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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 CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2012 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Version Date: 20140522 International Standard Book Number-13: 978-1-84076-616-5 (eBook - PDF) This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. 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Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com CONTENTS 5 ROSACEA – EPIDEMIOLOGY AND Abbreviations 4 Preface 5 PATHOPHYSIOLOGY 1 ACNE VULGARIS – EPIDEMIOLOGY AND PATHOPHYSIOLOGY 7 Introduction 7 Epidemiology 8 Clinical assessment of acne vulgaris 10 Pathophysiology of acne vulgaris 11 THERAPEUTICS 15 Introduction 15 Topical agents 15 Oral agents 20 Introduction 39 Classification of acne scars 39 Surgical options: punch excision, subcision, punch elevation 41 Dermaroller 43 Chemical reconstruction of skin scars (CROSS) technique 43 Injectables in the treatment of atrophic acne scars 44 Lasers and laser-like devices: traditional ablative resurfacing 45 Lasers and laser-like devices: traditional nonablative resurfacing 46 Lasers and laser-like devices: fractional resurfacing 47 Treatment of keloid and hypertropic acne scars 50 Introduction 59 General considerations 59 Topical agents 60 Oral agents 62 DEVICES IN THE TREATMENT OF ROSACEA 65 29 Introduction 65 General concepts and mechanism of action 65 Preoperative care 66 Pulsed-dye lasers 66 Intense pulsed light sources 68 KTP and Nd:YAG lasers 70 Future directions in light-based treatment of rosacea 72 39 8 LASERS AND SIMILAR DEVICES IN Introduction 29 Mid-infrared range lasers 29 Pulsed-dye lasers 32 Visible light sources and light-emitting diodes 33 Photodynamic therapy 34 Radiofrequency devices 36 4 TREATMENT OF ACNE SCARS 59 7 LASERS AND SIMILAR 3 LASERS AND SIMILAR DEVICES IN THE TREATMENT OF ACNE VULGARIS Introduction 51 Epidemiology 51 Definition of rosacea 52 Rosacea subtypes 52 Pathophysiology of rosacea 55 6 ROSACEA – CURRENT MEDICAL 2 ACNE VULGARIS – CURRENT MEDICAL THERAPEUTICS 51 THE TREATMENT OF SEBACEOUS HYPERPLASIA Introduction 73 Aging of the sebaceous glands and the pathophysiology of sebaceous hyperplasia 73 Clinical considerations 74 Lasers and similar technologies in the treatment of sebaceous hyperplasia 75 References Index 77 93 73 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 (laser) RARE retinoic acid response element 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 A CNE vulgaris is a common disorder of the pilosebaceous unit affecting millions of people worldwide. Although most frequently encountered in adolescents, acne may persist well into adulthood and lead to significant physical and psychological impairment in those affected. The severity of acne may vary significantly from the mildest comedonal forms (1) to a severe and debilitating condition (2). In addition to the face, the chest, back, and shoulders are also commonly affected (3, 4). 1 1 Mild comedonal acne on a patient’s face. 2 2 Severe cystic acne. 4 3 3 Acne papules and pustules on the chest. 4 Acne papules associated with extensive postinflammatory hyperpigmentation on a patient’s back. 8 5 5 In acné excoriée des jeunes filles, patients frequently manipulate their acne lesions, leading to prolonged healing time and often, scarring. Numerous factors, both intrinsic and extrinsic (5), may underlie the development and the progression of the disease. E P I D E M I O LO GY Acne is the most common cutaneous disorder in the Western world. In the United States, its prevalence has been variably estimated at between 17 and 45 million people (Berson et al. 2003; White 1998). This number is typically based on a landmark publication by Kraning & Odland (1979), which estimated the prevalence of acne in persons aged 12–24 years at 85%. Several studies have documented that a significant portion of acne sufferers are postadolescent or adult (Collier et al. 2008; Cunliffe & Gould 1979; Goulden et al. 1997; Poli et al. 2001, Stern 1992).A recent study based on 1013 surveys found the overall prevalence of acne in patients 20 years of age and older to be 73.3% (Collier et al. 2008). Among such patients, women are affected at higher rates than men in all age categories. Thus, more recent studies place the incidence of clinically-important adult acne at 12% of women and 3% of men over 25 years of age. If milder, ‘physiologic’ acne is taken into consideration, the prevalence increases to 54% of women and 40% of men (Goulden et al. 1997). Adult acne may present as a continuation of the teenage disease process or may arise de novo. Acne is also encountered in the preadolescent population, including neonates and, less commonly, infants and preteens (Cunliffe et al. 2001; Jansen et al. 1997; Lucky 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 patients than in their Black counterparts (Wilkins & Voorhees 1970). More recent evidence indicates that subclinical, microscopic inflammation may be more common in the latter group (Halder et al. 1996). It has also been suggested that certain nonwesternized societies demonstrate significantly lower prevalence of acne (Cordain et al. 2002; Schaefer 1971; Steiner 1946). The cause of such disparity is unclear and although nutritional factors have been suggested as the cause of lower acne rates, this inference has so far not been conclusively substantiated (Bershad 2003). The issue of nutrition and its influence, or lack thereof, on acne has long been a highly contested one (Adebamowo et al. 2005; Bershad 2003; Bershad 2005; Cordain 2005; Danby 2005; Kaymak et al. 2007; Logan 2003; Smith et al. 2007; Treloar 2003). Proponents of the link between acne and nutrition frequently cite nutritional influence on serum hormone levels, such as insulin-like growth factor (IGF)-1 and IGF binding protein-3, to demonstrate the purported effect on acne. Thus, foods with a low glycemic load–those that cause least elevation of blood glucose and have lowest carbohydrate content–as well as diets high in omega-3 essential fatty acids, have been advocated as beneficial for acne patients (Cordain 2005; Logan 2003; Smith et al. 2007; Treloar et al. 2008). Additionally, milk has been proposed as a potential culprit in acne causation, with arguments being raised as to the presence of various hormones in the consumed product (Adebamowo et al. 2005, Danby 2005). On the other hand, those refuting the link between acne and nutrition may cite two flawed studies from over 30 years ago (Anderson 1971; Fulton et al. 1969). In reality, controlling diet in a study is difficult, especially when it involves teenagers. As it stands now, there are far too few A C N E V U L G A R I S – E P I D E M I O LO G Y A N D PAT H O P H Y S I O LO G Y 6 6 Postinflammatory hyperpigmentation is a common consequence of acne in patients with darker skin tones, such as this Indian patient. large, well-designed, well-controlled prospective clinical 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; however, taking into consideration other, more serious health risks associated with smoking, cessation should 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 with polycystic ovarian syndrome, hyperandrogenism, and elevated serum cortisol levels have a significantly increased risk of developing acne (Lowenstein 2006; Mann et al. 2007; New & Wilson 1999; Stratakis et al. 1998; The Rotterdam ESHRE/ASRM-Sponsored PCOS consensus workshop group 2004; Voorhees et al. 1972) 7 7 Extensive postinflammatory hyperpigmentation in an African-American patient with acne. 8 8 A combination of acne and hirsutism, such as on the neck of this patient, may point to an underlying state of hyperandrogenism. (8). Additionally, there is a high level of concordance in acne severity between monozygotic twins, while adult acne has been demonstrated to occur with a much higher frequency in those with first-degree relatives suffering from the same condition (Bataille et al. 2002; Evans et al. 2005; Friedman 1984; Goulden et al. 1999; Lee & Cooper 2006). 9