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Official reprint from UpToDate

www.uptodate.com2014 UpToDate

Authors

Diane Thiboutot, MDAndrea Zaenglein, MD

Section Editors

Robert P Dellavalle, MD, PhD, MSPHMoise L Levy, MDMark V Dahl, MD

Deputy Editor

Abena O Ofori, MD

Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris

Disclosures

All topics are updated as new evidence becomes available and our peer review processis 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 individuScars can be disfiguring and lifelong. In one prospective study of 90 patients with acne, a significant improvement in

esteem was found with treatment of the acne [3]. Thus, it is imperative that clinicians are familiar with acne vulgaris

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 fo

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

Acne tends to resolve in the third decade, but it may persist into or develop de novo in adulthood. The exact prevale

in adults is uncertain, and studies using a clinical examination typically find a lower prevalence than surveys askin

patients to self-report acne.

Post-adolescent acne predominantly affects women, in contrast to adolescent acne which has a male predominance

In one survey of over 1000 adults, self-reported acne in men and women was documented as follows [5]:

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

20 to 29 years: 43 and 51 percent, respectively!



ages 50 and older: 7 and 15 percent, respectively!

Follicular hyperkeratinization!

Increased sebum production!

Propionibacterium acnes (P. acnes) within the follicle!
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The sequence of events leading to the development of an acne lesion is not fully understood. The earliest change in

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 obstructi

the follicle with sebum and keratin (the microcomedo). However, an influx of inflammatory cells in the perifollicular re

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 sebumproduction 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 identificati

the following bacterial properties that may contribute to the inflammatory response [8,9]:

A component of the host innate immune system, the toll-like receptor, is also thought to play an important role in the

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 contrib

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:

Role of androgens Androgens contribute to the development of acne through stimulating the growth and secreto

function of sebaceous glands. Most circulating androgens are produced by the adrenal gland and the gonads (figure

Androgen production also occurs within the sebaceous glands, which convert dehydroepiandrosterone sulfate (DHE

S), 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.

Inflammation!

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 respons!

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.!

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).

!
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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 wit

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 produ

by the immature adrenal gland in girls, and the immature adrenal gland and testes in boys. Androgen levels fall by a

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]; tho

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 no

androgen levels. Conditions in which hyperandrogenism is seen include polycystic ovarian syndrome, congenital ad

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 ruptu

comedos, promoting the development of inflammatory lesions [17]. Thus, patients with acne should refrain from rubb

their faces or picking their skin.

Turtlenecks, bra straps, shoulder pads, orthopedic casts, and sports helmets may all cause acne mechanica, in whic

occlusion of pilosebaceous follicles leads to comedone formation. Pomade acne is associated with the use of occlus

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

used retrospective data collection to determine diet during high school found an association between acne and intak

milk [22]. The authors suggested that natural hormonal components of milk or other bioactive molecules in milk coul

exacerbate acne [22,23]. Two subsequent large prospective cohort studies (one involving boys and the other involvigirls) 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)

moderate to severe acne (odds ratio [OR] 1.78, 95% CI 1.22-2.59) [26]. Similar to the other studies, food intake histo

was assessed via a retrospective patient questionnaire. No randomized trials have evaluated the relationship betwe

dairy products and acne.

Other studies have suggested that insulin-like growth factor (IGF) may play a role in acne [27,28]. Milk consumption

been associated with increased levels of serum IGF [29]. IGF is also increased by ingestion of high glycemic loads a

could potentially link diet and acne. A 12-week randomized trial that compared low and high glycemic load diets in 4

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 res

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 ac

[21].

Data on favorable effects of dietary factors such as zinc, omega-3 fatty acids, antioxidants, vitamin A, and dietary fib
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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 fam

members [26,33,34], and a large twin study of monozygotic and dizygotic twins also supported the heritable nature o

acne [35]. In cases of very severe acne, there is often a positive family history; but the role of genetics in mild acne i

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 o

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

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 hum

sebaceous glands [40]. Sebaceous gland cells exhibit stronger staining for CRH in acne-involved skin than in norma

uninvolved skin. Although additional studies are necessary, these findings suggest that the CRH system may partici

in the occurrence of stress-exacerbated acne.

Body mass index Few studies have evaluated the relationship between weight and acne vulgaris, and study res

vary on the connection between these factors [26,41-43]. Whereas a case-control study of adolescents and young a

(ages 10 to 24) found a correlation between low BMI and a reduced risk for acne that was most evident among male

[26], a cross-sectional, survey-based study of young adults (ages 18 and 19) found a statistically significant associa

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 th

have the largest, hormonally-responsive sebaceous glands, including the face, neck, chest, upper back, and upper a

In addition to the typical lesions of acne vulgaris (eg, open comedones, closed comedones, and inflammatory lesionscarring 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 fla

(picture 3) [44,45]. These women, in particular, seem to benefit from hormonal therapies for acne [44]. Premenstrua

flares of acne appear to be more common in women over the age of 33 than in women aged 20 to 33 years [46]. (Se

"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 lesion

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 sometime

inaccurately referred to as "cystic" or "nodulocystic" acne (picture 4A-B). In reality, true cysts are rare. Sinus tracts, w
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manifest as fluctuant linear lesions, are formed when nodules merge. These are seen in the most severe forms of ac

and are difficult to treat (picture 5). The presence of scarring or postinflammatory hyperpigmentation is also assesse

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 psychologic

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 inflamma

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 requir

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 a

friable plaques with hemorrhagic crusts suggests the diagnosis of acne fulminans, a systemic disorder (picture 6). T

rare condition affects adolescent males primarily. Lesions usually involve the trunk, but may be present elsewhere. A

fulminans is associated with leukocytosis, an elevated erythrocyte sedimentation rate, proteinuria, and osteolytic les

Patients with acne fulminans can be treated with systemic glucocorticoids (0.5 to 1 mg/kg) plus oral isotretinoinor or

antibiotics [49]. Treatment regimens vary, but oral glucocorticoids should be initiated about four weeks prior to startin

low-dose oral isotretinoin to prevent a flare of the condition [49]. Oral isotretinoin is started at 0.5 mg/kg/day or less a

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 m

(picture 7A-B). Lesions are most prominent on the back, chest, and buttocks, but can also appear in other sites. Larg

draining lesions, sinus tracts, and severe scarring may occur. Systemic symptoms are absent. Treatments have incl

systemic antibiotics, intralesional glucocorticoids, systemic glucocorticoids, and surgical intervention [48]. Patients c

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-alphainhibitors (etanercept[50], adalimumab[51], and combination therapy with infliximaband 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

disorder (picture 8). This diagnosis also requires systemic therapy [53]. (See "Major causes of musculoskeletal ches

pain", section on 'Sternocostoclavicular hyperostosis (SAPHO syndrome)'.), and (see "Treatment of musculoskeleta

chest pain"and "Neutrophilic dermatoses", section on 'SAPHO syndrome').

PAPA syndrome PAPA syndrome (sterile pyogenic arthritis, pyoderma gangrenosum, and acne) is an autoso

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. Inflammator

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. Patient

are treated with antibiotics with gram negative coverage. Recalcitrant cases are managed with oral isotretinoinfor fo

five months [44].
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Neonatal acne and infantile acne Neonatal acne (also called neonatal cephalic pustulosis) and infantile acn

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. Affec

children usually present with a mixture of comedones and inflammatory lesions on the face. An endocrinology worku

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, lea

to erosions and scarring (picture 10). An underlying psychiatric disorder can be associated, and treatment may invoantidepressants and psychotherapy.

Solid facial edema Solid facial edema (Morbihan's disease) is a rare complication of acne that presents as fa

soft tissue edema and erythema. The condition may wax and wane in severity, but usually does not spontaneously

resolve without treatment. Improvement with isotretinoinwith 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 vulga

A medication history should also be reviewed for acne-inducing drugs (table 2). Skin should be examined carefully, s

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 hyperandrogenThis 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 adult

One study of 51 women with acne (ages 15 to 46) found that 39 percent had menstrual abnormalities and 37 percen

had PCOS [56]. These observations suggest that all women with the combination of acne and oligomenorrhea shou

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. Patie

with Cushing's disease or syndrome and late-onset congenital adrenal hyperplasia may also experience acne vulga

Evidence of virilization includes a deepening voice, decreased breast size, clitoromegaly, alopecia, oligomenorrhea,

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

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 la

onset congenital adrenal hyperplasia, in which elevated levels of DHEA-S may also be seen. Referrals to endocrino

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 o

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-induce

acne. (See 'Drug-induced acne'below and 'EGFR inhibitor acneiform eruption'below and "Drug eruptions", section o

'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 12and picture 13), and postinflammatory

pigmentary changes (picture 14) should be noted. The skin examination is essential for determining the best treatme

course for an individual patient. (See "Treatment of acne vulgaris", section on 'Patient assessment'and "Treatment o

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 m

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

telangiectasias. Common features of rosacea include erythema, telangiectasias, and papules or pustules on th

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). W

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 mo

commonly occurs in adults with a history of oily skin. These growths are umbilicated yellowish papules are mos

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 1

B). Comedones are absent, and lesions are usually monomorphous, unlike the polymorphous lesion in differen

stages of development that are typical of acne. (See "Folliculitis".)

!

Keratosis pilaris In this common condition, caused by keratotic follicular plugging, patients typically presen

with small follicular papules on the extensor surfaces of the upper arms or thighs (picture 20A-B). Erythema m

be present. Lesions can also occur on the face, particularly in children. (See "Approach to the patient with pust

skin lesions", section on 'Keratosis pilaris'.)

!

Favre-Racouchot syndrome Favre-Racouchot syndrome is a condition resulting from cutaneous photodam

(sun damage) seen in middle-aged or older adults. Open and closed comedones are found in areas of

!
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Acneiform eruptions There are multiple disorders in which acne-like eruptions occur, unassociated with true acn

vulgaris. These include the following:

Drug-induced acne Drug-induced acne typically presents with a monomorphous inflammatory papular erupti

(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 areferred 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 availabl

Heavy, oil-based hair products are still commonly used and may contribute to the development of acne on the forehe

(pomade acne).

Irritant reactions to cosmetic products can also produce eruptions that resemble acne vulgaris. Inflammatory papule

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, neand upper trunk in the majority of patients receiving these medications (picture 25). (See "Cutaneous complications

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 tarderivatives, 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 monomorph

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 see

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 antibiotic

may also be used.

Radiation acne Treatment with ionizing radiation can result in the appearance of comedones as acute radiati

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 o

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

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

which multiple yellow or skin-colored sebum-filled cysts are found on the trunk, upper arms, or chest (picture 2

!

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".)

!
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the arms, buttocks, and thighs is seen. The acneiform eruption is difficult to treat. Isotretinoinhas 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 Bey

the Basics. The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, a

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 educ

pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 to 12 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 topic

your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info an

the keyword(s) of interest.)

SUMMARY

th th

th th

Basics topics (see "Patient information: Acne (The Basics)")!

Beyond the Basics topics (see "Patient information: Acne (Beyond the Basics)")!

Acne vulgaris is a common condition in adolescents that also affects adults. The psychological impact of acnevulgaris 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, whic

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 androg

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 indediets has been proposed, but prospective trials are necessary to ascertain the relationship between diet and ac

(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 papu

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, menstru

irregularity, or hirsutism is seen in women presenting with acne, evaluation for hyperandrogenism is indicated.

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 ot

diagnostic possibilities, including acneiform eruptions. (See 'Diagnostic evaluation'above and 'EGFR inhibitor

acneiform eruption'above.)

!
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GRAPHICS

Pathogenesis of follicular distention, rupture, and

inflammation in acne vulgaris





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)





and open (C) comedones form. Excessive sebum secretion occurs, and the

bacterium P. acnesproliferates. 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 LippincottWilliams & Wilkins.

Graphic 57892 Version 1.0





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.

http://www.dermatlas.org/





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.






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.






Inflammatory acne

Erythematous papules and pustules are present.

Reproduced with permission from: www.visualdx.com. Copyright Logical

Images, Inc.

http://www.visualdx.com/





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: 5-

alpha-reductase; DHEA: dehydroepiandrosterone; DHEAS: DHEA sulfate; A: aromatase

(CYP19); SK: sulfokinase; SL: sulfotransferase.






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)


"

"





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.






Acne nodules

Severe nodular acne on the forehead.






Nodular acne

Erythematous papules, pustules, and nodules are present on the face.

This patient also has postinflammatory hyperpigmentation and

scarring.

Reproduced with permission from: www.visualdx.com. Copyright Logical

Images, Inc.

http://www.visualdx.com/





Acne sinus tract

Multiple sinus tracts in an adolescent male with severe nodular acne.


5/28/2018 Pathogenesis, clinical manifestations, and

pathogenesis, clinical manifestations, and diagnosis of acne vulgaris.pdf

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