<unk>  is caused by increased activation of growth factor receptor proteins, usually due to endocrine dysfunction. This is most commonly insulin-mediated activation of IGF receptors on keratinocytes, as a result of hyperinsulinaemia or insulin resistance, as seen in diabetes mellitus. Factors involved in the development of<unk>  include: * Increased circulating insulin. This activates keratinocyte IGF receptors, particularly IGF-1. At high concentrations, insulin may also displace IGF-1 from insulin-like growth factor-binding protein (IGFBP). Increased circulating IGF may lead to keratinocyte and dermal fibroblast proliferation. * In hereditary forms of<unk> , fibroblast growth factor receptor (FGFR) defects * Increased transforming growth factor (TGF), which appears to be the mechanism for malignancy-associated<unk> . TGF acts on epidermal tissue via the epidermal growth factor receptor (EGFR). In conjunction with increased end levels of IGF, it is likely that perspiration and friction may be necessary predeterminants for lesions, since the level of insulin is usually not enough to activate IGF receptors across the body.
Acanthosis nigricans
Metabolic syndrome
Hypertrichosis
Green nails
Xanthosis
Blue nails
Hypertrichosis cubiti
Generalized lentiginosis