Acquired, chronic hypermelanosis characterized by symmetrical, irregularly bordered hyperpigmented macules and patches
Epidemiology
- Common in women of reproductive age
- Female : male ≈ 9 : 1
- More prevalent in Fitzpatrick skin types III–V
- Higher incidence in tropical regions
- Strong association with sun exposure, pregnancy, and hormonal factors
Aetiology
- Ultraviolet (UV) radiation (most important)
- Hormonal influences:
- Pregnancy (chloasma)
- Oral contraceptives
- Genetic predisposition
- Photosensitizing drugs and cosmetics
- Thyroid dysfunction (association)
Pathophysiology
- Hyperfunctional melanocytes with normal cell count
- Increased melanin synthesis and transfer
- UV exposure induces:
- ↑ α-MSH
- ↑ tyrosinase activity
- Dermal inflammation and vascular changes
Clinical presentation
- Symmetric, irregularly shaped brown to gray-brown macules/patches
- Well-defined but irregular borders
- No scaling, erythema, or symptoms
- Gradual onset, chronic course
- Exacerbated by sun exposure

Investigations
- Clinical diagnosis
- Wood’s lamp: helps determine pigment depth (limited in darker skin)
- Dermoscopy: reticulated brown pigmentation
- Biopsy: rarely required
Management
General Measures (Cornerstone)
- Strict photoprotection
- Broad-spectrum sunscreen (SPF ≥30–50)
- Physical blockers (zinc oxide, titanium dioxide)
- Protective clothing
Topical Therapy (First-line)
Agent | Mechanism |
Hydroquinone 2-5% | Tyrosinase inhibition |
Triple combination cream | Hydroquinone + tretinoin + corticosteroid |
Azelaic acid 20% | Inhibits tyrosinase |
Kojic acid | Melanin inhibition |
Retinoids | Increase epidermal turnover |
Procedural Therapy
- Chemical peels (glycolic, salicylic acid)
- Laser and light-based therapy (with caution)
- Microneedling (adjunctive)