Q:

What is the risk of evolution toward overt hypersecretion?

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A 35-year-old farmer sustains chest injuries following an accident at the farm for which he is subjected to CT imaging of thorax and abdomen which reveals bilateral adrenal mass, measuring 4 cm × 3 cm × 4 cm, homogeneous, smooth walled, isodense with liver and well enhancing on contrast administration. He is asymptomatic prior to the accident. Examination reveals a normally built male, normal vitals, no postural drop in blood pressure. No obvious hyperpigmentation. Biochemical evaluation are all normal except a serum sodium levels of 129 mEq/L. TSH, total T4 levels are normal. At 8 am cortisol is 5 mg/dL with a corresponding ACTH of 100 pg/mL. A synacthen stimulation test with 250 mg given IV is done and 60 min cortisol of 13 mg/dL is obtained. A diagnosis of Addison’s disease is made. Chest X-ray and Mantoux test are normal. 24-hour urine collection for metanephrines is normal. A CT-guided FNAC is performed which reveals 2–4 μm oval, budding yeast forms with a probable diagnosis of histoplasmosis. ELISA for human immunodeficiency virus is negative. Patient is started on hydrocortisone 15 mg/day in two split doses. Patient is given intravenous amphotericin B for two weeks followed by oral itraconazole for one year.

What is the risk of evolution toward overt hypersecretion?

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Development of overt Cushing’s syndrome during the follow-up was observed in <1% of cases, whereas appearance of silent biochemical alterations was reported in a 0–11% cases across different studies. Masses of 3 cm or greater are more likely to develop silent hyperfunction than smaller tumors, and the risk seems to plateau after 3–4 years.

The onset of catecholamine overproduction or hyperaldosteronism during long-term follow-up is very rare.

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