A 15-year-old boy with obesity (BMI 33 kg/m²) presents with a 2-year history of progressive discoloration on the back of his neck and axillae that does not wash off. On examination, the lesions marked **A** in the diagram show a characteristic velvety, palpably thickened surface with symmetric distribution across the posterior neck and axillae. Laboratory investigations reveal fasting glucose 108 mg/dL, HbA1c 6.0%, and fasting insulin 32 μIU/mL (HOMA-IR 8.6). There is no history of malignancy, rapid weight loss, or dysphagia. Which of the following best explains the morphologic hallmark of the lesions marked **A**?

Question

Accepted Answer

B. Hyperkeratosis and papillomatosis of the epidermis due to insulin-stimulated IGF-1 receptor signaling on keratinocytes and fibroblasts. ## Why option 1 is correct

The velvety, palpably thickened surface texture marked **A** is the morphologic hallmark of benign acanthosis nigricans and results from hyperkeratosis and papillomatosis of the epidermis. In insulin resistance, elevated circulating insulin binds to insulin-like growth factor-1 (IGF-1) receptors on keratinocytes and fibroblasts, driving epidermal proliferation and the characteristic papillomatous texture. This boy's elevated fasting insulin (32 μIU/mL) and HOMA-IR (8.6) confirm significant insulin resistance, which is the pathogenic driver. The symmetric distribution in flexural areas (neck, axillae, antecubital fossae) and the absence of malignancy features (rapid onset, weight loss, dysphagia, oral involvement) confirm benign acanthosis nigricans related to metabolic disease, not paraneoplastic syndrome.

## Why each distractor is wrong

- **Option 2 (Lichenoid infiltration with melanin incontinence)**: This describes postinflammatory hyperpigmentation or lichen planus, which lack the distinctive velvety, papillomatous texture and do not correlate with insulin resistance or HOMA-IR elevation. The texture in this case is palpably thickened, not flat.
- **Option 3 (Sebaceous gland hyperplasia and follicular plugging)**: This describes comedonal lesions or seborrheic dermatitis, which are not associated with insulin resistance and do not produce the characteristic velvety texture or symmetric flexural distribution seen in acanthosis nigricans.
- **Option 4 (Dermal fibrosis and collagen deposition)**: This describes scleroderma or morphea, which present with induration and loss of skin mobility, not velvety texture. Scleroderma is not a cutaneous manifestation of insulin resistance and would not improve with weight loss and metformin.

**High-Yield:** The velvety, palpably thickened papillomatous texture is the single most specific morphologic clue that differentiates benign acanthosis nigricans (insulin resistance) from postinflammatory hyperpigmentation, seborrheic dermatitis, or malignant acanthosis nigricans.

[cite: Phiske MM. Acanthosis nigricans. Indian Dermatol Online J. 2023. ADA pediatric T2DM screening 2024.]

Answer

A. Sebaceous gland hyperplasia with follicular plugging due to androgen excess in insulin resistance

Answer

C. Lichenoid infiltration of the dermis with melanin incontinence secondary to chronic sun exposure

Answer

D. Dermal fibrosis and collagen deposition from chronic inflammation mimicking scleroderma

Explanation

Why option 1 is correct

Why each distractor is wrong

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