Disorders of the cutaneous melanocytes — expanded notes
Clinical approach to hyperpigmentation
Establish whether the pigment is epidermal, dermal or mixed; ask about preceding inflammation, UV exposure, pregnancy/hormones, medications and systemic symptoms. Brown colour commonly reflects epidermal melanin; grey-blue colour may reflect dermal pigment or melanophages. Consider Wood lamp and dermoscopy where useful.
Melasma
Melasma causes symmetrical brown macules and patches on sun-exposed face, often centrofacial, malar or mandibular. Risk factors include UV and visible light, pregnancy, hormonal therapy, genetic predisposition and darker phototypes. It is chronic and relapsing. Management requires photoprotection, including visible-light protection, and selected topical depigmenting agents such as hydroquinone, azelaic acid or retinoids under appropriate guidance.
Post-inflammatory hyperpigmentation
PIH follows acne, eczema, burns, trauma or procedures. Inflammation stimulates melanogenesis and can damage the basal layer, allowing melanin to enter the dermis where melanophages retain it. Control the primary inflammation, avoid irritation and use photoprotection; pigment-lightening therapy may be added carefully.
Vitiligo pathogenesis and types
Vitiligo is an acquired depigmenting disorder involving loss of functional melanocytes. Autoimmune cytotoxic T-cell mechanisms, oxidative stress, genetic predisposition and melanocyte stress contribute. Non-segmental disease is often symmetrical and may progress; segmental disease is often unilateral and tends to stabilise earlier. Leukotrichia suggests follicular melanocyte involvement and may predict reduced repigmentation.
Diagnosis and associations
Diagnosis is clinical and supported by Wood lamp, which accentuates complete depigmentation. Assess extent, activity, Koebner phenomenon, mucosal involvement and psychosocial impact. Vitiligo is associated with autoimmune thyroid disease; investigate thyroid function when indicated. Differential diagnoses include pityriasis alba, post-inflammatory hypopigmentation, tinea versicolor, chemical leukoderma and hypopigmented scars.
Treatment
Treatment depends on extent, site, activity and patient preference. Options include topical corticosteroids for limited body sites, topical calcineurin inhibitors for face/flexures, narrowband UVB for more extensive disease and selected surgical techniques for stable localised lesions. Counsel that response is slow and variable and relapse may occur. Provide sun protection and psychological support.