A 49-year-old Indian gentleman attended A&E reporting a three-day history of fever, rigors and lower back pain. A CT KUB incidentally revealed a left adrenal mass and widespread abdominal lymphadenopathy. A subsequent CT NCAP showed lymphadenopathy above and below the hemidiaphragm with bilateral adrenal masses. A PET scan showed avidity in these locations. A right axillary lymph node biopsy revealed granulomatous lymphadenitis with focal necrosis. No microorganisms, including acid-fast bacilli were seen on staining. His Mantoux test was positive (34mm). Given his epidemiological risks factors, positive Mantoux test and evidence of necrotising granulomas on biopsy, tuberculosis was considered the most likely diagnosis, although lymphoma remained within the differential. He commenced standard first-line anti-tuberculosis treatment. One week later he re-presented reporting fever, dyspnoea, vomiting, generalised abdominal pain and increased skin pigmentation. He was tachycardic, hypotensive and hypoglycaemic (HR 129, BP 105/73, BM 3.8). Investigations showed a marked hyponatraemia, metabolic acidosis (Na+ 115, pH 7.24) and deranged liver function tests (ALT 510). ACTH was raised (869 ng/L) and a short Synacthen test showed no rise in serum cortisol. His tuberculosis medication was held and he was treated for Addisonian crisis with intravenous hydrocortisone and oral fludrocortisone. It is likely that commencing rifampicin induced metabolism of endogenous steroid, thus precipitating the crisis. Potentially, he was already compensating for low endogenous steroid production prior to initiation of rifampicin, caused by adrenal tuberculosis. He subsequently improved and was discharged with oral hydrocortisone and fludrocortisone. His tuberculosis medications with be restarted as an Outpatient.

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