History and exam

Key diagnostic factors

common

black or Hispanic ancestry

One study found acanthosis nigricans affecting 19.4% of Americans with black ancestry, 23.1% of Hispanic people, and 4.2% of Caucasians.[5]

new pigmented velvety skin lesions in axillary or flexural areas

Symmetric, hyperpigmented plaques ranging in color from yellow to dark brown are most commonly found on flexural surfaces.

lesions distributed on the posterior neck, axillae, vulva, umbilicus, inner thighs, and groin

These are the most frequently affected sites.

weight gain

Obesity-related acanthosis nigricans may follow weight gain.

uncommon

generalized distribution

May be seen in benign (familial) or malignant acanthosis nigricans.

sudden appearance of multiple seborrheic keratoses

Associated with malignant acanthosis nigricans.

Other diagnostic factors

common

age >40 years

The onset of malignant acanthosis nigricans is usually seen in patients over 40 years of age.[8]

child/young adult

Obesity-associated acanthosis nigricans (AN) is seen in children and young adults.[2][5][24]​ Benign AN also has an onset in childhood.[4]

female sex

Women are slightly more predisposed to acanthosis nigricans.[5]

acrochordons (skin tags)

Acrochordons frequently appear in affected areas.[22]​​

uncommon

acral distribution

The acral form of acanthosis nigricans presents with lesions on the extensor surfaces of extremities, without involvement of intertriginous areas.[2][23]

pruritus

Generalized pruritus occurs in 41% of patients with malignant acanthosis nigricans.[11]

mucosal or palmoplantar lesions

Mucosal involvement and hyperkeratosis of the palms and soles (also known as "tripe palms") may be present in 25% of malignant acanthosis nigricans.[11]

weight loss

Associated with malignant acanthosis nigricans that often occurs abruptly and spreads rapidly.[2][8][9]

Risk factors

strong

obesity

Incidence of acanthosis nigricans (AN) is positively associated with increased body mass index (BMI).[5][17]​​ As incidence of obesity increases in a population, so does the incidence of AN.[1]​ Skin lesions tend to regress with weight loss.[1]​​

AN is found in 46% of children with BMI ≥ 95th percentile, 62% ≥ to 98th percentile and 70% ≥ to 99th percentile.[5]

insulin resistance

Acanthosis nigricans (AN) and obesity are positively and independently associated with hyperinsulinemia.[17] Children with AN are 4.2 times as likely to have hyperinsulinemia as those without.[7][17]​​​ AN is also noted in genetic syndromes with marked hyperinsulinemia such as type A and type B insulin resistance syndromes, leprechaunism, and genetic lipodystrophies.[19]

positive family history of AN or genetic syndrome

Genetic syndromes, particularly those in which insulin resistance, obesity, or fibroblastic growth factor defects are present have high incidence of acanthosis nigricans.[4][19]

family history of diabetes mellitus

Children with a family history of diabetes mellitus are more often affected with acanthosis nigricans.[5]

malignancy

Malignant acanthosis nigricans is rare but most commonly associated with gastric adenocarcinomas.[2][8][9][10]​​ It tends to rapidly worsen as tumor burden increases and remits with treatment of the underlying malignancy.[2][8]

weak

medication

Rarely induced by medications (e.g., systemic corticosteroids, nicotinic acids, estrogens, oral contraceptives, insulin, methyltestosterone, topical fusidic acid, or pituitary extract).[1][2]​​​​

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