Post-inflammatory Hypopigmentation

PIH: Intro & Pathophys - Fading Fast

• Acquired disorder: ↓ or absent skin pigment post-inflammation or injury.
• More frequent and visually prominent in individuals with darker skin tones (Fitzpatrick types III-VI).
• Usually temporary, but resolution can be slow (months to years).
• Pathophysiology involves:
  • ↓ Melanin synthesis within melanocytes.
  • Impaired transfer of melanosomes to surrounding keratinocytes.
  • Actual loss or destruction of melanocytes in severe cases.
• Inflammatory mediators (e.g., certain cytokines, leukotrienes) are key culprits.

⭐ PIH often follows conditions like eczema, psoriasis, acne, burns, or even cosmetic procedures, especially in pigmented skin types.

PIH: Etiology & Clinical - Spot the Lesions

• Etiology (Common Triggers):
  • Inflammatory dermatoses: Eczema, Psoriasis, Lichen planus.
  • Infections: Pityriasis versicolor, Herpes zoster.
  • Physical injury: Burns, Cryotherapy, Laser, Chemical peels.
  • Medications: Topical steroids (prolonged).
• Clinical Presentation (Lesions):
  • Appearance: Hypopigmented macules/patches, not completely depigmented.
  • Color: Lighter than skin; varies from subtle loss to pallor.
  • Borders: Indistinct, "smudged," follows prior inflammation pattern.
  • Distribution: Localized to sites of previous inflammation or injury.
  • Symptoms: Usually asymptomatic; may have pruritus from prior cause.

⭐ On Wood's lamp, PIH shows some retained pigment (incomplete loss), unlike vitiligo's stark, chalky-white fluorescence.

PIH: Diagnosis & DDx - The Right White

• Diagnosis:

  • Key: History of prior inflammation (e.g., eczema, psoriasis, acne, burn).
  • Lesions: Hypopigmented (not achromic/depigmented); borders often ill-defined.
  • Wood's Lamp: May accentuate hypopigmentation; no bright blue-white fluorescence (unlike vitiligo).
  • Biopsy (rarely needed): ↓ melanin in epidermis; melanocyte count usually normal.

• Key DDx - Distinguishing Features:

  • Vitiligo: Complete depigmentation (achromia); well-demarcated; chalky-white fluorescence on Wood's lamp.

    ⭐ PIH typically shows normal melanocyte numbers with reduced melanin production/transfer, while vitiligo often demonstrates a complete absence of melanocytes.

  • Pityriasis Alba: Ill-defined, fine scales, faint erythema; common in atopic individuals, face/extensors.
  • Tinea Versicolor: Multiple, well-demarcated, scaly macules; KOH positive ("spaghetti & meatballs"); variable Wood's lamp fluorescence (e.g., yellowish-green).
  • Idiopathic Guttate Hypomelanosis (IGH): Small (2-5mm), discrete, "porcelain-white" macules; sun-exposed limbs.

PIH: Management & Prognosis - Restore the Hue

• Primary Goal: Treat underlying dermatosis; reassure patient (often self-limiting).
• Sun Protection: Essential daily; broad-spectrum sunscreen helps ↓contrast with normal skin.
• Topical Therapies:
  • Mild corticosteroids (e.g., hydrocortisone 1%): Short-term for any residual inflammation.
  • Topical Calcineurin Inhibitors (TCIs): Pimecrolimus, tacrolimus (preferred for face, flexures).
• Phototherapy (Persistent/Widespread PIH):
  • Excimer laser (308 nm): Targeted therapy for localized, stable lesions.
  • Narrowband UVB (NB-UVB): Option for more extensive PIH.
• Cosmetic Camouflage: Medicated or commercial concealers (e.g., Dermablend).
• Prognosis:
  • Generally good; spontaneous repigmentation common over months to years.
  • Slower if significant dermo-epidermal junction damage or delayed treatment of primary cause.

  ⭐ Repigmentation typically initiates perifollicularly (around hair follicles) or from the lesion's periphery, gradually coalescing centrally.

High‑Yield Points - ⚡ Biggest Takeaways

• Acquired loss of pigmentation following cutaneous inflammation or injury.
• Caused by impaired melanocyte function or reduced melanocyte numbers, leading to decreased melanin.
• Clinically appears as ill-defined macules or patches lighter than normal skin.
• Distribution typically follows the pattern of the original dermatosis.
• Diagnosis is usually clinical, relying on patient history and lesion appearance.
• Generally self-limiting, with spontaneous repigmentation occurring over months to years.
• Strict sun protection is vital to minimize contrast and support repigmentation.