Post-inflammatory Hyperpigmentation

PIH Basics - Spotting the Spots

• Definition: Acquired hypermelanosis (excess pigment) after cutaneous inflammation or injury.
• Pathophysiology: Inflammation triggers ↑ melanocyte activity or altered melanin distribution.
  • Epidermal PIH: ↑ melanin in keratinocytes; tan, brown, or dark brown.
  • Dermal PIH: Melanin in dermal macrophages (melanophages); blue-grey hue.
  • 📌 Epidermal = Easier to treat; Dermal = Deeper, Difficult.
• Key Cells:
  • Melanocytes: Primary melanin producers.
  • Macrophages: Ingest dermal melanin.

⭐ Epidermal PIH, characterized by increased melanin in keratinocytes, generally has a better prognosis and response to topical therapy compared to dermal PIH (melanin in dermal macrophages).

Causes & Culprits - The Inflammation Story

Any skin inflammation or injury can stimulate melanocytes, leading to PIH. Common triggers:

• Acne vulgaris: Especially inflammatory types.
• Eczema: Atopic dermatitis, contact dermatitis.
• Psoriasis: After plaque resolution.
• Lichen planus: Often leaves significant PIH.
• Trauma: Burns, abrasions, post-surgical.
• Infections: Fungal (e.g., tinea versicolor), viral (e.g., herpes zoster).
• Drug Reactions: E.g., tetracyclines, NSAIDs, fixed drug eruptions.
• Cosmetic Procedures: E.g., chemical peels, lasers, if improperly managed.

⭐ In Indian skin, acne vulgaris and lichen planus are particularly common precursors to persistent post-inflammatory hyperpigmentation.

Clinical Picture - Shades of Evidence

• Morphology: Ill-defined macules and/or patches.
• Color: Varies from tan, brown to greyish-blue, depending on melanin depth (epidermal vs. dermal).
• Distribution: Occurs at sites of previous inflammation (e.g., acne, eczema, trauma).

⭐ Wood's lamp examination is a crucial non-invasive tool to differentiate epidermal PIH (appears more obvious/accentuated) from dermal PIH (no accentuation or may appear less distinct).

Treatment Toolkit - Fading the Marks

• Core Strategy: Sun Protection
  • Mandatory: Broad-spectrum sunscreen SPF 30+ (reapply). Prevents worsening and recurrence.
• Treatment Pathway:

• Key Topical Agents:

  Agent	MOA (Simplified)	Key Note / Common Side Effect
  Hydroquinone (HQ) 2-4%	Tyrosinase inhibitor	Irritation, ochronosis (long-term)
  Azelaic Acid (AA) 15-20%	Tyrosinase inhibitor, anti-inflam.	Mild irritation, less hypopig.
  Topical Retinoids	↑Epidermal turnover, ↓melanin transfer	Irritation, photosensitivity
  (Tretinoin 0.025-0.1%, Adapalene)		Start low, go slow

• Other Topical Options: Kojic acid, Niacinamide (Vit B3), Vitamin C, Thiamidol. Often used in combination products.
• Procedural Interventions:
  • Chemical Peels: Glycolic acid, salicylic acid (superficial peels).
  • Lasers: Q-switched Nd:YAG, Picosecond lasers (target dermal melanin, for resistant cases).

⭐ Strict photoprotection is paramount in managing PIH; without it, other treatments are significantly less effective and recurrence is high.

High‑Yield Points - ⚡ Biggest Takeaways

• PIH is an acquired hypermelanosis post-inflammation or injury.
• More common and severe in darker skin (Fitzpatrick III-VI).
• Epidermal type: brown, transient. Dermal type: blue-grey, persistent (due to melanin incontinence).
• Wood's lamp: epidermal enhances, dermal does not.
• Common triggers: acne, eczema, lichen planus, burns, procedures.
• Sun protection is crucial for prevention and treatment.
• Treat underlying cause; use topical depigmenting agents (hydroquinone, retinoids, azelaic acid).