ODP016 A case of adrenal incidentaloma in a patient with latent tuberculosis

Abstract

An adrenal incidentaloma can be either a nonfunctioning adrenocortical adenoma or may cause disease, such as adrenocortical carcinoma, pheochromocytoma, hormone-producing adenoma or metastasis. However, less commonly, it can be a manifestation of infection such as tuberculosis. The case is a 40-year-old male who emigrated from China two years ago, referred to the endocrine clinic after he was found to have a 3 cm right adrenal macroadenoma on MRCP after hospitalization for acute cholecystitis. The patient was also found to have positive Quantiferon, but CXR was clear. He was started on isoniazid therapy for latent tuberculosis and was later switched to rifampin postoperatively. One month after hospital discharge, he was evaluated by Endocrinology. Vital signs, including BP were normal with no symptoms of dizziness or orthostatic hypotension. He had no symptoms of adrenal insufficiency or excess. Electrolytes, renal, liver function tests, and CBC were within normal. Albumin was 4.3g/dL(RR 3.4-5). Fasting 8 AM labs: ACTH 9 pg/mL (RR 0-47), cortisol 10.10 ug/dL (RR 5.3-22.5), DHEA S 130 mcg/dL (RR 80-560), plasma metanephrines and normetanephrines and midnight salivary cortisol were normal, aldosterone 10 ng/dL, renin 1.49 ng/mL/h with ARR of 6.7. Adrenal CT w/wo contrast showed right adrenal mass with absolute washout 78% and relative washout 53% consistent with adenoma, as well as bilateral subcentimeter lipid rich adenomas and marked mesenteric lymphadenopathy. Mycobacterium tuberculosis complex spreads to the adrenal glands hematogenously. Clinical manifestations of adrenal insufficiency in tuberculosis may take years to take effect, after 90% of gland destruction occurs. The majority of patients with active or recently acquired disease (<2 years) have bilateral adrenal enlargement, while calcification and atrophy is found with remote infection or inactive disease. The adrenals can be enlarged in patients with pulmonary tuberculosis even without active involvement of the glands solely due to stress and inflammation. The hypothalamic-pituitary-adrenal (HPA) axis can be activated or even under-activated in active pulmonary tuberculosis. Cortisol levels return to baseline after anti-tuberculous treatment. Rarely tuberculosis can cause adrenal incidentaloma. Adrenal biopsy is not necessary for primary adrenal insufficiency with bilateral adrenal enlargement in a patient with proven extra-adrenal tuberculosis. However, about 12% of patients with adrenal tuberculosis have no evidence of active extra-adrenal tuberculosis. Adrenal biopsy was refused but is generally necessary in these patients to prove adrenal involvement by tuberculosis. Our case highlights the fact that tuberculosis should be considered in the differential of adrenal masses. Reference: Fassnacht M, Arlt W, Bancos I, et al. Management of adrenal incidentalomas: European Society of Endocrinology Clinical Practice Guideline in collaboration with the European Network for the Study of Adrenal Tumors. Eur J Endocrinol. 2016 Aug;175(2): G1-G34. doi: 10.1530/EJE-16-0467. PMID: 27390021.

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