Melasma Flashcards
(17 cards)
Incidence
Incidence: 90% F
9% Hispanics
40% south east Asians
Exacerbating factors
Exacerbating factors: pregnancy, OCP, UV light, visible light (darker pigmentation, more sustained), autoimmune thyroid disease, phenytoin, phototoxic drugs
Aetiology
UV induced upregulation of melanocyte stimulating cytokines
Increased vascularity and increased VEGF in epidermis. Which is why Pulsed dye and transexamic acid may help
Locations
Brown macules or pattern in centrofacial (most common), malar or mandibular region. Most often overlapping. Rarely affects below the mandible. Face> forearms
Problem with wood’s lamp
Wood’s lamp may help, but often limiting – in theory epidermal more obvious. Usually mixed: epidermal/dermal
Scoring system
MASI: melasma area & severity index. (0-48)
A)area of involvement
D) darkness
H) homogeneity in the forehead, right malar, left malar, chin
Then consider % surface area
DDx
DDx: Naevus of Ota, Hori’s naevus, Medication induced hyperpigmentation Erythema dyschromia perstans LPP Lichenoid drug Riehl’s melanosis Post inflammatory pigmentation Maturational dyschromia Periorbital hyperpigmentation Acanthosis nigricans Lentigines Exogenous ochronosis.
DDx if lateral forehead or nasolabial folds
If lateral forehead- think drug induced or LPP
Nasolabial folds spared (drug – often involved)
Histology
Histo: melanocytes contain and increased no of melanosomes. Increased melanin deposition is in all layers of the epidermis.
Treatment - general measures
Photoprotection, particularly with physical blockers and iron oxide 3.2% containing sunscreens or make up. Consider computer screen protectors and tinted car windows.
Consider checking baseline Vit D levels
Cosmetic camouflage
DDx of facial hyperpigmentation
Squamous: Riehl’s melanosis (contact allergy) or Berloque dermatitis, PIH, erythromelanosis follicularis faceiei et colli
Infiltrates: mastocytosis
Naevus of ota like macules
Drugs: minocycline, photosensitive drug, amiodarone, argyria, exogenous ochronosis , OCP
Immune: LP, actinic type, LPP, erythema dyschromicum perstans
Physical: facial erythema ab igne, PMLE, poikiloderma of civatte
Metabolic: Liver disease, haemachromatosis.
Endocrine: Melasma, addisons
Nutritional: Kwashiorkor, pellagra, sprue, Vit B12 deficiency
Kligman-Willis combination?
Kligman-Willis combination and variants : dex 0.1%, hydroquinone 5%, tretinoin 0.1%. Daily for 12/52, then twice weekly maintenance.
Peels that could be used
Glycolic acid – alpha hydroxyl acid 20-70% Lactic acid Sal acid TCA 10-20% Tretinoin Other
Glycolic acid peels
Reduction in melasma, but similar from hydroquinone or dual topicals. Optimal concentration is 53%. May marginally help in combination with 5% Hydroquinone 0.05% tretinoin 1% HC
Laser?
Last resort considering risk of PIH
IPL 560nm cut off filters: avoid in darker skin types
Q switched lasers eg Nd:YAG
Erb: YAG: not effective
Non ablative 1550nm fractional laser (erb: glass) – as effective as 15% TCA peel
Fractional 1927 laser – studies not convincing
Systemics
Oral transexamic acid : thought it decreases tyrosinase activity and possibly increases VEGF
SE: menstrual irregularity, headaches, naeusa and back pain
No evidence for increase in thrombotic events in doses up to 3.9-4g/day for 4-5/7 per cycle
500mg daily if failed or are intolerant of hydroquinone. Trial 6-12 months. Attempt to transition to topical maintenance with sunscreen + topical retinoid.
Possible regimes
1) 0.1% tretinoin, 1% HC, 4-6% HQ +0.5% Ascorbic acid in aqueous cream nocte
2) 20% topical azelaic acid for epidermal
3) 4% HQ twice daily
RV at 8 weeks
4) 30% GA peel up to 3min then increasing in duration and concentration every 4-6 weeks as tolerated
5)2.5% kojic acid + 2.5% hydroquinone + 1% HC
