A 58-year-old man presents with a 6-month history of progressive skin lesions characterized by migratory annular erosive erythema with central clearing and peripheral spread, predominantly affecting the intertriginous areas, perineum, and perioral region. The lesions follow a cyclical pattern of erythema, vesiculation, erosion, and crusting over 7–14 days. He also reports recent-onset mild diabetes mellitus and has been found to have a normochromic normocytic anemia. Imaging reveals a 3 cm mass in the pancreatic head. The structure marked **A** in the diagram represents the distinctive cutaneous manifestation seen in this patient. Which of the following is the most likely underlying diagnosis?

Why Glucagonoma with necrolytic migratory erythema as a paraneoplastic dermatosis is right

The clinical presentation—migratory annular erosive erythema with intertriginous and periorificial distribution, cyclical 7–14 day pattern, accompanied by mild diabetes and anemia—is the pathognomonic triad of glucagonoma syndrome. Necrolytic migratory erythema (NME) is the cutaneous hallmark of glucagonoma, occurring in 70–90% of cases and often preceding diagnosis by months to years. The structure marked A (migratory annular erosive erythema) is the distinctive morphologic feature that, combined with the pancreatic mass and metabolic derangements (hypoaminoacidemia, hypozincemia, essential fatty acid deficiency), confirms the diagnosis. The pathogenesis involves glucagon-driven gluconeogenesis causing amino acid deficiency and impaired epidermal protein synthesis, similar to nutritional necrolytic dermatoses (acrodermatitis enteropathica, pellagra). Somatostatin analogs (octreotide, lanreotide) rapidly improve NME by suppressing glucagon secretion.

Why each distractor is wrong

Harrison's 21e Ch 81; Bolognia 5e Ch 53