Andrei Metelitsa, MD, FRCPC, FAAD Co-Director, Institute for Skin Advancement Clinical Associate Professor, Dermatology University of Calgary, Canada

Transcription

1 Andrei Metelitsa, MD, FRCPC, FAAD Co-Director, Institute for Skin Advancement Clinical Associate Professor, Dermatology University of Calgary, Canada

2 Copyright 2017 by Sea Courses Inc. All rights reserved. No part of this document may be reproduced, copied, stored, or transmitted in any form or by any means graphic, electronic, or mechanical, including photocopying, recording, or information storage and retrieval systems without prior written permission of Sea Courses Inc. except where permitted by law. Sea Courses is not responsible for any speaker or participant s statements, materials, acts or omissions.

3 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

4 Learning Objectives Hyperpigmentation Melasma Drug-Induced PIH Neurofibromatosis Lentigines Hypo/Depigmentation Vitiligo Tuberous Sclerosis Pityriasis Alba

5 1. Disorders of Hyperpigmentation

6 i. Melasma

7 i. Melasma

8 i. Melasma

9 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

10 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

11 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

12 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

13 ii. Drug-Induced Pigmentation Minocycline Antidepressants (imipramine) Amiodarone Antimalarials Chlorpromazine Heavy metals

14 Drug-Induced Pigmentation

15 Drug-Induced Pigmentation

16 iii. Postinflammatory Hyperpigmentation

17 Postinflammatory Hyperpigmentation Very common Typically affects dark-skinned people Usually develops following previous inflammation or injury to the skin Typically resolves within 1 year

18 iv. Neurofibromatosis

19 iv. Neurofibromatosis

20 iv. Neurofibromatosis

21 Neurofibromatosis

22 iv. Neurofibromatosis

23 iv. Neurofibromatosis

24 v. Lentigo

25 2. Disorders of Hypo/Depigmentation

26 a) Vitiligo

27 a) Vitiligo

28 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

29 Vitiligo Treatment General measures Sun Protection, Makeup Topical steroids Topical calcineurin inhibitors Phototherapy Laser Depigmentation therapy

30 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 Jun 24.

31 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

32 Forehead photos

33 Hands photos

34 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

35 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

36 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)

37 b) Tuberous Sclerosis

38 Tuberous Sclerosis

39 c) Pityriasis Alba

40 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

41 Pityriasis Alba - Treatment May persist for months-years Resolves spontaneously Topical Steroids Topical Calcineurin Inhibitors

42 d) Tinea Versicolor

43 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)

44 Tinea Versicolor Treatment: Topical antifungals E.g. ketoconazole, terbinafine Systemic antifungals Itroconazole, ketoconazole, fluconazole

45 PEARLs Sunprotection is critical Increased pigmentation Brown vs. slate-grey (medication induced) Loss of pigmentation Depigmentation (vitiligo) vs. hypopigmentation