A group of inherited genetic disorders characterized by reduced or absent melanin production due to defects in melanocyte function or melanin synthesis, despite a normal number of melanocytes.
Epidemiology
- Prevalence: approximately 1 in 17,000–20,000 worldwide
- Occurs in all ethnic groups
- Usually present from birth
- Most forms are autosomal recessive
Aetiology
Albinism results from mutations affecting melanin biosynthesis or melanosome function, including:
- TYR (tyrosinase) – OCA type 1
- P protein defect — OCA type 2
- TYRP1 – OCA type 3
- SLC45A2 – OCA type 4
Pathophysiology
- Melanocytes are present in normal numbers
- Defective conversion of tyrosine → DOPA → melanin
- Leads to hypopigmentation of skin, hair, and eyes
Clinical presentation
Classification
Oculocutaneous Albinism (OCA)
Involves skin, hair, and eyes.
Type | Defect | Key Features |
OCA1 | Tyrosinase deficiency | Severe, little/no pigment |
OCA2 | P protein | Partial pigmentation |
OCA3 | TYRP1 | Reddish-brown pigment |
OCA4 | SLC45A2 | Similar to OCA2 |
Ocular Albinism
- Mainly affects the eyes
- X-linked (GPR143 mutation)
- Minimal skin involvement
Clinical Features
Cutaneous
- Generalized hypopigmentation from birth
- White to light-yellow hair
- Very fair skin
- Inability to tan

Ocular (Hallmark)
- Nystagmus
- Photophobia
- Reduced visual acuity
- Strabismus
- Foveal hypoplasia
- Translucent iris
Investigations
Test | Purpose |
Ophthalmologic exam | Visual abnormalities |
Hair bulb test | Reduced tyrosinase activity |
Genetic testing | Confirm subtype |
Management
No curative treatment
Supportive Care
- Strict photoprotection
- Sunscreens (SPF ≥30)
- Protective clothing
- Regular skin cancer screening
Ophthalmologic Care
- Corrective lenses
- Visual aids
- Early intervention for amblyopia