Clinical descriptions of acanthosis nigricans (AN) usually emphasize its velvety texture and relative hyperpigmentation. However, these characteristic findings are not the result of increased melanin production or thickening (acanthosis) of the epidermis, as is sometimes assumed. Rather, they are a reflection of an increased folding of the superficial layers of the skin leading to an accordionlike configuration that is best appreciated by gently stretching the skin. Recognition of this phenomenon aids in the identification of AN in unusual locations and provides some insight into suggested treatment options.
The most common locations for AN are the flexural surfaces of the body—in particular, the neck and axillae (see Fig. 5). However, AN can involve extensor surfaces, especially the skin overlying the elbows, knees, and the small joints of the hands and feet. Although the diagnosis of AN always prompts a mental review of associated systemic diseases or syndromes, the most common underlying disease is obesity, with its associ-
ated insulin resistance and hyperinsulinemia. Some dermatologists prefer to refer to the form of AN associated with obesity as "pseudo-AN," but given the overlap in underlying pathophysiology between this form of the disease and AN associated with diabetes, use of the term "pseudo" may be unnecessary. Although AN is a hallmark of insulin resistance with hyperinsulinemia and, hence, is typically seen in type 2 diabetes, it may occur in the obese patient with type 1 diabetes or atypical diabetes mellitus.
Insulin resistance with AN is characteristic of Kahn's type A syndrome, which is the result of defects in the insulin receptor or downstream targets and Kahn's type B syndrome, which is the result of circulating anti-insulin receptor antibodies (39). In the type B syndrome, cutaneous manifestations of other autoimmune disorders such as lupus erythematosus and Sjogren's syndrome may be present. Clinical signs of hyper-androgenemia (e.g., hirsutism, acne vulgaris, and androgenetic alopecia) can be seen in prepubertal and postpubertal women with insulin resistance, explained in part by insulin-ovary interactions and often referred to as the HAIR-AN syndrome (HyperAn-drogenism; Insulin Resistance; Acanthosis Nigricans).
One explanation proposed for the epidermal hyperplasia seen in AN is binding of excess amounts of circulating insulin to insulinlike growth factor receptors on ker-atinocytes and fibroblasts (40). Therapies for AN include weight loss and topical agents such as urea, tretinoin, and a-glycolic acids (24,41). For widespread and severe cases of AN, there are scattered case reports of the use of oral retinoids (42). However, the side effects of oral retinoids, which include hypertriglyceridemia and fetal abnormalities, must be balanced against their use, especially in light of the observation that AN reappears soon after discontinuation of the medication.
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