Adrenal atrophy overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maryam Hadipour, M.D.[2]
Adrenal glands, also known as suprarenal glands, are small, triangular-shaped glands located on top of both kidneys. They produce hormones that help regulate your metabolism, immune system, blood pressure, response to stress and other essential functions. Adrenal atrophy may be caused by loss of ACTH and trophic support of the adrenal cortex (due to exogenous corticosteroid overuse) or direct damage to the tissue caused by infections (TB, CMV, histoplasmosis, paracoccidioidomycosis), vascular impairments (hemorrhage from sepsis, adrenal vein thrombosis, HIT), deposition disease (hemochromatosis, amyloidosis, sarcoidosis), or drugs (azole anti-fungals, etomidate, rifampin, anticonvulsants) or cytotoxic agents such as mitotane. The onset of clinical manifestations is dependent to the etiology of the atrophy. However, the symptoms of the adrenal atrophy usually develop in patient’s 30s to 50s and in their 60s in the case of secondary adrenal atrophy. Common complications of the adrenal atrophy and its malfunction include hypoglycemia, dehydration, weight loss, and disorientation. Prognosis is generally poor, due to the irreversibility of atrophy and the one out of 200 patients with adrenal atrophy die each year due to the adrenal crisis. As the disease consists of the irreversible atrophy of the adrenal gland treatment of the adrenal atrophy is a conservative treatment, including hormone replacement therapy and managing the adrenal crisis state.