Postinflammatory hypopigmentation in Child
Postinflammatory hypopigmentation can occur in patients of all ages, sexes, and skin types, and is more visibly pronounced in those with darker skin phototypes. It can be seen as a sequela of many inflammatory skin diseases (atopic dermatitis, seborrheic dermatitis, psoriasis, lichen striatus, pityriasis lichenoides chronica, lichen planus, sarcoidosis, discoid lupus erythematosus), infections (zoster, pityriasis versicolor, impetigo), procedures (chemical peels, laser, dermabrasion), and burns.
Time to resolution of hypopigmentation is dependent on the underlying cause and severity of inflammation, ranging from a few weeks in minimally hypopigmented lesions to several years in depigmented lesions (eg, discoid lupus erythematosus and burns).
Related topic: Drug-induced hypopigmentation
L81.9 – Disorder of pigmentation, unspecified
277787003 – Post-inflammatory hypopigmentation
Differential Diagnosis & Pitfalls
- Pityriasis alba – Scaly, oval, ill-defined macules and patches with mild hypopigmentation; more common in children.
- Progressive macular hypomelanosis – Punctiform red fluorescence under Wood's lamp.
- Pityriasis versicolor – Coppery orange under Wood's lamp; potassium hydroxide (KOH) prep of scale shows a characteristic "spaghetti and meatballs" appearance.
- Leprosy – Associated with hypoesthesia.
- Mycosis fungoides – Early-stage variant involving hypopigmentation on the trunk and extremities that may be pruritic.
- Scleroderma – Circumscribed hypopigmentation with perifollicular pigment retention.
- Eruptive hypomelanosis – Acute onset of symmetric, monomorphic, hypopigmented macules with or without fine scaling. Usually preceded by viral prodrome and spontaneously resolves within 2-8 weeks.
- Medication – Particularly high-potency topical and intralesional corticosteroids.
- Chronic arsenic exposure – Hypopigmented lesions resemble idiopathic guttate hypomelanosis presentation but are scattered on a hyperpigmented base.
- Lichen striatus