Pathogenesis, Clinical Manifestations, and Diagnosis of Acne Vulgaris PDF

Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris
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Official reprint from UpToDate www.uptodate.com 2014 UpToDate
Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris Authors Diane Thiboutot, MD Andrea Zaenglein, MD Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Feb 2014. | This topic last updated: Dec 9, 2013. INTRODUCTION Acne vulgaris is the most common cutaneous disorder affecting adolescents and young adults. Patients with acne can experience significant psychological morbidity and, rarely, mortality due to suicide [1,2]. The psychological effects of embarrassment and anxiety can impact the social lives and employment of affected individuals. Scars can be disfiguring and lifelong. In one prospective study of 90 patients with acne, a significant improvement in selfesteem was found with treatment of the acne [3]. Thus, it is imperative that clinicians are familiar with acne vulgaris and its treatment. The pathogenesis, clinical manifestations, diagnosis, and differential diagnosis of acne vulgaris will be reviewed here. The treatment of acne vulgaris is discussed elsewhere. (See "Treatment of acne vulgaris" and "Hormonal therapy for women with acne vulgaris" and "Oral isotretinoin therapy for acne vulgaris" and "Light-based, adjunctive, and other therapies for acne vulgaris".) EPIDEMIOLOGY Estimates of the prevalence of acne vulgaris in adolescents range from 35 to over 90 percent [4,5]. Acne tends to resolve in the third decade, but it may persist into or develop de novo in adulthood. The exact prevalence in adults is uncertain, and studies using a clinical examination typically find a lower prevalence than surveys patients to self-report acne. asking for Section Editors Robert P Dellavalle, MD, PhD, MSPH Moise L Levy, MD Mark V Dahl, MD Deputy Editor Abena O Ofori, MD
Post-adolescent acne predominantly affects women, in contrast to adolescent acne which has a male predominance [6]. In one survey of over 1000 adults, self-reported acne in men and women was documented as follows [5]:
! 20 to 29 years: 43 and 51 percent, respectively ! 30 to 39 years: 20 and 35 percent, respectively ! 40 to 49 years: 12 and 26 percent, respectively ! ages 50 and older: 7 and 15 percent, respectively The difference in the prevalence of acne in males and females was statistically significant in each age group. PATHOGENESIS Pilosebaceous follicles Acne vulgaris is a disease of pilosebaceous follicles. Four factors are involved (figure 1): ! Follicular hyperkeratinization ! Increased sebum production ! Propionibacterium acnes (P. acnes) within the follicle
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! Inflammation The sequence of events leading to the development of an acne lesion is not fully understood. The earliest change in the pilosebaceous unit was initially thought to be follicular hyperkeratinization, which is associated with both increased proliferation and decreased desquamation of keratinocytes lining the follicular orifice. This results in partial obstruction of the follicle with sebum and keratin (the microcomedo). However, an influx of inflammatory cells in the perifollicular region may precede the changes in keratinization [7]. Initiating factors for this inflammatory process are unknown. Sebaceous glands enlarge with adrenarche (the prepubertal period in which levels of DHEA-S rise) and sebum production increases. Sebum provides a growth medium for P. acnes, an anaerobic diphtheroid that is a normal component of skin flora. Microcomedones provide an anaerobic lipid-rich environment that allows these bacteria to thrive; they utilize triglycerides in sebum as a nutrient source by hydrolyzing them into free fatty acids and glycerol. Inflammation results from the proliferation of P. acnes. Sequencing of the P. acnes genome has led to the identification of the following bacterial properties that may contribute to the inflammatory response [8,9]: ! Enzymes produced by P. acnes may promote the degradation of the follicular wall and follicular rupture. ! P. acnes surface proteins may play a role in antigenicity, triggering humoral and cell-mediated immune responses. ! Heat shock proteins, which promote inflammation via the innate immune system, are produced by P. acnes. ! Porphyrins produced by P. acnes may contribute to adjacent tissue damage and inflammation. A component of the host innate immune system, the toll-like receptor, is also thought to play an important role in the P. acnes mediated inflammatory response [10]. Toll-like receptor-2, located on perifollicular macrophages, binds to P. acnes, and triggers the release of proinflammatory cytokines (including IL-8 and IL-12) [11]. These cytokines contribute to the attraction of neutrophils and the release of neutrophil lysosomal enzymes that promote follicular rupture. (See "Toll-like receptors: Roles in disease and therapy".) Differences in the host inflammatory response to P. acnes or the pathogenicity of specific strains of P. acnes that colonize skin may contribute to the variation in the prevalence and severity of acne [12,13]. Types of acne lesions The microcomedo is considered the precursor for the clinical lesions of acne vulgaris, including closed comedos, open comedos, and inflammatory papules, pustules, and nodules. The process by which microcomedones evolve into other acne lesions remains to be elucidated, but may involve the following: ! Accumulation of sebum and keratinous material converts a microcomedo into a closed comedo (a whitehead) (picture 2C). ! The follicular orifice is opened with continued distension, forming an open comedo (a blackhead) (picture 1). Densely packed keratinocytes, oxidized lipids, and melanin all contribute to the dark color of the open comedo. ! Follicular rupture contributes to the development of inflammatory lesions. Following follicular rupture, proinflammatory lipids and keratin are extruded into the surrounding dermis, leading to inflammatory papule or nodule formation (picture 2A-B). Role of androgens Androgens contribute to the development of acne through stimulating the growth and secretory function of sebaceous glands. Most circulating androgens are produced by the adrenal gland and the gonads (figure 2). Androgen production also occurs within the sebaceous glands, which convert dehydroepiandrosterone sulfate (DHEAS), an adrenal androgen precursor, to testosterone via the action of several enzymes (table 1). Testosterone is subsequently converted to 5-alpha-dihydrotestosterone (DHT) via the action of type I 5-alpha reductase in the sebaceous gland.
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Androgen receptors that bind DHT and testosterone are present in the sebaceous glands and the outer root sheath keratinocytes of the follicular epithelium. DHT has greater affinity for androgen receptors than testosterone. Men with androgen insensitivity (lacking androgen receptors) do not produce sebum and do not develop acne, suggesting an important role of androgen receptors in the pathogenesis of acne [14]. Infantile acne (with typical onset at age three to six months) occurs as a result of elevated levels of androgens produced by the immature adrenal gland in girls, and the immature adrenal gland and testes in boys. Androgen levels fall by age one to two, and acne subsequently improves. (See "Benign skin and scalp lesions in the newborn and young infant", section on 'Neonatal acne' and "Benign skin and scalp lesions in the newborn and young infant", section on 'Infantile acne'.) The onset of acne in children correlates with the rise in serum levels of DHEA-S that occurs as puberty approaches (adrenarche). Higher serum levels of DHEA-S are found in prepubertal girls with acne than in those without [15]; those with the highest levels develop the most severe acne [16]. Although androgen excess due to a variety of conditions can cause acne, the majority of patients with acne have normal androgen levels. Conditions in which hyperandrogenism is seen include polycystic ovarian syndrome, congenital adrenal hyperplasia, and adrenal or ovarian tumors. (See "Pathogenesis and causes of hirsutism", section on 'Etiology'.) External factors Soaps, detergents, and astringents remove sebum from the skin surface but do not alter sebum production. Repetitive mechanical trauma caused by scrubbing with these agents may worsen the disorder by rupturing comedos, promoting the development of inflammatory lesions [17]. Thus, patients with acne should refrain from rubbing their faces or picking their skin. Turtlenecks, bra straps, shoulder pads, orthopedic casts, and sports helmets may all cause acne mechanica, in which occlusion of pilosebaceous follicles leads to comedone formation. Pomade acne is associated with the use of occlusive, oil-based hair products. (See 'Acne cosmetica' below.) Diet A potential role for diet in acne is controversial [18-21]. A study of 47,355 women in the Nurses' Health Study that used retrospective data collection to determine diet during high school found an association between acne and intake of milk [22]. The authors suggested that natural hormonal components of milk or other bioactive molecules in milk could exacerbate acne [22,23]. Two subsequent large prospective cohort studies (one involving boys and the other involving girls) also reported an association of milk ingestion and acne [24,25]. All three studies were questionnaire-based, requiring subjects to recall their dietary intake and self-diagnose acne and disease severity. A case-control study of 205 patients with clinician-confirmed moderate to severe acne and 358 controls with mild or nonexistent acne also found a possible association between milk consumption (more than three portions per week) and moderate to severe acne (odds ratio [OR] 1.78, 95% CI 1.22-2.59) [26]. Similar to the other studies, food intake history was assessed via a retrospective patient questionnaire. No randomized trials have evaluated the relationship between dairy products and acne. Other studies have suggested that insulin-like growth factor (IGF) may play a role in acne [27,28]. Milk consumption has been associated with increased levels of serum IGF [29]. IGF is also increased by ingestion of high glycemic loads and could potentially link diet and acne. A 12-week randomized trial that compared low and high glycemic load diets in 43 male patients with acne found a greater reduction in lesion counts with the low glycemic load diet [30]. However, the participants on that diet also lost more weight than those on the high glycemic load diet, so it is possible that the results were due to changes in weight rather than the composition of the diet. There is no reliable evidence that ingestion of chocolate is associated with an increased prevalence or severity of acne [21]. Data on favorable effects of dietary factors such as zinc, omega-3 fatty acids, antioxidants, vitamin A, and dietary fiber
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on acne vulgaris are limited [31]. Further studies are necessary to determine the roles of these supplements in acne vulgaris. Family history Individuals with close family members with acne are at increased risk for the disorder [26,32,33]. Case-control studies have demonstrated a more than three-fold risk among individuals with affected first-degree family members [26,33,34], and a large twin study of monozygotic and dizygotic twins also supported the heritable nature of acne [35]. In cases of very severe acne, there is often a positive family history; but the role of genetics in mild acne is uncertain due to the almost ubiquitous occurrence in young adolescents. Stress Patients and clinicians commonly believe that psychological stress can exacerbate acne [36,37]. A prospective cohort study in 94 secondary school students compared acne severity and sebum production at times of high stress (midterm examinations) and low stress (summer holidays) [38]. Sebum production did not appear to be related to stress, but acne severity, as assessed by an examiner blinded to the hypothesis of the study, did appear to be associated with stress, particularly in boys. Similarly, a study of 22 university students found that acne severity appeared to have some correlation with stress around the time of school examinations [39]. Receptors for corticotropin releasing hormone (CRH), a hormone involved in the stress response, are present in human sebaceous glands [40]. Sebaceous gland cells exhibit stronger staining for CRH in acne-involved skin than in normal or uninvolved skin. Although additional studies are necessary, these findings suggest that the CRH system may participate in the occurrence of stress-exacerbated acne. Body mass index Few studies have evaluated the relationship between weight and acne vulgaris, and study results vary on the connection between these factors [26,41-43]. Whereas a case-control study of adolescents and young adults (ages 10 to 24) found a correlation between low BMI and a reduced risk for acne that was most evident among males [26], a cross-sectional, survey-based study of young adults (ages 18 and 19) found a statistically significant association between rising BMI and increased risk for acne only among females [42]. CLINICAL MANIFESTATIONS AND CLASSIFICATION Acne vulgaris typically affects those areas of the body that have the largest, hormonally-responsive sebaceous glands, including the face, neck, chest, upper back, and upper arms. In addition to the typical lesions of acne vulgaris (eg, open comedones, closed comedones, and inflammatory lesions), scarring and postinflammatory hyperpigmentation can occur, which can be greatly distressing for patients. Postinflammatory hyperpigmentation is most common in patients with darker complexions, and an individual hyperpigmented macule may take several months or more to resolve without treatment. (See "Treatment of acne vulgaris", section on 'Therapy for postinflammatory hyperpigmentation'.) Adult women may present with acne involving the lower face and neck that is often associated with premenstrual flares (picture 3) [44,45]. These women, in particular, seem to benefit from hormonal therapies for acne [44]. Premenstrual flares of acne appear to be more common in women over the age of 33 than in women aged 20 to 33 years [46]. (See "Hormonal therapy for women with acne vulgaris".) Classification There is no universal classification system for acne vulgaris; the extensive variety of clinical presentations would make it challenging to develop and implement such a system. A description of the actual lesions encountered will be most useful when considering management of acne. Young adolescents often have primarily comedonal acne consisting of noninflammatory lesions (closed and/or open comedones) involving the forehead, nose and chin. As the acne progresses, patients develop inflammatory lesions (papules, pustules, and nodules (picture 2A-C)) Comedones can become extensive in some patients (picture 1). Nodules are tender inflammatory acne lesions that are larger than 5 mm in diameter [47]. Nodular acne is sometimes inaccurately referred to as "cystic" or "nodulocystic" acne (picture 4A-B). In reality, true cysts are rare. Sinus tracts, which
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manifest as fluctuant linear lesions, are formed when nodules merge. These are seen in the most severe forms of acne and are difficult to treat (picture 5). The presence of scarring or postinflammatory hyperpigmentation is also assessed. Estimations of acne severity are patient-specific, and depend on a number of factors. The clinical type of lesions, presence of scarring, presence of draining lesions or sinus tracts, lack of therapeutic response, and the psychological impact of acne are some of the features taken into account [47]. As an example, patients with inflammatory, nodular acne are often considered to have severe acne. Similarly, a patient without nodules but who has numerous inflammatory papules and pustules and notable scarring could also be classified as having severe disease. Acne variants Occasionally, patients with acne vulgaris may exhibit variants of the disease, some of which require aggressive treatment [44,48]. These variants are discussed below. Acne fulminans The presence of fever and arthralgias with an acute eruption of large inflammatory nodules and friable plaques with hemorrhagic crusts suggests the diagnosis of acne fulminans, a systemic disorder (picture 6). This rare condition affects adolescent males primarily. Lesions usually involve the trunk, but may be present elsewhere. Acne fulminans is associated with leukocytosis, an elevated erythrocyte sedimentation rate, proteinuria, and osteolytic lesions. Patients with acne fulminans can be treated with systemic glucocorticoids (0.5 to 1 mg/kg) plus oral isotretinoin or oral antibiotics [49]. Treatment regimens vary, but oral glucocorticoids should be initiated about four weeks prior to starting low-dose oral isotretinoin to prevent a flare of the condition [49]. Oral isotretinoin is started at 0.5 mg/kg/day or less and can be gradually increased. After several weeks of therapy, glucocorticoids are tapered as tolerated. In rare cases, treatment of acne vulgaris with isotretinoin can precipitate an acne fulminans-like eruption. Acne conglobata Acne conglobata is a severe form of nodular acne that is most commonly seen in young males (picture 7A-B). Lesions are most prominent on the back, chest, and buttocks, but can also appear in other sites. Large draining lesions, sinus tracts, and severe scarring may occur. Systemic symptoms are absent. Treatments have included systemic antibiotics, intralesional glucocorticoids, systemic glucocorticoids, and surgical intervention [48]. Patients can respond well to isotretinoin, although they may experience severe flares at the start of isotretinoin therapy. For this reason, lower doses of isotretinoin (0.5 mg/kg/day or less) plus systemic glucocorticoids before or during isotretinoin therapy are often required [48]. A few case reports have documented improvement in acne conglobata during treatment with biologic TNF-alpha inhibitors (etanercept [50], adalimumab [51], and combination therapy with infliximab and isotretinoin [52]). However, further study is necessary before treatment with these agents can be recommended. SAPHO syndrome The SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) is another rare disorder (picture 8). This diagnosis also requires systemic therapy [53]. (See "Major causes of musculoskeletal chest pain", section on 'Sternocostoclavicular hyperostosis (SAPHO syndrome)'.), and (see "Treatment of musculoskeletal chest pain" and "Neutrophilic dermatoses", section on 'SAPHO syndrome'). PAPA syndrome PAPA syndrome (sterile pyogenic arthritis, pyoderma gangrenosum, and acne) is an autosomal dominant inflammatory disorder that is discussed separately. (See "Periodic fever syndromes and other autoinflammatory diseases: An overview", section on 'PAPA syndrome'.) Gram-negative folliculitis Patients with pre-existing acne vulgaris who have been treated with long-term systemic antibiotics (usually tetracyclines) may develop gram-negative folliculitis. These patients exhibit an initial response to the oral antibiotic, followed by apparent resistance to the treatment and worsening of acne. Inflammatory papules, pustules, and nodules typically appear on perinasal skin and the central face. A culture of lesions will yield gram-negative organisms, such as Enterobacter, Klebsiella, Pseudomonas, Proteus, or Escherichia species. Patients are treated with antibiotics with gram negative coverage. Recalcitrant cases are managed with oral isotretinoin for four to five months [44].
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Neonatal acne and infantile acne Neonatal acne (also called neonatal cephalic pustulosis) and infantile acne are distinct conditions. Neonatal acne appears within the first few weeks of life (picture 9); infantile acne usually appears around three to six months of age. (See "Benign skin and scalp lesions in the newborn and young infant", section on 'Neonatal acne' and "Benign skin and scalp lesions in the newborn and young infant", section on 'Infantile acne'.) Childhood acne Mid-childhood acne (acne that occurs in children ages one to six years) is uncommon. Affected children usually present with a mixture of comedones and inflammatory lesions on the face. An endocrinology workup to evaluate for hyperandrogenism is indicated when acne develops in a child in this age group [54]. Unlike mid-childhood acne, pre-adolescent acne (acne in children aged 7 to 12 years) is common. Acne may be the initial sign of puberty [15]. A predominance of comedones with relatively few inflammatory lesions is typically seen in affected children. An endocrinologic work-up usually is not necessary for children with pre-adolescent acne in the absence of other clinical signs of hyperandrogenism [54,55]. However, the possibility of polycystic ovarian syndrome should be considered in girls with unusually severe acne, other signs of hyperandrogenism, or a poor response to treatment [54]. (See "Adrenal hyperandrogenism", section on 'Clinical manifestations' and "Clinical features and diagnosis of polycystic ovary syndrome in adolescents", section on 'Clinical features'.) Acne excorie des jeunes filles This scarring acne condition is often, but not always, seen in young women. Relatively mild acne comedones or inflammatory papules are chronically and obsessively picked and excoriated, leading to erosions and scarring (picture 10). An underlying psychiatric disorder can be associated, and treatment may involve antidepressants and psychotherapy. Solid facial edema Solid facial edema (Morbihan's disease) is a rare complication of acne that presents as facial soft tissue edema and erythema. The condition may wax and wane in severity, but usually does not spontaneously resolve without treatment. Improvement with isotretinoin with or without ketotifen, systemic glucocorticoids, or clofazimine has been reported [48]. DIAGNOSTIC EVALUATION Particular attention to endocrine function is essential in the evaluation of acne vulgaris. A medication history should also be reviewed for acne-inducing drugs (table 2). Skin should be examined carefully, since an assessment of the type and location of lesions is critical for determining the most appropriate treatments. Hyperandrogenism In women, polycystic ovary syndrome (PCOS) is the most common cause of hyperandrogenism. This disorder is characterized by menstrual irregularity, hirsutism, acne, ovarian cysts, and varying degrees of insulin resistance and acanthosis nigricans (picture 11). (See "Clinical manifestations of polycystic ovary syndrome in adults".) One study of 51 women with acne (ages 15 to 46) found that 39 percent had menstrual abnormalities and 37 percent had PCOS [56]. These observations suggest that all women with the combination of acne and oligomenorrhea should be evaluated for PCOS. (See "Diagnosis of polycystic ovary syndrome in adults".) The rapid appearance of acne in conjunction with virilization suggests an underlying adrenal or ovarian tumor. Patients with Cushing's disease or syndrome and late-onset congenital adrenal hyperplasia may also experience acne vulgaris. Evidence of virilization includes a deepening voice, decreased breast size, clitoromegaly, alopecia, oligomenorrhea, and hirsutism. These patients may require imaging studies of the adrenal glands and ovaries, and hormonal evaluation. Referral to an endocrinologist should be considered in these cases. (See "Epidemiology and clinical manifestations of Cushing's syndrome" and "Adrenal hyperandrogenism".) Recommendations for initial screening tests for hyperandrogenism vary. DHEA-S, total testosterone, and free testosterone levels are reasonable initial tests. A 17-hydroxyprogesterone level may also be obtained to screen for lateonset congenital adrenal hyperplasia, in which elevated levels of DHEA-S may also be seen. Referrals to endocrinology and gynecology should be considered if abnormalities are noted. Patients should not be taking oral contraceptives during testing for hyperandrogenism.
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Medications A complete list of medications, including vitamin supplements, should be obtained. Known causes of acne or acneiform eruptions include glucocorticoids, phenytoin, lithium, isoniazid, epidermal growth factor inhibitors, iodides, bromides, androgens, and other drugs (table 2) [57]. Vitamins B2, B6, and B12 may also cause drug-induced acne. (See 'Drug-induced acne' below and 'EGFR inhibitor acneiform eruption' below and "Drug eruptions", section on 'Halogenoderma'.) Physical examination The physical examination should focus upon the skin and in women, evidence of hyperandrogenism. The type and location of lesions, scarring (picture 12 and picture 13), and postinflammatory pigmentary changes (picture 14) should be noted. The skin examination is essential for determining the best treatment course for an individual patient. (See "Treatment of acne vulgaris", section on 'Patient assessment' and "Treatment of acne vulgaris", section on 'Overview of treatment'.) Hirsutism or virilization should prompt further laboratory and imaging studies or referral. (See "Evaluation of premenopausal women with hirsutism".) DIFFERENTIAL DIAGNOSIS Although acne vulgaris is a common condition that clinicians may feel they can accurately diagnose, a variety of disorders need to be considered in the differential diagnosis. In addition, patients may present with acneiform eruptions, which have similar features, but are unrelated to acne vulgaris. Non-acne dermatoses Some of the conditions in the differential diagnosis of acne include: ! Rosacea Acne vulgaris is distinguished from acne rosacea by the presence of comedones and the absence of telangiectasias. Common features of rosacea include erythema, telangiectasias, and papules or pustules on the central face (picture 15). (See "Rosacea: Pathogenesis, clinical features, and diagnosis".) ! Perioral dermatitis Perioral dermatitis (also known as periorificial dermatitis) is characterized by small, grouped, erythematous papules in a perioral (or occasionally perinasal or periorbital) distribution (picture 16). When the perioral skin is involved, a rim of spared skin is usually seen around the vermilion border of the lip. (See "Perioral (periorificial) dermatitis".) ! Sebaceous hyperplasia Visible enlargement of sebaceous glands is termed sebaceous hyperplasia. It most commonly occurs in adults with a history of oily skin. These growths are umbilicated yellowish papules are most commonly found on the forehead and cheeks (picture 17). These lesions may resemble basal cell carcinomas. ! Pseudofolliculitis barbae and acne keloidalis nuchae These two conditions occur most commonly in individuals of African origin, and are likely related to the configuration of the hair follicle. It is thought that short shaved or clipped hairs curl back towards the skin, penetrate the skin, and cause a foreign-body inflammatory reaction. Inflammatory papules and pustules occur, which may result in keloidal scarring as the lesions heal (picture 18A-C). The beard area (pseudofolliculitis barbae) and the nuchal area (acne keloidalis nuchae) are typically involved. (See "Pseudofolliculitis barbae" and "Keloids".) ! Folliculitis Staphylococcal, eosinophilic, or pseudomonal folliculitis may mimic inflammatory acne (picture 19AB). Comedones are absent, and lesions are usually monomorphous, unlike the polymorphous lesion in different stages of development that are typical of acne. (See "Folliculitis".) ! Keratosis pilaris In this common condition, caused by keratotic follicular plugging, patients typically present with small follicular papules on the extensor surfaces of the upper arms or thighs (picture 20A-B). Erythema may be present. Lesions can also occur on the face, particularly in children. (See "Approach to the patient with pustular skin lesions", section on 'Keratosis pilaris'.) ! Favre-Racouchot syndrome Favre-Racouchot syndrome is a condition resulting from cutaneous photodamage (sun damage) seen in middle-aged or older adults. Open and closed comedones are found in areas of
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photodamage, usually on the lateral upper cheeks (picture 21). ! Nevus comedonicus A lesion presenting at birth or in childhood, in which grouped or a linear arrangement of comedones are noted. ! Adnexal tumors Benign follicular tumors, such as trichoepitheliomas, trichodiscomas, or fibrofolliculomas typically present as flesh-colored facial papules. ! Steatocystoma multiplex Steatocystoma multiplex is an autosomal dominant or sporadic genetic disorder in which multiple yellow or skin-colored sebum-filled cysts are found on the trunk, upper arms, or chest (picture 22). ! Tuberous sclerosis Facial angiofibromas associated with tuberous sclerosis usually appear in childhood. These lesions commonly present as persistent, 1 to 3 mm pink or red papules on the nose and medial cheeks (picture 23). (See "Tuberous sclerosis complex: Genetics, clinical features, and diagnosis".) Acneiform eruptions There are multiple disorders in which acne-like eruptions occur, unassociated with true acne vulgaris. These include the following: Drug-induced acne Drug-induced acne typically presents with a monomorphous inflammatory papular eruption (as opposed to the polymorphous eruption with lesions in varying stages seen with acne vulgaris) (picture 24). Medications associated with drug-induced acne are listed in a table (table 2). Glucocorticoid-induced eruptions are also referred to as "steroid folliculitis." (see 'Medications' above). Acne cosmetica Cosmetic products that contain comedogenic ingredients can induce the formation of acne lesions. This type of acne has lessened as products designed to be less comedogenic have become widely available. Heavy, oil-based hair products are still commonly used and may contribute to the development of acne on the forehead (pomade acne). Irritant reactions to cosmetic products can also produce eruptions that resemble acne vulgaris. Inflammatory papules or pustules may occur within hours after the application of the inciting product. EGFR inhibitor acneiform eruption Epidermal growth factor receptor (EGFR) inhibitors and other tyrosine kinase inhibitors used to treat cancers are known to cause an inflammatory acneiform eruption involving the face, neck and upper trunk in the majority of patients receiving these medications (picture 25). (See "Cutaneous complications of molecularly targeted therapy and other biologic agents used for cancer therapy".) Occupational acne Comedones, inflammatory papules, pustules, nodules, or cysts can occur in response to exposure to certain chemicals, including insoluble cutting oils, coal tar derivatives, and chlorinated hydrocarbons. Chloracne is the term used to describe occupational acne that occurs with exposure to chlorinated hydrocarbons (eg, dioxin) via percutaneous contact, inhalation, or ingestion. Clinically, chloracne is characterized by large monomorphic comedones with evolution into severely inflammatory and scarring lesions. Chloracne is most common on the face, neck, postauricular skin, axillae, and scrotum, although other sites may be involved. Tropical acne Tropical acne occurs upon exposure to elevated environmental temperatures, and may be seen in tropical countries or other situations (eg, occupations) in which individuals are exposed to extreme heat. Large inflammatory nodules are seen on the trunk and buttocks. Treatment involves avoidance of heat. Systemic antibiotics may also be used. Radiation acne Treatment with ionizing radiation can result in the appearance of comedones as acute radiation dermatitis resolves. Ionizing radiation induces follicular epithelial metaplasia, creating follicular hyperkeratotic plugs. Apert syndrome Apert syndrome (ie, acrocephalosyndactyly type I) is an autosomal dominant disorder associated with synostoses of bone in the hands, feet, cranium, and vertebral bodies. A diffuse acneiform eruption on
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the arms, buttocks, and thighs is seen. The acneiform eruption is difficult to treat. Isotretinoin has been used with success in some cases. (See "Craniosynostosis syndromes", section on 'Apert syndrome'.) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond the Basics. The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the keyword(s) of interest.) ! Basics topics (see "Patient information: Acne (The Basics)") ! Beyond the Basics topics (see "Patient information: Acne (Beyond the Basics)") SUMMARY ! Acne vulgaris is a common condition in adolescents that also affects adults. The psychological impact of acne vulgaris can be significant. (See 'Introduction' above and 'Epidemiology' above.) ! Acne vulgaris is a disorder of the pilosebaceous follicles. Follicular hyperkeratinization, sebum production, Propionibacterium acnes (P. acnes), and inflammation are involved in the pathogenesis. Follicular rupture, which releases proinflammatory lipids and keratin into the dermis, can intensify the inflammation seen in acne. (See 'Pathogenesis' above.) ! Androgens induce sebum production, and are an important factor in the development of acne vulgaris. Hyperandrogenism may cause acne in some patients, but most patients with acne vulgaris do not have androgen excess. (See 'Role of androgens' above.) ! The role of diet and stress in acne vulgaris remain unclear. A contributory effect of milk and high-glycemic index diets has been proposed, but prospective trials are necessary to ascertain the relationship between diet and acne. (See 'Diet' above and 'Stress' above.) ! Typically, acne vulgaris occurs on areas of the body with hormonally-sensitive sebaceous glands, including the face, neck, chest, upper back, and upper arms. Open comedones, closed comedones, and inflammatory papules, pustules, or nodules may be seen. The term "cystic acne" is a misnomer, as true cysts are rare in acne vulgaris. Adult women may present with lower face and neck acne associated with premenstrual flares. (See 'Clinical manifestations and classification' above.) ! A number of uncommon acne variants exist. Highly inflammatory conditions such as acne fulminans and acne conglobata require aggressive therapy to prevent scarring. (See 'Acne variants' above.) ! The diagnosis of acne vulgaris rests upon the patient's history and physical examination. If virilization, menstrual irregularity, or hirsutism is seen in women presenting with acne, evaluation for hyperandrogenism is indicated. A medication history should evaluate for the use of drugs that may cause acne or acneiform eruptions. (See 'Diagnostic evaluation' above.) ! Although acne vulgaris is a common condition that is often easily diagnosed, clinicians should be mindful of other diagnostic possibilities, including acneiform eruptions. (See 'Diagnostic evaluation' above and 'EGFR inhibitor acneiform eruption' above.)
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Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Cotterill JA, Cunliffe WJ. Suicide in dermatological patients. Br J Dermatol 1997; 137:246. 2. Dalgard F, Gieler U, Holm J, et al. Self-esteem and body satisfaction among late adolescents with acne: results from a population survey. J Am Acad Dermatol 2008; 59:746. 3. Newton JN, Mallon E, Klassen A, et al. The effectiveness of acne treatment: an assessment by patients of the outcome of therapy. Br J Dermatol 1997; 137:563. 4. Stathakis V, Kilkenny M, Marks R. Descriptive epidemiology of acne vulgaris in the community. Australas J Dermatol 1997; 38:115. 5. Collier CN, Harper JC, Cafardi JA, et al. The prevalence of acne in adults 20 years and older. J Am Acad Dermatol 2008; 58:56. 6. Goulden V, Clark SM, Cunliffe WJ. Post-adolescent acne: a review of clinical features. Br J Dermatol 1997; 136:66. 7. Jeremy AH, Holland DB, Roberts SG, et al. Inflammatory events are involved in acne lesion initiation. J Invest Dermatol 2003; 121:20. 8. Brggemann H, Henne A, Hoster F, et al. The complete genome sequence of Propionibacterium acnes, a commensal of human skin. Science 2004; 305:671. 9. Brggemann H. Insights in the pathogenic potential of Propionibacterium acnes from its complete genome. Semin Cutan Med Surg 2005; 24:67. 10. Shibata M, Katsuyama M, Onodera T, et al. Glucocorticoids enhance Toll-like receptor 2 expression in human keratinocytes stimulated with Propionibacterium acnes or proinflammatory cytokines. J Invest Dermatol 2009; 129:375. 11. Kim J, Ochoa MT, Krutzik SR, et al. Activation of toll-like receptor 2 in acne triggers inflammatory cytokine responses. J Immunol 2002; 169:1535. 12. Lomholt HB, Kilian M. Population genetic analysis of Propionibacterium acnes identifies a subpopulation and epidemic clones associated with acne. PLoS One 2010; 5:e12277. 13. Sugisaki H, Yamanaka K, Kakeda M, et al. Increased interferon-gamma, interleukin-12p40 and IL-8 production in Propionibacterium acnes-treated peripheral blood mononuclear cells from patient with acne vulgaris: host response but not bacterial species is the determinant factor of the disease. J Dermatol Sci 2009; 55:47. 14. Imperato-McGinley J, Gautier T, Cai LQ, et al. The androgen control of sebum production. Studies of subjects with dihydrotestosterone deficiency and complete androgen insensitivity. J Clin Endocrinol Metab 1993; 76:524. 15. Lucky AW, Biro FM, Huster GA, et al. Acne vulgaris in premenarchal girls. An early sign of puberty associated with rising levels of dehydroepiandrosterone. Arch Dermatol 1994; 130:308. 16. Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130:30. 17. Gollnick H, Cunliffe W, Berson D, et al. Management of acne: a report from a Global Alliance to Improve Outcomes in Acne. J Am Acad Dermatol 2003; 49:S1. 18. Cordain L, Lindeberg S, Hurtado M, et al. Acne vulgaris: a disease of Western civilization. Arch Dermatol 2002; 138:1584. 19. Thiboutot DM, Strauss JS. Diet and acne revisited. Arch Dermatol 2002; 138:1591. 20. Bershad S. The unwelcome return of the acne diet. Arch Dermatol 2003; 139:940. 21. Spencer EH, Ferdowsian HR, Barnard ND. Diet and acne: a review of the evidence. Int J Dermatol 2009; 48:339. 22. Adebamowo CA, Spiegelman D, Danby FW, et al. High school dietary dairy intake and teenage acne. J Am Acad Dermatol 2005; 52:207. 23. Danby FW. Acne and milk, the diet myth, and beyond. J Am Acad Dermatol 2005; 52:360.
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24. Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in adolescent girls. Dermatol Online J 2006; 12:1. 25. Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in teenaged boys. J Am Acad Dermatol 2008; 58:787. 26. Di Landro A, Cazzaniga S, Parazzini F, et al. Family history, body mass index, selected dietary factors, menstrual history, and risk of moderate to severe acne in adolescents and young adults. J Am Acad Dermatol 2012; 67:1129. 27. Thiboutot D. Acne: hormonal concepts and therapy. Clin Dermatol 2004; 22:419. 28. Cappel M, Mauger D, Thiboutot D. Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women. Arch Dermatol 2005; 141:333. 29. Holmes MD, Pollak MN, Willett WC, Hankinson SE. Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations. Cancer Epidemiol Biomarkers Prev 2002; 11:852. 30. Smith RN, Mann NJ, Braue A, et al. The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: a randomized, investigator-masked, controlled trial. J Am Acad Dermatol 2007; 57:247. 31. Bowe WP, Joshi SS, Shalita AR. Diet and acne. J Am Acad Dermatol 2010; 63:124. 32. Ballanger F, Baudry P, N'Guyen JM, et al. Heredity: a prognostic factor for acne. Dermatology 2006; 212:145. 33. Xu SX, Wang HL, Fan X, et al. The familial risk of acne vulgaris in Chinese Hans - a case-control study. J Eur Acad Dermatol Venereol 2007; 21:602. 34. Goulden V, McGeown CH, Cunliffe WJ. The familial risk of adult acne: a comparison between first-degree relatives of affected and unaffected individuals. Br J Dermatol 1999; 141:297. 35. Bataille V, Snieder H, MacGregor AJ, et al. The influence of genetics and environmental factors in the pathogenesis of acne: a twin study of acne in women. J Invest Dermatol 2002; 119:1317. 36. Rasmussen JE, Smith SB. Patient concepts and misconceptions about acne. Arch Dermatol 1983; 119:570. 37. Green J, Sinclair RD. Perceptions of acne vulgaris in final year medical student written examination answers. Australas J Dermatol 2001; 42:98. 38. Yosipovitch G, Tang M, Dawn AG, et al. Study of psychological stress, sebum production and acne vulgaris in adolescents. Acta Derm Venereol 2007; 87:135. 39. Chiu A, Chon SY, Kimball AB. The response of skin disease to stress: changes in the severity of acne vulgaris as affected by examination stress. Arch Dermatol 2003; 139:897. 40. Ganceviciene R, Graziene V, Fimmel S, Zouboulis CC. Involvement of the corticotropin-releasing hormone system in the pathogenesis of acne vulgaris. Br J Dermatol 2009; 160:345. 41. Tsai MC, Chen W, Cheng YW, et al. Higher body mass index is a significant risk factor for acne formation in schoolchildren. Eur J Dermatol 2006; 16:251. 42. Halvorsen JA, Vleugels RA, Bjertness E, Lien L. A population-based study of acne and body mass index in adolescents. Arch Dermatol 2012; 148:131. 43. Galobardes B, Davey Smith G, Jeffreys M, et al. Acne in adolescence and cause-specific mortality: lower coronary heart disease but higher prostate cancer mortality: the Glasgow Alumni Cohort Study. Am J Epidemiol 2005; 161:1094. 44. Zaenglein AK, Thiboutot DM. Acne Vulgaris. In: Dermatology, 2nd ed, Bolognia JL, Jorizzo JL, Rapini RP, et al (Eds), Elsevier, 2008. p.495. 45. Lucky AW. Quantitative documentation of a premenstrual flare of facial acne in adult women. Arch Dermatol 2004; 140:423. 46. Stoll S, Shalita AR, Webster GF, et al. The effect of the menstrual cycle on acne. J Am Acad Dermatol 2001; 45:957. 47. Pochi PE, Shalita AR, Strauss JS, et al. Report of the Consensus Conference on Acne Classification. Washington, D.C., March 24 and 25, 1990. J Am Acad Dermatol 1991; 24:495.
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48. Zaenglein AK, Graber EM, Thiboutot DM, et al. Acne vulgaris and acneiform eruptions. In: Dermatology in General Medicine, 7th ed, Wolff K, Goldsmith LA, Katz SI, et al (Eds), McGraw Hill, 2008. p.690. 49. Seukeran DC, Cunliffe WJ. The treatment of acne fulminans: a review of 25 cases. Br J Dermatol 1999; 141:307. 50. Campione E, Mazzotta AM, Bianchi L, Chimenti S. Severe acne successfully treated with etanercept. Acta Derm Venereol 2006; 86:256. 51. Sand FL, Thomsen SF. Adalimumab for the treatment of refractory acne conglobata. JAMA Dermatol 2013; 149:1306. 52. Shirakawa M, Uramoto K, Harada FA. Treatment of acne conglobata with infliximab. J Am Acad Dermatol 2006; 55:344. 53. Suei Y, Taguchi A, Tanimoto K, et al. Case report. synovitis, acne, pustulosis, hyperostosis and osteitis (SAPHO) syndrome. Dentomaxillofac Radiol 1996; 25:287. 54. Eichenfield LF, Krakowski AC, Piggott C, et al. Evidence-based recommendations for the diagnosis and treatment of pediatric acne. Pediatrics 2013; 131 Suppl 3:S163. 55. Friedlander SF, Baldwin HE, Mancini AJ, et al. The acne continuum: an age-based approach to therapy. Semin Cutan Med Surg 2011; 30:S6. 56. Timpatanapong P, Rojanasakul A. Hormonal profiles and prevalence of polycystic ovary syndrome in women with acne. J Dermatol 1997; 24:223. 57. Goldstein SM, Wintroub BU. Adverse Cutaneous Reactions to Medication: A Physician's Guide, CoMedica Inc, New York 1994. p.55. Topic 39 Version 10.0
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GRAPHICS Pathogenesis of follicular distention, rupture, and inflammation in acne vulgaris
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Acne is a disease of the follicular canal of a sebaceous folicle. A compact stratum corneum and a thickened granular layer in the infrainfundibulum are the beginning of the formation of a comedone. Microcomedones (A) and closed (B)
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and open (C) comedones form. Excessive sebum secretion occurs, and the bacterium P. acnes proliferates. The organism produces chemotactic factors, leading to neutrophil migration into the intact comedone. Neutrophilic enzymes are released and the comedone ruptures, inducing a cycle of chemotaxis and intense neutrophilic inflammation (D and E).
Reproduced with permission from: Rubin E, MD and Farber JL, MD. Pathology, 3rd Edition. Philadelphia: Lippincott Williams & Wilkins, 1999. Copyright 1999 Lippincott Williams & Wilkins. Graphic 57892 Version 1.0
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Mild acne
This 14-year-old girl has multiple closed comedones and scattered, small inflammatory papules and pustules on the forehead.
Courtesy of Douglas Hoffman, MD, Dermatlas; http://www.dermatlas.org. Graphic 62816 Version 4.0
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Noninflammatory acne
Numerous open comedones are present on the chin.

Reproduced with permission: Goodheart HP. Goodheart's Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams & Wilkins, Philadelphia 2003. Copyright 2003 Lippincott Williams & Wilkins. Graphic 80536 Version 3.0
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Inflammatory and noninflammatory acne
The face of this teenager shows open and closed comedones, papules, and pustules.
Reproduced with permission: Goodheart, HP. Goodheart's Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams & Wilkins, Philadelphia 2003. Copyright 2003 Lippincott Williams & Wilkins. Graphic 68412 Version 1.0
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Inflammatory acne
Erythematous papules and pustules are present.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc. Graphic 70809 Version 3.0
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Synthetic pathways for adrenal steroid synthesis
The first step in adrenal steroid synthesis is the combination of acetyl CoA and squalene to form cholesterol, which is then converted into pregnenolone. The enclosed area contains the core steroidogenic pathway utilized by the adrenal glands and gonads.
17!: 17-alpha-hydroxylase (CYP17, P450c17); 17,20: 17,20 lyase (also mediated by CYP17); 3": 3-beta-hydroxysteroid dehydrogenase; 21: 21-hydroxylase (CYP21A2, P450c21); 11": 11-beta-hydroxylase; (CYP11B1, P450c11); 18 refers to the two-step process of aldosterone synthase (CYP11B2, P450c11as), resulting in the addition of an hydroxyl group that is then oxidized to an aldehyde group at the 18-carbon position; 17"R: 17-beta-reductase; 5!R: 5alpha-reductase; DHEA: dehydroepiandrosterone; DHEAS: DHEA sulfate; A: aromatase (CYP19); SK: sulfokinase; SL: sulfotransferase. Graphic 70372 Version 3.0
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Androgen production in the sebaceous gland

Dehydroepiandrosterone sulfate (DHEA-S)
! Steroid sulfatase
Dehydroepiandrosterone (DHEA)
! 3 " -hydroxysteroid dehydrogenase
Androstenedione
! 17 " -hydroxysteroid dehydrogenase
Testosterone
! 5! -reductase type I
Dihydrotestosterone (DHT)
Graphic 68437 Version 1.0
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Postadolescent acne
Characteristic location of acne along the jaw line in a woman. Multiple papules have been excoriated.
Reproduced with permission from: Goodheart, HP, MD. Goodheart's Photoguide of Common Skin Disorders, 2nd ed. Lippincott Williams & Wilkins, Philadelphia 2003. Copyright 2003 Lippincott Williams & Wilkins. Graphic 81886 Version 2.0
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Acne nodules
Severe nodular acne on the forehead.

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Nodular acne
Erythematous papules, pustules, and nodules are present on the face. This patient also has postinflammatory hyperpigmentation and scarring.
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Acne sinus tract
Multiple sinus tracts in an adolescent male with severe nodular acne.

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Acne fulminans
This healthy adolescent with severe nodulocystic acne developed ulcerations and crusts shortly after starting oral 13-cisretinoic acid. Oral corticosteroids were added to his regimen and slowly tapered over 2 months.
Copyright Bernard Cohen, MD, Dermatlas; http://www.dermatlas.org. Graphic 64372 Version 3.0
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Cystic acne conglobata
This 22-year-old man with a 2 year history of severe nodulocystic acne was treated with oral 13-cis retinoic acid.
Copyright Yahia Albaili, DO, Dermatlas; http://www.dermatlas.org. Graphic 55681 Version 4.0
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Acne conglobata
Reproduced with permission from: Lippincott Williams & Wilkins. Copyright 2008. Graphic 75599 Version 1.0
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SAPHO Syndrome
A 37-year-old woman with a history of palmoplantar pustulosis presented with severe chest pain. The patient was first diagnosed with palmoplantar pustulosis at the age of 36 and soon afterwards suffered from upper chest pain. Although the pain and skin lesion had been relieved for three years after excision of the left first sternocostal articulation, she experienced subsequent relapse of sternal pain and palmoplantar pustulosis. Medication for rheumatoid arthritis, such as prednisolone, bucillamine, and methotrexate, or antibiotic therapy failed to ameliorate the symptoms. At the age of 45, she underwent palatine tonsillectomy with resolution of symptoms. At present, the patient has neither palmoplantar skin lesions nor sternal pain.
Copyright Shimizu Tominaga, MD, PhD, Dermatlas; http://www.dermatlas.org. Graphic 68169 Version 4.0
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Neonatal acne
Erythematous papules and pustules on the cheeks of a 3-week-old neonate.

Reproduced with permission from: George A Datto, III, MD. Graphic 56615 Version 2.0
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Acne excorie des jeunes filles
Multiple excoriations are present on the face.

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Major causes of drug-induced acne

Glucocorticoids Phenytoin Lithium Isoniazid Epidermal growth factor receptor inhibitors Iodides Bromides Androgens Corticotropin Cyclosporine Disulfiram Psoralens Thiourea Vitamins B2, B6, and B12 Azathioprine Graphic 76762 Version 2.0
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Hirsutism in an 18-year-old woman with late-onset congenital adrenal hyperplasia
Clinical features are similar to those of polycystic ovary syndrome: acne, hirsutism, menstrual irregularities, and obesity.
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Hypertrophic scars
These lesions are characteristic of acne scars that occur on the trunk.
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Keloids from acne
Reproduced with permission from: Stedman's Medical Dictionary. Copyright 2008 Lippincott Williams & Wilkins. Graphic 61382 Version 4.0
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Postinflammatory hyperpigmentation
In this patient, healing acne was the cause of the postinflammatory hyperpigmented patch.
Reproduced with permission from: Goodheart HP. Goodheart's Photoguide of Common Skin Disorders, 2nd ed. Lippincott Williams & Wilkins, Philadelphia 2003. Copyright 2003 Lippincott Williams & Wilkins. Graphic 78119 Version 4.0
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Papulopustular rosacea
As seen here, rosacea is characterized by inflammatory papules and pustules and telangiectasias located on the central third of the face. Comedones are absent.
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Perioral dermatitis
Small acne-like papules and scale are typically present in perioral dermatitis. The skin nearest to the mouth is characteristically spared.
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Sebaceous hyperplasia
Multiple yellowish papules are present.

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Pseudofolliculitis barbae
Tight, curly hairs that have been sharpened by shaving penetrate the skin. Inflammatory papules and pustules that resemble acne are evident.
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Pseudofolliculitis barbae
Pseudofolliculitis barbae. A loop of hair exiting and entering the skin is visible at the site of the erythematous papule.
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Acne keloidalis
Hypertrophic scarring and flesh-colored papules are seen in this patient.

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Staphylococcal folliculitis
A) Pustules and papules can be seen on this woman's thigh. B) This is a close-up view of Panel A.
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Pseudomonal folliculitis
Hot tub folliculitis ("hot tub buns"). Multiple pruritic follicular papules and pustules occurred on the buttocks and trunk of this woman 3 days after she had bathed in a hot tub. Bacterial culture grew Pseudomonas aeruginosa.
Reproduced with permission from: Goodheart, HP. Goodheart's Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams & Wilkins, Philadelphia 2003. Copyright 2003 Lippincott Williams & Wilkins. Graphic 82321 Version 1.0
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Keratosis pilaris
Keratosis pilaris. Multiple follicularly-based hyperpigmented papules are present.

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Keratosis pilaris
Keratosis pilaris. Multiple mildly erythematous follicularly-based papules are present.

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Favre-Racouchot Syndrome
This 87-year-old man, with a history of chronic sun exposure, developed prominent asymptomatic open comedones on the upper cheeks and sides of his nose.
Copyright Shahbaz A. Janjua, MD, Dermatlas; http://www.dermatlas.org. Graphic 59339 Version 3.0
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Steatocystoma multiplex
This healthy 25-year-old man complained of increasing numbers of firm cream colored papules and nodules on his chest.
Copyright Mary Tonsager, Dermatlas; http://www.dermatlas.org. Graphic 71097 Version 5.0
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Angiofibromas of the face in a child with tuberous sclerosis complex
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Systemic glucocorticoid-induced acneiform eruption
A) Drug-induced acneiform eruption. This patient was taking prednisone for sarcoidosis. B) This patient is taking systemic glucocorticoids for severe asthma.
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Acneiform eruption secondary to epidermal growth factor receptor (EGFR) inhibitor therapy
Diffuse erythematous follicular papules on the back of this patient treated with gefitinib.
Courtesy of Aimee S. Payne, MD, PhD. Graphic 55753 Version 2.0
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Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris

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