Lecture 38 Dyspigmentation disorders Flashcards
What does the tx/management of melasma look like?
Baseline: photoprotection ⇒ look for iron oxides to help block blue light
Topicals: hydroquinone, niacinamide - inhibits transfer of melanosomes from melanocytes to skin cells
ascorbic acid - may reduce activity of tyrosinase
azelaic acid - may reduce tyrosinase activity and promote cell turnover
kojic acid - may reduce tyrosinase activity
compounded combo cream (hydroquinone + tretinoin + TCS)
Systemic Agents: tranexamic acid (ensure pt doesn’t have hx of PEs, DVTs or coagulation issues)
Procedural: chemical peels - use acids to exfoliate and speed up cell turnover
microneedling - alternative to peels and laser in darker phenotypes, can combo with topical for better results, penetrates skin to trigger wound healing
laser - target deeper pigment using specific wavelengths
How does hydroquinone work in melasma treatment (MOA, product, dosing/admin, contra/AE)
MOA: Tyr-kinase inhibitor, inhibits enzymatic oxidation of tyrosinase (normally converts L-3,4-dihydroxyphenylalanine ⇒ melanin), destroys melanocytes, degrades melanosomes, inhibits DNA and RNA synthesis
Product/Dose/Admin: monotherapy 4% or in combo cream, limit duration to about 6 months
Contra: pregnancy
AE: irritant contact dermatitis, allergic contact dermatitis, erythema, inflammation, xeroderma, stinging, leukoderma, ochronosis
How does tranexamic acid (TXA) work in melasma tx (MOA, dose, contra)?
MOA: plasmin inhibitor, UV light increases plasmin activity (keratinocytes) ⇒ increased melanocytic stimulating mediators, this drug inhibits UV-induced plasma activity in keratinocytes
Dose: 250 (325) mg PO BID for 8-12 weeks, topical may also be used
Contra: hypercoagulable comorbidities (ex. VTE, malignancy, OCP), females on combo hormonal contraception
relative ones - recent infection, smoking
What is post-inflammatory hypopigmentation (presentation, causes)?
more common in Fitzpatrick skin scores III >/= but can happen to anyone, may present as partial or total loss of pigment in affected area, presents as patch or area of loss that recently was inflamed or injured, most are self-limiting and will heal on their own
Causes: cutaneous inflammation including cutaneous infection (ex. dermatitis, acne vulgaris, cellulitis, tinea versicolor), cutaneous injury (ex. fall with damage to skin), cutaneous procedures (surgical excision site)
How is post-inflammatory hypopigmentation managed?
Topical Corticosteroids: reduce inflammation helping accelerate re-pigmentation
Topical Calcineurin Inhibitors: reduce inflammation helping accelerate re-pigmentation, can be used on more sensitive areas (ex. genitalia, axilla, face) as doesn’t promote atrophy
Topical Antifungals: used when tx tinea versicolor infections, topical or oral options, topical ones like ketoconazole 2% may be used for weeks to months, if not responding then oral options like itraconazole or fluconazole may be sued for short duration or pulsed
How is vitiligo managed tx wise?
Phototherapy: UVB commonly used 2-3 x week and induces re-pigmentation in most pt with early and localized disease
Topical Corticosteroids: reduce inflammation helping accelerate re-pigmentation, used on combo with phototherapy
Topical Calcineurin Inhibitors: reduce inflammation helping accelerate re-pigmentation, can be used on sensitive areas due to not causing atrophy, used on combo with phototherapy
Jak-Kinase Inhibitor Ruxolitinib: binds to JAK1 and 2 and thought to inhibit IFN-gamma mediated JAK-STAT signaling
Systemic Corticosteroids: suppress autoimmune response thought to attack melanocytes, can cause mood changes, weight gain, insomnia, Cushing’s sx, adrenal suppression
Methotrexate: immunosuppressant, may be considered in severe and steroid resistant
