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Andrei Metelitsa, MD, FRCPC, FAAD
Co-Director, Institute for Skin Advancement
Clinical Associate Professor, Dermatology
University of Calgary, Canada
Copyright © 2017 by Sea Courses Inc.
All rights reserved. No part of this document may be reproduced, copied, stored, or transmitted in any
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Sea Courses is not responsible for any speaker or participant’s statements, materials, acts or
omissions.
Faculty/Presenter Disclosure
Faculty: [Andrei Metelitsa MD FRCPC FAAD]
Relationships with commercial interests:
▪ Grants/Research Support: N/A
▪ Speakers Bureau/Honoraria: N/A
▪ Consulting Fees: N/A
3
Learning Objectives
Hyperpigmentation
▪ Melasma
▪ Drug-Induced
▪ PIH
▪ Neurofibromatosis
▪ Lentigines
Hypo/Depigmentation
▪ Vitiligo
▪ Tuberous Sclerosis
▪ Pityriasis Alba
▪ Tinea Versicolor
1. Disorders of Hyperpigmentation
i. Melasma
i. Melasma
i. Melasma
Melasma
Seen primarily in women
▪ at least 90% of patients
Increased prevalence in individuals who are
Hispanic, Asian or of African descent
Most common location is the face, followed by
the forearms
Symmetric patches of hyperpigmentation with
irregular borders due to increased melanin
within the epidermis and/or dermis
Melasma Treatment
Daily sun protection is critical
▪ Sunblock is preferred
Topical agents
▪ Hydroquinone
▪ Azelaic Acid
▪ Kojic Acid
▪ Retinoids
▪ Kligman formula
Chemical peels
Lasers
▪ Fractionated non-ablative
Melasma Treatment
Modified Kligman Formula▪ 2%HC + 5%HQ +0.05% tretinoin cream
8 week data▪ Triple combo: 26% clearance
▪ HQ + tretinoin 9% clearance
▪ HQ + fluocinolone 1.9% clearance
Triple combo vs HQ alone▪ 35% vs 4% improvement
Hydroquinone
Typically 4% preparation▪ Usually suggest limiting use to 3 months
Exogenous ochronosis (blue-gray discoloration) is very rare▪ Usually associated with higher concentration of hydroquionone
(8%)
▪ More prolonged use
ii. Drug-Induced Pigmentation
Minocycline Antidepressants (imipramine) Amiodarone Antimalarials Chlorpromazine Heavy metals
Drug-Induced Pigmentation
Drug-Induced Pigmentation
iii. Postinflammatory Hyperpigmentation
Postinflammatory Hyperpigmentation
Very common Typically affects dark-skinned people Usually develops following previous inflammation
or injury to the skin Typically resolves within 1 year
iv. Neurofibromatosis
iv. Neurofibromatosis
iv. Neurofibromatosis
Neurofibromatosis
iv. Neurofibromatosis
iv. Neurofibromatosis
v. Lentigo
2. Disorders of Hypo/Depigmentation
a) Vitiligo
a) Vitiligo
Vitiligo
Acquired, idiopathic disorder characterized by circumscribed depigmented macules and patches
Usually asymptomatic Clinical variants include localized, generalized
and universal Association with immune disorders
▪ especially thyroid Wood’s lamp accentuates areas of vitiligo
Vitiligo Treatment
General measures
▪ Sun Protection, Makeup
Topical steroids
Topical calcineurin inhibitors
Phototherapy
Laser
Depigmentation therapy
Woman in her 50’s with progressive vitiligo > 1 year
Increasing involvement of hands and face
Past treatments: triamcinolone, tacrolimus and short course of nUVB
▪ Poor efficacy
Patient requested alternate therapy
Craiglow BG, King BA. Tofacitinib Citrate for the Treatment of Vitiligo: A Pathogenesis-Directed Therapy. JAMA Dermatol. 2015 Jun 24.
Oral tofacitinib citrate 5 mg every other day
3 weeks, the dosage was increased to 5 mg/d
▪ half the approved dose for RA which is 5 mg twice daily
2 months of therapy, partial repigmentation of the face and upper extremities was evident
5 months, repigmentation of the forehead and hands was nearly complete
▪ Remaining involved areas demonstrated partial repigmentation
Forehead photos
Hands photos
Tofacitinib is a JAK 1/3 inhibitor that was FDA approved in 2012 for the treatment of moderate to severe rheumatoid arthritis
Recently described in the treatment of alopecia universalis
Alopecia areata and vitiligo share genetic risk and appear to share pathogenesis
Interferon-gamma–induced expression of C-X-C motif chemokine 10 (CXCL10) in keratinocytes is an important mediator of depigmentation in vitiligo
Hypothesis: Tofacitinib effectively leads to blockade of interferon gamma signaling and downstream CXCL10 expression, thus giving rise to repigmentation in vitiligo
Interferon-gamma–induced expression of C-X-C motif chemokine 10 (CXCL10) in keratinocytes is an important mediator of depigmentation in vitiligo
Oral Tofacitinib (Jak 1/3 inhibitor) Topical Ruxolitinib (Jak 1/2 inhibitor)
b) Tuberous Sclerosis
Tuberous Sclerosis
c) Pityriasis Alba
Pityriasis Alba
Low grade dermatosis Minor feature of atopic dermatitis More common among dark-skinned
children Presents with ill-defined hypopigmented
patches▪ Face most common site
▪ Initially can be more erythematous
▪ More apparent in summer
Pityriasis Alba - Treatment
▪ May persist for months-years
▪ Resolves spontaneously
▪ Topical Steroids
▪ Topical Calcineurin Inhibitors
d) Tinea Versicolor
Tinea Versicolor
Etiology: Common superficial cutaneous fungal eruption caused by Malassezia furfur
History: ▪ Usually affects young adults
▪ Humid Environments Physical:
▪ Oval macules and patches on the trunk
▪ Hyperpigmented and hypopigmented variants Diagnosis:
▪ KOH – classic spaghetti and meatballs (hyphae and spores)
Tinea Versicolor
Treatment:
▪ Topical antifungals▪ E.g. ketoconazole, terbinafine
▪ Systemic antifungals▪ Itroconazole, ketoconazole, fluconazole
PEARLs
Sunprotection is critical
Increased pigmentation
▪ Brown vs. slate-grey (medication induced)
Loss of pigmentation
▪ Depigmentation (vitiligo) vs. hypopigmentation