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acanthosis-nigricans-pathogenesis-and-clinical-findings

Acanthosis Nigricans: Pathogenesis and clinical findings Authors: Laura Chin Reviewers: Taylor Woo Crystal Liu Laurie Parsons* * MD at time of publication Medications E.g. systemic glucocorticoids, injected insulin, oral contraceptives Hyperinsulinemia Insulin inhibits IGFBP 1&2 secretion Genetic Syndromes E.g. Down syndrome, Rabson- Mendenhall syndrome, congenital generalized lipodystrophy Defects in insulin receptor or anti-insulin receptor antibody production Insulin Resistance ↑ IGFR1 binding Type 2 Diabetes Mellitus Polycystic Ovarian Syndrome Obesity Neoplasms E.g. gastric carcinomas Excess IGF-1, TGFα, and FGF production TGFα is structurally similar to EGFα TGFα can bind to EGFR ↑ EGFR binding Inheritable Mutations E.g. FGFR3 activating mutation ↑ free IGF-1 ↑ FGFR binding Moist environment and rubbing of intertriginous skin Skin inflammation and thinning Bacterial or yeast infection Erosions Malodour Dermal keratinocyte and fibroblast growth and differentiation of neck and intertriginous areas, occasionally mucosal surfaces Hyperkeratosis Abbreviations: • IGF-1 – insulin-like growth factor • IGFR1 – insulin-like growth factor receptor-1 • IGFBPs – insulin-like growth factor binding proteins • FGFR – fibroblast growth factor receptor • TGFα – transforming growth factor-alpha • EGFα – epidermal growth factor-alpha • EGFR – epidermal growth factor receptor Hyperpigmentation Crusting Velvety plaques Pain Pruritis Pus Acanthosis Nigricans Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 14, 2019 on www.thecalgaryguide.com