A 28-year-old woman has fatigue, weight loss, and generalized skin darkening, most marked over pressure points and palmar creases. BP is 92/60 mmHg, sodium 128 mEq/L, potassium 5.6 mEq/L, and plasma ACTH is markedly elevated. The hyperpigmentation in this patient results directly from:

• A Autoantibodies cross-reacting with melanocyte antigens
• B Elevated cortisol acting on dermal melanocytes
• C Increased melanocyte-stimulating activity derived from pro-opiomelanocortin produced along with ACTH ✓
• D Hyperkalemia stimulating melanin synthesis

Explanation

Primary adrenocortical insufficiency (Addison disease) causes low cortisol, which removes negative feedback and drives very high ACTH secretion. ACTH is cleaved from pro-opiomelanocortin (POMC), the same precursor that yields melanocyte-stimulating hormones, so chronically elevated POMC products stimulate melanocytes and darken skin, especially at pressure points, scars, and mucosa. Cortisol is low here, ruling out B. This hyperpigmentation distinguishes primary from secondary (pituitary) adrenal insufficiency, where ACTH is low and pigmentation does not occur.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.