importance of considering this diagnosis in patients with severe TB and unexplained hydro-electrolytic disturbances.
Presentation of Case: A 37-year-old man, chronic smoker (3 pack-years), was admitted for severe deterioration of general condition with recent-onset dyspnea (mMRC stage 3), post-prandial vomiting, major weight loss, anorexia, asthenia, low-grade fever, and night sweats. On examination he was febrile (38 °C), drowsy, tachypneic (26 cycles/min), hypotensive (90/50 mmHg), and hypoxemic (SpO2 70% on room air). Laboratory tests showed hyponatremia (118 mmol/L), hyperkalemia (5.6 mmol/L), and a markedly depressed morning serum cortisol level of 29.5 nmol/L (reference range approximately 138–690 nmol/L), consistent with acute adrenal insufficiency. Chest imaging revealed bilateral macronodular consolidations predominating in the upper and middle lung zones, associated with a “mimosa flower” micronodular pattern and mediastinal lymphadenopathy, together with a positive QuantiFERON-TB test, leading to a clinical diagnosis of pulmonary tuberculosis.
Discussion: AAI complicating TB may result from direct tuberculous destruction of the adrenal cortex or from a functional cortisol response inadequate to the demands of severe infectious stress, further aggravated by rifampicin-induced acceleration of cortisol clearance. Prompt recognition and immediate glucocorticoid replacement are essential to prevent hemodynamic collapse.
Conclusion: Substitutive hydrocortisone therapy combined with standard antituberculous chemotherapy (2RHZE/4RH) led to marked clinical improvement. Clinicians should systematically consider AAI in patients with severe TB presenting with marked general impairment and electrolyte disturbances.