Acanthosis nigricans--decreased extracellular matrix viscosity: cancer, obesity, diabetes, corticosteroids, somatotrophin.
Acanthosis nigricans is a reaction pattern to over a dozen different causes. The skin, most classic in the axilla, is dark, soft, velvet-like with fine folding and papillae. The mechanism of this skin change is decreased viscosity of extracellular matrix (ECM) combined with mechanical extrusion of ECM into papillae extending out from the upper dermis. It occurs in obesity (increased mechanical pressure on ECM), diabetes (decreased quality of glycosaminoglycans) (GAG), excess corticosteroids (decreased quality of GAG), pineal tumors (increased ECM and edema), other endocrine disorders (alterations in the quality of GAG), multiple genetic variants (structural and chemical change), from drugs such as nicotinic acid, estrogens, corticosteroids (weakened or altered GAG) and adenocarcinoma (fractions of depolymerized or altered GAG released from the tumor area are incorporated into and weaken the skin GAG). Acanthosis nigricans was first reported in 1890 as a cutaneous sign of internal malignancy. Acanthosis nigricans presents an opportunity to better understand what is occurring in the ECM in many disorders. The understanding of the association of AN and internal malignancy will expand our understanding of how a neoplasm decreases generalized ECM viscosity.
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D000052:Acanthosis Nigricans / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D000305:Adrenal Cortex Hormones / Q000502:physiology*; D048909:Diabetes Complications; D005109:Extracellular Matrix / Q000473:pathology / Q000502:physiology; D005260:Female; D014644:Genetic Variation; D013006:Growth Hormone / Q000502:physiology*; D006801:Humans; D009369:Neoplasms / Q000150:complications*; D009525:Niacin / Q000009:adverse effects; D009765:Obesity / Q000150:complications*; D014783:Viscosity
D000305:Adrenal Cortex Hormones; D009525:Niacin; D013006:Growth Hormone