Acanthosis Nigricans and PIH Overview

Acanthosis Nigricans

• Characterized by velvety, papillomatous, brown or hyperpigmented patches/plaques.
• Also shows darkening and thickening (hyperkeratosis) or leathery skin.
• Most commonly found on the neck, axilla, groin, and inframammary region.
• Prevalence varies across ethnic groups (13.3% African American, 5.5% Latino, 34.2% Native American).
• Primarily linked to insulin resistance (obesity, diabetes, etc.).
• Can rarely be associated with internal malignancy (malignant AN: middle-aged, non-obese, abrupt onset).
• Prevention: Unknown, but often associated with lifestyle changes.
• Treatment: topical retinoids, microdermabrasion, keratolytics (e.g., lactic, glycolic, salicylic or trichloroacetic acid).

Post Inflammatory Hyperpigmentation (PIH)

• Hyperpigmented macular patches or plaques, a temporary pigmentation following skin injury/inflammation.
• Most common in darker skin tones (Fitzpatrick 4-6).
• Diagnosis: usually clinical, potentially biopsy.
• Treatment: addressing the inflammatory source, sunscreen. Lesions usually resolve spontaneously (6-12 months).
• Speeding resolution: Skin lighteners (hydroquinone 4-8% qhs, 1-2 months), retinoids, topical steroids, microdermabrasion, chemical peels (salicylic or glycolic acid).

Melasma

• Hyperpigmented macular patches/plaques on sun-exposed areas (face, neck, arms).
• Gradual onset, no inflammation present.
• Bilateral, asymptomatic, light-to-dark brown macules/patches with irregular borders.
• Common patterns: centrofacial (forehead, cheeks, nose, upper lip), malar (cheeks), mandibular (jawline, chin), extrafacial (forearms/shoulders).
• More common in women (20-40 years old, Fitzpatrick skin types III-IV).
• Risk factors: pregnancy, estrogen (oral contraceptives, HRT), sun exposure.
• Prognosis: gradually fades after pregnancy/contraceptive discontinuation.
• Treatment: sun protection (broad-spectrum sunscreen), antioxidants (omega-3/6, vitamin E), topical skin lighteners (kojic acid, ascorbic acid, azelaic acid, hydroquinone), hormone modification, microdermabrasion, lasers, chemical peels.

Lichen Sclerosus

• Ivory white, atrophic papules with faint pink rims.
• Flat-roofed, slightly raised papules coalescing into oval plaques with dull/glistening white, atrophic surfaces (wrinkled).
• Mucosal surfaces exhibit atrophic, white, glistening, wrinkled lesions.
• Etiology: unclear but potentially genetic, hormonal, irritant, traumatic, infectious.
• Autoimmune component suspected (ECM-1 antibodies in 60-80% of women).
• Primarily affects non-hair-bearing areas of the vulva (can extend to perineum, labia, clitoris, surrounding skin, anal/perianal areas, 50% of women).
• Increased risk of anogenital cancer (squamous cell carcinoma, SCC), up to 5% (risk highest with uncontrolled inflammation).
• Diagnosis: often from biopsy (early cases)
• Treatment: emollients, avoidance of tight clothing/friction, topical steroids (high-potency), other treatments such as Cyclosporine and surgery if necessary.

Vitiligo

• Acquired depigmentation of the skin, well-circumscribed white macules/patches.
• Hairs in affected areas can be normal or white.
• Etiology: autoimmune destruction of melanocytes; 1% of population is affected, often onset before 20 years old, equal genders, and family history (30%) is present. Strongly associated with thyroid disease (15% adults, 5-10% children).
• Diagnosis: Wood's lamp (accentuates hypopigmentation), skin biopsy (melanocyte absence, sparse lymphocytic inflammation).
• Prognosis: variable and potentially progressive, increased skin cancer risk in depigmented areas due to sunburns.
• Treatment: topical corticosteroids, calcineurin inhibitors (pimecrolimus, tacrolimus), topical vitamin D derivatives (calcipotriol, tacalcitol), ruxolitinib, Jak1 and 2 inhibitors, PD-1 inhibitors, phototherapy (UVB), lasers.
• Older Systemic Treatments: systemic steroids, methotrexate, cyclosporine, mycophenolate mofetil, or oral minocycline.