Idiopathic Guttate Hypomelanosis

Common acquired disorder of small, sharply defined, porcelain white macules on sun exposed skin of adults, mainly the shins and forearms. The cause is unknown.

• It affects women more than men, from the third decade onwards, and the prevalence rises with age (about 50 to 80% in people over 50, and almost universal over 70). It occurs in all skin types but is most visible in dark skin.
• Proposed causes: chronic ultraviolet damage, ageing of melanocytes, genetic predisposition, trauma, and local autoimmune or degenerative processes. Histology shows reduced melanin and a decreased number of dopa positive melanocytes, with mild epidermal atrophy.
• It is benign, slowly progressive, and does not repigment spontaneously. It carries no risk of malignancy, but the skin around lesions is sun damaged and carries the usual risk of skin cancer.

• Discrete, round, oval or angular white macules, 2 to 6 mm (up to 10 mm), flat, well defined, and with no scale, redness or itch. Some appear slightly atrophic. Their number increases slowly over years, up to dozens.
• Distribution: extensor forearms and anterior shins most often, then upper arms and thighs. The face, neck and trunk are involved less often, and the palms and soles are spared.
• Differential diagnosis: vitiligo (larger, confluent, Koebner phenomenon, wider body distribution), post-inflammatory hypopigmentation, pityriasis alba, pityriasis versicolor, guttate morphoea and lichen sclerosus (surface change and atrophy), stellate pseudoscars (steroid use, easy bruising), hypopigmented mycosis fungoides, tuberous sclerosis macules (childhood), and scars from previous solar keratoses treated with cryotherapy.
• Complications: cosmetic concern only.

• Clinical, from age, distribution, size, and the stable porcelain white appearance.
• Wood lamp shows well demarcated, bright white macules. Dermoscopy shows a homogeneous white area with a sharp border and no scale or vessel change.
• Biopsy only if the diagnosis is uncertain. It shows reduced melanin, a reduction in melanocytes, and flattening of the rete ridges.
• Examine the surrounding skin for actinic keratoses, solar lentigines and skin cancer.

• Reassure the patient that the condition is harmless, common and usually permanent, and that no treatment is required.
• Photoprotection: sunscreen SPF 50, broad spectrum, on exposed skin, protective clothing, and avoidance of tanning and sunbeds, because ultraviolet damage contributes to progression and tanned skin increases the contrast.
• Cosmetic treatment for patients who request it (response is variable and evidence is limited):
  • Cryotherapy with liquid nitrogen, a light spray for 5 to 10 seconds, one freeze thaw cycle, repeated every 4 to 8 weeks. Repigmentation occurs in some patients, but over treatment causes hypopigmentation or scarring, so it is used with caution in dark skin.
  • Tacrolimus 0.1% ointment twice daily for 3 to 6 months.
  • Tretinoin 0.025 to 0.05% cream at night, or calcipotriol 0.005%, as adjuncts.
  • Intralesional triamcinolone acetonide 2.5 mg/mL, a very small volume per lesion, carries a risk of atrophy and is rarely appropriate.
  • Fractional carbon dioxide laser combined with topical fluorouracil 5% or 308 nm excimer, and punch grafting or suction blister grafting for small numbers of lesions in specialist centres.
  • Camouflage cosmetics and self-tanning products are safe.
• Special groups:
  • Pregnancy: sunscreen only. Avoid retinoids and fluorouracil.
  • Dark skin: avoid cryotherapy and laser unless carefully supervised.
  • Immunosuppression and long term sun exposed skin: check the skin yearly for actinic damage and cancer.
• Follow up: not needed for the condition itself. Advise an annual skin check where there is sun damage, and refer if a lesion changes or if the diagnosis is uncertain.