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Integumentary system ORGAN SYSTEMS

Acanthosis nigricans (AN)

Introduction

Common cutaneous condition characterized by thick velvety hyperpigmented plaques of the intertriginous, flexural, and less commonly extensor areas of the skin.


Aetiology

Associated conditions:

  • Disorders associated with insulin resistance (M/C)
    • Obesity-associated AN (M/C type)
    • Type 2 diabetes
    • PCOS
  • Internal malignancy
  • Endocrine disorders
  • Drug reactions

Pathophysiology

Etiopathogenesis of acanthosis nigricans: Insulin has been demonstrated to cross dermoepidermal junction (DEJ) to reach keratinocytes. At low concentrations, insulin regulates carbohydrate, lipid and protein metabolism and can weakly promote growth by binding to “classic” insulin receptors. At higher concentrations, however, insulin can exert more potent growth-promoting effects through binding to insulin-like growth factor 1 receptors (IGF-1Rs) that are similar in size and subunit structure to insulin receptors, but bind IGF-1 with 100- to 1000-fold greater affinity than insulin. The binding stimulates proliferation of keratinocytes and fibroblasts, leading to AN | Jeong KH, Oh SJ, Chon S, Lee MH. Generalized acanthosis nigricans related to type B insulin resistance syndrome: A case report. Cutis. 2010;86:299–302. (Image courtesy of Dr. Ashwin Kosambia, Consultant Dermatologist, Mumbai, India)

Clinical features

  • Asymptomatic area of darkening and thickening of the skin, pruritus, and lesions that are velvety, hyperpigmented macules and patches and progress to palpable plaques.
  • Typically occur in areas of skin folds like the groin, axillae, or posterior neck (M/C)
Relapse of AN after successful kidney cancer treatment on the neck (a), groins, scrotum and thighs (b), and axillae (c, d). In the axillae, skin tags are seen | Wollina, U., Hansel, G., Lotti, T., Tchernev, G., Vojvodic, A., & Temelkova, I. (2019). Acanthosis Nigricans – A Two-Sided Coin: Consider Metabolic Syndrome and Malignancies!. Open access Macedonian journal of medical sciences, 7(18), 3081–3084. https://doi.org/10.3889/oamjms.2019.258

Management

Topical retinoids

First-line treatment
  • Tretinoin 0.1% cream/gel
  • Triple therapy: Tretinoin 0.05% + hydroxyquinone 4% + fluocinolone acetonide 0.01%
  • Adapalene gel

Topical vitamin D analogs

Inhibit keratinocyte proliferation and promote differentiation by increasing keratinocyte intracellular calcium and cyclic GMP levels
  • Calcipotriene

Superficial chemical peels

Relatively safe and effective treatment option for AN
  • Trichloroacetic acid (TCA): Chemical exfoliating agent that causes destruction of the epidermis with subsequent repair and rejuvenation

Oral retinoids (isotretinoin and acitretin)

Normalization of epithelial growth and differentiation

Metformin and rosiglitazone

Treatment of AN associated with insulin resistance
  • Metformin increases peripheral insulin responsiveness, resulting in reduction of glucose production, hyperinsulinemia, body weight, and fat mass, as well as an increase in insulin sensitivity in patients with insulin resistance and AN

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