Post-Inflammatory Hypopigmentation

Loss of skin colour in an area of previous inflammation or injury. It results from reduced melanin production, impaired transfer of melanosomes to keratinocytes, or, in severe or deep injury, destruction of melanocytes.

• It is commoner and more visible in darker skin, but occurs in all skin types.
• Common causes:
  • Inflammatory dermatoses: atopic dermatitis, pityriasis alba, psoriasis, lichen planus, lichen striatus, pityriasis rosea, seborrhoeic dermatitis, discoid lupus erythematosus, sarcoidosis, and acne.
  • Infection: pityriasis versicolor, tinea, and healed impetigo.
  • Physical and procedural injury: burns, cryotherapy, laser and light treatments, chemical peels, dermabrasion, electrosurgery, and friction.
  • Drugs and chemicals: intralesional or superpotent topical corticosteroids, phenolic and catechol compounds in cosmetics and rubber (chemical leukoderma), and hydroquinone misuse.
• Pigment returns over 6 to 12 months if melanocytes are preserved. If the melanocyte reservoir has been destroyed (deep burn, scar, discoid lupus, repeated cryotherapy), the change is permanent.

• Hypopigmented macules or patches matching the earlier area of inflammation or injury. The edge is indistinct and the colour is lighter than normal but not chalk white.
• Fine scale may persist while the original dermatosis is active. Islands of normal pigment around hair follicles are common during repigmentation, and are a favourable sign.
• Scar texture, atrophy or hair loss indicates deep injury or scarring disease (discoid lupus).
• Differential diagnosis: vitiligo (sharply marginated depigmentation, no preceding inflammation, often symmetrical, Koebner phenomenon), idiopathic guttate hypomelanosis, pityriasis versicolor, nevus depigmentosus, leprosy, lichen sclerosus, morphoea, hypopigmented mycosis fungoides, piebaldism, chemical leukoderma, and tuberous sclerosis.
• Complications: cosmetic distress, sunburn of pale skin, and persistent change when melanocytes are lost.

• Clinical, based on a clear history of preceding inflammation, injury or procedure.
• Wood lamp: hypopigmented, not the bright white of vitiligo. Dermoscopy shows retained perifollicular pigment.
• Potassium hydroxide preparation for pityriasis versicolor and tinea.
• Check for reduced sensation if leprosy is a possibility, and take a slit skin smear and biopsy when suspected.
• Biopsy for atypical, progressive or scarring lesions, or to exclude mycosis fungoides, which shows epidermotropic lymphocytes.
• Check for current use of potent steroids, depigmenting agents and exposure to phenolic chemicals.

• Treat the cause: control the underlying dermatosis, stop causative agents, and avoid further trauma, friction, cryotherapy and aggressive peels in the area.
• Observation is the first approach. Expect gradual repigmentation over 6 to 12 months, or longer for deep injury.
• Photoprotection: sunscreen SPF 50, broad spectrum, daily to the affected area, because pale skin burns easily and tanned surrounding skin increases the contrast.
• Topical therapy to stimulate repigmentation (evidence is limited):
  • Tacrolimus 0.1% ointment twice daily for 3 to 6 months. It also treats residual inflammation. Use 0.03% in children aged 2 to 15 years.
  • A low potency steroid for only a short period if inflammation persists.
  • Calcipotriol 0.005% once or twice daily, alone or with phototherapy.
• Phototherapy (specialist): narrowband UVB 2 to 3 times weekly for 3 to 6 months, with starting dose and 10 to 20% increments set by skin type and minimal erythema dose. The 308 nm excimer laser or lamp is used for localised patches, twice weekly for 3 to 6 months. Repigmentation depends on residual follicular melanocytes, and is poor in scars.
• Camouflage with water resistant cosmetic cover, self-tanning products (dihydroxyacetone), or micropigmentation (tattooing) for stable patches.
• Surgical melanocyte transfer (suction blister grafting, punch grafting, non-cultured epidermal cell suspension) is offered for stable, localised, scarred patches after at least 12 months of stability, by specialist teams.
• Chemical leukoderma: stop exposure to the causative chemical, and use the same repigmentation measures.
• Special groups:
  • Children: observe, protect from the sun, and avoid phototherapy if repigmentation is likely.
  • Pregnancy: sunscreen and camouflage, with narrowband UVB if needed. Avoid psoralen treatments.
  • Dark skin: avoid cryotherapy and aggressive laser or peels for any benign condition, because of the risk of permanent loss.
• Follow up: review at 3 months and 6 months with photographs. Refer to dermatology if there is progression, a possible diagnosis of vitiligo, scarring, or a request for phototherapy or surgery.