Poikiloderma
Specialty: Skin.
Why it occurs
- Long-term accumulated chronic sun damage (main cause on the lateral side of the neck and décolleté, respecting the shaded submental area)
- Atrophic vascular poikiloderma (initial phase or variant of mycosis fungoides / cutaneous T-cell lymphoma)
- Chronic systemic or discoid lupus erythematosus (chronic inflammation of the dermal-epidermal junction with peripheral and pigmentary vascular damage)
- Chronic radioderma secondary to previous treatments with oncological radiotherapy
- Rare hereditary genetic syndromes (such as Rothmund-Thomson syndrome or dyskeratosis congenita).
Initial workup
Clinical diagnosis based on the classic triad: skin atrophy, fine telangiectasias and mottled hyperpigmentation mixed with areas of hypopigmentation. Skin biopsy with a 4 mm punch of the area of greatest atrophy or erythema for histopathological study, follicular immunohistochemistry and ruling out lymphoproliferative malignancy.
red flags
Presence of generalized poikilodermic plaques with an asymmetric distribution that are associated with intractable pruritus, palpable lymphadenopathy of stone consistency in accessible lymph node chains, or unexplained weight loss (strong suspicion of cutaneous T-cell lymphoma).
Standard management
- 2% hydroquinone cream combined with azelaic acid — local depigmentation treatment focused on attenuating the hyperpigmentation component of the lesion
- Emollient creams rich in lipids and intense moisturizers to improve the thinned skin barrier
- Strict physical photoprotection with zinc oxide or titanium dioxide SPF 50+ daily to stop progression induced by ultraviolet radiation
- Referral to a specialist for treatment of telangiectasias and pigment using pulsed dye laser (LCP) or intense pulsed light (IPL).
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Skin
- Listed causes
- 5
- Treatment options
- 4