Acne Vulgaris

http://emedicine.medscape.com/article/1069804-overview

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Acne Vulgaris
Author: James Fulton Jr, MD, PhD; Chief Editor: Dirk M Elston, MD more... Updated: Aug 26, 2011

Background
Acne vulgaris is a common skin disease that affects 60-70% of Americans at some time during their lives. Twenty percent will have severe acne, which results in permanent physical and mental scarring. Acne vulgaris is American's most common disease and is characterized by noninflammatory, open or closed comedones and by inflammatory papules, pustules, and nodules. Acne vulgaris affects the areas of skin with the densest population of sebaceous follicles; these areas include the face, the upper part of the chest, and the back. Other eMedicine articles on acne include Acne Conglobata,Acne Fulminans,Acne Keloidalis Nuchae, and Acneiform Eruptions. Also see the Medscape Acne Resource Center.

Pathophysiology
The pathogenesis of acne vulgaris is multifactorial. The key factor is genetics.[1] If both parents had acne, 3 of 4 children will have acne. If 1 parent had acne, then 1 of 4 of the children will have acne. However, similar to other genetic conditions, not every family will have the same pattern, with acne vulgaris sometimes skipping generations. What is inherited is the propensity for follicular epidermal hyperproliferation with subsequent plugging of the follicle. Additional aggravating factors include excess sebum, the presence and activity of Propionibacterium acnes, and inflammation. Retention hyperkeratosis is the first recognized event in the development of acne vulgaris. The exact underlying cause of this hyperproliferation is not known. Currently, 3 leading hypotheses have been proposed to explain why the follicular epithelium produces cells at a rapid rate that are retained in individuals with acne. First, androgen hormones have been implicated as the initial trigger. Comedones, the clinical lesion that results from follicular plugging, begin to appear around adrenarche in persons with acne in the T-zone area. Furthermore, the degree of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S).[4] Additionally, androgen hormone receptors are present in sebaceous glands; individuals with malfunctioning androgen receptors do not develop acne.
[5] [3] [2]

Excess sebum is another key factor in the development of acne vulgaris. Sebum production and excretion are regulated by a number of different hormones and mediators. In particular, androgen hormones promote sebum production and release.[6] Still, most men and women with acne have normal circulating levels of androgen hormones. An end-organ hyperresponsiveness to androgen hormones has been hypothesized. Androgen hormones are not the only regulators of the human sebaceous gland. Numerous other agents, including growth hormone and insulinlike growth factor, also regulate the sebaceous gland and may contribute to the development of acne. P acnes is an anaerobic organism present in acne lesions. The presence of P acnes promotes inflammation through a variety of mechanisms. P acnes stimulates inflammation by producing proinflammatory mediators that diffuse

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Acne Vulgaris

http://emedicine.medscape.com/article/1069804-overview

through the follicle wall. Studies have shown that P acnes activates the toll-like receptor 2 on monocytes and neutrophils. Activation of the toll-like receptor 2 then leads to the production of multiple proinflammatory cytokines, including interleukins 12 and 8 and tumor necrosis factor. Hypersensitivity to P acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not.
[8] [7]

Inflammation may be a primary phenomenon or a secondary phenomenon. Most of the evidence to date suggests a secondary inflammatory response to P acnes. However, interleukin 1-alpha expression has been identified in microcomedones, and it may play a role in the development of acne.
[9]

Epidemiology
Frequency
United States Acne vulgaris affects 60-70% of Americans at some time during their lives. Twenty percent have severe acne with permanent physical and mental scarring. International Persons of some races are affected more than others. Cystic acne is prevalent in the Mediterranean region from Spain to Iran.
[11, 12] [10]

Mortality/Morbidity
Acne can cause psychosocial suffering. Acne can lead to physical scarring. A severe inflammatory variant of acne, acne fulminans, can be associated with fever, arthritis, and other systemic symptoms.
[13]

Race
Acne is common in North American whites. Spanish persons tend to more commonly develop cystic acne. African Americans have a higher prevalence of pomade acne, likely stemming from the use of hair pomades.

Sex
During adolescence, acne vulgaris is more common in males than in females. In adulthood, acne vulgaris is more common in women than in men.
[14]

Age
Acne vulgaris may be present in the first few weeks and months of life, when a newborn is still under the influence of maternal hormones and when the androgen-producing portion of the adrenal gland is disproportionately large. This neonatal acne tends to resolve spontaneously. However, the neonate should be treated with a mild retinoid to clear out the impacted follicles. Adolescent acne usually begins with the onset of puberty, when the gonads begin to produce and release more androgen hormone. Acne is not limited to adolescence. Twelve percent of women and 5% of men at age 25 years have acne. By age 45 years, 5% of both men and women still have acne.
[15]

Contributor Information and Disclosures

Author James Fulton Jr, MD, PhD Center for Cosmetic Dermatology; Consultant, Vivant Pharmaceuticals, LLC James Fulton Jr, MD, PhD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, American Society for Laser Medicine and Surgery, Dermatology Foundation, International Society of Cosmetic and Laser Surgeons, and Skin Cancer Foundation Disclosure: Vivant Pharmaceuticals Grant/research funds Consulting

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Specialty Editor Board Alexa F Boer Kimball, MD, MPH Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology Disclosure: Nothing to disclose. David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa Disclosure: Nothing to disclose. Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society Disclosure: Nothing to disclose. Joel M Gelfand, MD, MSCE Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator Chief Editor Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology Disclosure: Nothing to disclose. Acknowledgments The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Julie C. Harper, MD, to the development and writing of this article.

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