Acne and Rosacea: Epidemiology, Diagnosis and Treatment

97 Pages·2011·3.366 MB·English

by  David J Goldberg, (Dermatologist), Alexander L Berlin

Acne and Rosacea:
Epidemiology, Diagnosis and
Treatment
David J. Goldberg, MD, JD
Clinical Professor of Dermatology & Director of Laser Research,
Mount Sinai School of Medicine,
New York, NY
Clinical Professor of Dermatology & Chief of Dermatologic Surgery
UMDNJ New Jersey Medical School,
Newark, NJ
Adjunct Professor of Law
Fordham Law School,
New York, NY
Director, Skin Laser & Surgery Specialists,
New York, NY
Alexander L. Berlin, MD
Clinical Assistant Professor of Dermatology,
UMDNJ New Jersey Medical School,
Newark, NJ
Director of Mohs & Cosmetic Surgery,
US Dermatology Medical Group - Mullanax Dermatology Associates
Arlington, TX.
MANSON
PUBLISHING
Copyright © 2012 Manson Publishing Ltd
ISBN: 978-1-84076-150-4
All rights reserved. No part of this publication may be reproduced, stored in a
retrieval system or t ransmitted in any form or by any means without the written
permission of the copyright holder or in accordance with the provisions of the
Copyright Act 1956 (as amended), or under the terms of any licence permitting
limited copying issued by the Copyright Licensing Agency, 33–34 Alfred Place,
London WC1E 7DP, UK.
Any person who does any unauthorized act in relation to this publication may be
liable to criminal prosecution and civil claims for damages.
A CIP catalogue record for this book is available from the British Library.
For full details of all Manson Publishing Ltd titles please write to:
Manson Publishing Ltd, 73 Corringham Road, London NW11 7DL, UK.
Tel: [phone]
Fax: [phone]
Email: [email protected]
Website: www.mansonpublishing.com
Commissioning editor:Jill Northcott
Project manager:Kate Nardoni
Copy editor:Ruth Maxwell
Design:Ayala Kingsley
Layout:DiacriTech, Chennai, India
Colour reproduction: Tenon & Polert Colour Scanning Ltd, Hong Kong
Printed by: Butler Tanner & Dennis, Frome, England
CONTENTS
5 ROSACEA – EPIDEMIOLOGY AND
Abbreviations 4
PATHOPHYSIOLOGY 51
Preface 5
Introduction 51
1 ACNE VULGARIS – EPIDEMIOLOGY Epidemiology 51
AND PATHOPHYSIOLOGY 7 Definition of rosacea 52
Rosacea subtypes 52
Introduction 7
Pathophysiology of rosacea 55
Epidemiology 8
Clinical assessment of acne vulgaris 10
6 ROSACEA – CURRENT MEDICAL
Pathophysiology of acne vulgaris 11
THERAPEUTICS 59
2 ACNE VULGARIS – CURRENT Introduction 59
MEDICAL THERAPEUTICS 15 General considerations 59
Topical agents 60
Introduction 15
Oral agents 62
Topical agents 15
Oral agents 20
7 LASERS AND SIMILAR
3 LASERS AND SIMILAR DEVICES DEVICES IN THE TREATMENT
OF ROSACEA 65
IN THE TREATMENT OF
ACNE VULGARIS 29 Introduction 65
General concepts and mechanism
Introduction 29
of action 65
Mid-infrared range lasers 29
Preoperative care 66
Pulsed-dye lasers 32
Pulsed-dye lasers 66
Visible light sources and light-emitting diodes 33
Intense pulsed light sources 68
Photodynamic therapy 34
KTP and Nd:YAG lasers 70
Radiofrequency devices 36
Future directions in light-based
treatment of rosacea 72
4 TREATMENT OF ACNE SCARS 39 8 LASERS AND SIMILAR DEVICES IN
THE TREATMENT OF SEBACEOUS
Introduction 39
HYPERPLASIA 73
Classification of acne scars 39
Surgical options: punch excision, subcision, Introduction 73
punch elevation 41
Aging of the sebaceous glands and the
Dermaroller 43 pathophysiology of sebaceous hyperplasia 73
Chemical reconstruction of skin scars Clinical considerations 74
(CROSS) technique 43
Lasers and similar technologies in the treatment
Injectables in the treatment of atrophic acne scars 44 of sebaceous hyperplasia 75
Lasers and laser-like devices: traditional
ablative resurfacing 45
References 77
Lasers and laser-like devices: traditional
nonablative resurfacing 46 Index 93
Lasers and laser-like devices: fractional resurfacing 47
Treatment of keloid and hypertropic acne scars 50
ABBREVIATIONS
ALA aminolevulinic acid MMP matrix metal loproteinase
AP activator protein MTZ microscopic treatment zone
CAP cationic antimicrobial protein Nd:YAG neodymium:yttrium–aluminum–garnet
CRABP cytosolic retinoic acid-binding protein PABA para-aminobenzoic acid
CROSS chemical reconstruction of skin scars PDL pulsed-dye laser
DHEA-S dehydroepiandrosterone sulfate PDT photodynamic therapy
DHT dihydrotestosterone Pp protoporphyrin
DISH diffuse idiopathic skeletal hyperostosis PP papulopustular (rosacea)
Er:YAG erbium:yttrium–aluminum–garnet (laser) RAR retinoic acid receptor
Er:YSGG erbium:yttrium–scandium–gallium-garnet RARE retinoic acid response element
(laser)
RF radiofrequency
ET erythematotelangiectatic (rosacea)
ROS reactive oxygen species
FDA Food and Drug Administration
RXR retinoid X receptor
G6PD glucose-6-phosphate dehydrogenase
SCTE stratum corneum tryptic enzyme
HIV human immunodeficiency virus
TCA trichloroacetic acid
ICAM intercellular adhesion molecule
TLR Toll-like receptor
IGF insulin-like growth factor
TNF tumor necrosis factor
IL interleukin
TRT thermal relaxation time
IPL intense pulsed light
UV ultraviolet
KTP potassium titanyl phosphate (laser)
VEGF vascular endothelial growth factor
LED light-emitting diode
MAL methyl aminolevulinate
PREFACE
Acne and rosacea are two incredibly common skin problems that have both a medical and cosmetic impact on the
daily lives of millions of people. Much has been written in books and journal articles about the medical treatment of
acne and rosacea. Similarly, much has been written in books and journal articles about the cosmetic treatment of
acne and rosacea. This book is unique in that it presents an objective look at both the medical and cosmetic
treatments of these two skin disorders.
The first four chapters deal with acne and acne scars and the medical and laser/light treatments used to treat
patients with these problems. The next three chapters take the same approach to rosacea. Finally, the last chapter
discusses the treatment of sebaceous hyperplasia.
We greatly appreciate the information provided by Professor Anthony Chu of Hammersmith Hospital, London,
UK, on the availability of various therapeutic agents outside of the US.
David J. Goldberg
Alexander L. Berlin
New York, NY
and Arlington, TX
Disclaimer
The advice and information given in this book are believed to be true and accurate at the time of going to press. However,
not all drugs, formulations, and devices are currently available in all countries, and readers are advised to check local
availability and prescribing regimens.
This page intentionally left blank
7
1
ACNE VULGARIS –
EPIDEMIOLOGY AND
PATHOPHYSIOLOGY
INTRODUCTION
ACNEvulgaris is a common disorder of the psychological impairment in those affected. The severity
pilosebaceous unit affecting millions of of acne may vary significantly from the mildest
people worldwide. Although most frequently comedonal forms (1) to a severe and debilitating
encountered in adolescents, acne may persist well condition (2). In addition to the face, the chest, back,
into adulthood and lead to significant physical and and shoulders are also commonly affected (3, 4).
1 2
1 Mild comedonal acneon a patient’s face. 2 Severe cystic acne.
3 4
3 Acne papules andpustuleson the chest. 4 Acne papulesassociated with extensive
postinflammatory hyperpigmentation on a patient’s back.
8
preteens (Cunliffe et al. 2001; Jansen et al. 1997; Lucky
5 1998).
The prevalence of acne in individuals with skin of
color has, likewise, been investigated in several studies
(6, 7). Thus, Halder et al. (1983) reported acne being
present in 27.7% of the Black patients and 29.5% of the
Caucasian patients. Additional studies of adult patients
in the United Kingdom and Singapore have placed the
prevalence of adult acne at 13.7% of the Black patients
and 10.9% of the Indian and Asian patients (Child et al.
1999; Goh & Akarapanth 1994). It has also been
shown that the presence of significant inflammation,
resulting in the clinical appearance of nodulocystic
acne, is more common in Caucasian and Hispanic
5 Inacné excoriée des jeunes filles,patients frequently patients than in their Black counterparts (Wilkins &
manipulate their acne lesions, leading to prolonged healing Voorhees 1970). More recent evidence indicates that
time and often, scarring. subclinical, microscopic inflammation may be more
common in the latter group (Halder et al. 1996).
It has also been suggested that certain non-
westernized societies demonstrate significantly lower
Numerous factors, both intrinsic and extrinsic (5), may prevalence of acne (Cordain et al. 2002; Schaefer 1971;
underlie the development and the progression of the Steiner 1946). The cause of such disparity is unclear and
disease. although nutritional factors have been suggested as the
cause of lower acne rates, this inference has so far not
EPIDEMIOLOGY
been conclusively substantiated (Bershad 2003).
Acne is the most common cutaneous disorder in the The issue of nutrition and its influence, or lack
Western world. In the United States, its prevalence has thereof, on acne has long been a highly contested one
been variably estimated at between 17 and 45 million (Adebamowo et al. 2005; Bershad 2003; Bershad 2005;
people (Berson et al. 2003; White 1998). This Cordain 2005; Danby 2005; Kaymak et al. 2007; Logan
number is typically based on a landmark publication 2003; Smith et al. 2007; Treloar 2003). Proponents of
by Kraning & Odland (1979), which estimated the the link between acne and nutrition frequently cite
prevalence of acne in persons aged 12–24 years at 85%. nutritional influence on serum hormone levels, such as
Several studies have documented that a significant insulin-like growth factor (IGF)-1 and IGF binding
portion of acne sufferers are postadolescent or adult protein-3, to demonstrate the purported effect on acne.
(Collieret al. 2008; Cunliffe & Gould 1979; Goulden Thus, foods with a low glycemic load–those that cause
et al. 1997; Poli et al. 2001, Stern 1992).A recent study least elevation of blood glucose and have lowest
based on 1013 surveys found the overall prevalence of carbohydrate content–as well as diets high in omega-3
acne in patients 20 years of age and older to be 73.3% essential fatty acids, have been advocated as beneficial
(Collier et al. 2008). Among such patients, women are for acne patients (Cordain 2005; Logan 2003; Smith
affected at higher rates than men in all age categories. et al. 2007; Treloar et al. 2008). Additionally, milk has
Thus, more recent studies place the incidence of been proposed as a potential culprit in acne causation,
clinically-important adult acne at 12% of women and with arguments being raised as to the presence of
3% of men over 25 years of age. If milder, ‘physiologic’ various hormones in the consumed product
acne is taken into consideration, the prevalence (Adebamowo et al. 2005, Danby 2005). On the other
increases to 54% of women and 40% of men (Goulden hand, those refuting the link between acne and
et al. 1997). Adult acne may present as a continuation of nutrition may cite two flawed studies from over 30 years
the teenage disease process or may arise de novo. Acne is ago (Anderson 1971; Fulton et al. 1969). In reality,
also encountered in the preadolescent population, controlling diet in a study is difficult, especially when it
including neonates and, less commonly, infants and involves teenagers. As it stands now, there are far too few
ACNE VULGARIS – EPIDEMIOLOGY AND PATHOPHYSIOLOGY 9
6 7
6 Postinflammatory hyperpigmentationis a common 7 Extensive postinflammatory hyperpigmentationin
consequence of acne in patients with darker skin tones, an African-American patient with acne.
such as this Indian patient.
large, well-designed, well-controlled prospective clinical 8
studies to substantiate either point of view. This is in
accordance with the current guidelines of care from the
American Academy of Dermatology (Strauss et al.
2007).
Smoking and its influence on acne prevalence and
severity has been investigated in several published
clinical trials (Chuh et al. 2004; Firooz et al. 2005; Jemec
et al. 2002; Klaz et al. 2006; Mills et al. 1993; Rombouts
et al. 2007; Schafer et al. 2001). Of these studies, two
suggested a positive association between smoking and
acne, three proposed a negative one, and two found no
association. Thus, the evidence so far is inconclusive; 8 A combination of acne and hirsutism,such as on the
however, taking into consideration other, more serious neck of this patient, may point to an underlying state of
health risks associated with smoking, cessation should hyperandrogenism.
always be encouraged.
Very importantly, acne may arise in a number of
genetic and endocrinologic conditions, and the genetic
component of acne vulgaris has been well documented.
For example, patients with the XYY genotype and those (8). Additionally, there is a high level of concordance in
with polycystic ovarian syndrome, hyperandrogenism, acne severity between monozygotic twins, while adult
and elevated serum cortisol levels have a significantly acne has been demonstrated to occur with a much
increased risk of developing acne (Lowenstein 2006; higher frequency in those with first-degree relatives
Mannet al. 2007; New & Wilson 1999; Stratakis et al. suffering from the same condition (Bataille et al. 2002;
1998; The Rotterdam ESHRE/ASRM-Sponsored PCOS Evanset al. 2005; Friedman 1984; Goulden et al. 1999;
consensus workshop group 2004; Voorhees et al. 1972) Lee & Cooper 2006).