INTRODUCTION — Acne vulgaris is a common cutaneous disorder. Patients with acne can experience significant psychological morbidity and, rarely, mortality due to suicide [1,2]. The psychological effects of embarrassment, anxiety, and shame have an impact upon both social lives and employment. Scars can be disfiguring. In one prospective study of 90 patients with acne, a significant improvement in self-esteem 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 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 asking for patients to self-report acne.
In one survey, self-reported acne in men and women was documented as follows [5]:
- 20 to 29 years: 43 and 51 percent
- 30 to 39 years: 20 and 35 percent
- 40 to 49 years: 12 and 26 percent
- ages 50 and older: 7 and 15 percent
Post-adolescent acne predominantly affects women, in contrast to adolescent acne which has a male predominance [6]. Approximately one-third of affected women have features of hyperandrogenicity, while one-half have a family history of postadolescent acne [6].
PATHOGENESIS
Pilosebaceous follicles — Acne vulgaris is a disease of pilosebaceous follicles. Four factors are involved (figure 1):
- Follicular hyperkeratinization/abnormal desquamation
- Increased sebum production
- Propionibacterium acnes (P. acnes) within the follicle
- Inflammation
The earliest change in the pilosebaceous unit is follicular hyperkeratinization, which is associated with both increased proliferation and decreased desquamation of keratinocytes lining the follicular orifice. The result is formation of a hyperkeratotic plug composed of sebum and keratin (the microcomedo) in the follicular canal. Why this process occurs is not known.
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 [7,8]:
- 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 are highly immunogenic, are produced by P. acnes.
- Porphyrins produced by P. acnes may contribute to adjacent tissue damage and inflammation.
A component of the host immune system, the toll-like receptor, is also thought to play an important role in the P. acnes mediated inflammatory response. Toll-like-receptors are cell surface receptors that are involved in the innate and acquired immune defenses against microorganisms [9]. 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) [10]. These cytokines contribute to the attraction of neutrophils and the release of neutrophil lysosomal enzymes that promote follicular rupture. (See "Toll-like receptors".)
Development of the acne lesion — Depending upon the degree of follicular hyperkeratinization, sebum production, P. acnes growth, and inflammation, the microcomedo evolves into a noninflammatory closed comedo, an open comedo, or an inflammatory pustule, papule, or nodule (figure 1).
- Accumulation of sebum and keratinous material converts a microcomedo into a closed comedo (a whitehead) (picture 1).
- The follicular orifice is opened with continued distension, forming an open comedo (a blackhead) (picture 2). Densely packed keratinocytes, oxidized lipids, and melanin all contribute to the dark color of the open comedo.
- Inflammatory lesions develop when the follicular contents rupture into the surrounding dermis. Following follicular rupture, proinflammatory lipids and keratin are extruded into the surrounding dermis, leading to inflammatory papule or nodule formation (picture 3).
Role of androgens — Although androgen excess due to a variety of conditions can cause acne, most patients with acne do not overproduce androgens. 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'.)
Androgens induce sebum production, a critical factor in the pathogenesis of acne. Most circulating androgens are produced by the adrenal gland and the gonads (algorithm 1). Androgen production also occurs within the sebaceous glands, which convert dehydroepiandrosterone sulfate (DHEA-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.
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 [11].
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 [12]; those with the highest levels develop the most severe acne [13].
Infantile acne (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 typically 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'.)
External factors — Cosmetics may contribute to the development of acne. Oils in hair products and cosmetic creams or lotions can exacerbate the skin lesions, while water-based products are less comedogenic [14].
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 promoting the development of inflammatory lesions [15]. 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.
Diet — A potential role for diet in acne is controversial [16-19]. 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 [20]. The authors suggest that natural hormonal components of milk and/or other bioactive molecules in milk could exacerbate acne [20,21]. Two subsequent large prospective cohort studies (one involving boys and the other involving girls) also reported an association of milk ingestion and acne [22,23]. All three studies were questionnaire-based, requiring subjects to recall their dietary intake and self-diagnose acne.
Other studies have suggested that insulin-like growth factor (IGF) may play a role in acne [24,25]. Milk consumption has been associated with increased levels of serum IGF [26]. 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 [27]. 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 chocolate ingestion is associated with an increased prevalence or severity of acne [19].
Stress — Patients and clinicians commonly believe that psychological stress can exacerbate acne [28,29]. 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) [30]. 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 [31].
Receptors for corticotropin releasing hormone (CRH), a hormone involved in the stress response, are present in human sebaceous glands [32]. 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.
CLINICAL MANIFESTATIONS AND CLASSIFICATION — Acne vulgaris typically affects those areas of the body that have the greatest number of 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 some patients. Hyperpigmentation is most common in patients with darker complexions, and an individual lesion 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 associated with premenstrual flares (picture 4) [33,34]. These women, in particular, seem to benefit from hormonal therapies for acne [33]. Premenstrual flares of acne appear to be more common in women over the age of 33 than in women aged 20 to 33 years [35]. (See "Hormonal therapy for 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.
Patients may have primarily comedonal acne consisting of noninflammatory lesions (closed and/or open comedones) (picture 1 and picture 2), primarily inflammatory acne with papules, pustules, and/or nodules (picture 5), or a variable mixture of both (picture 3). In inflammatory acne, lesions that are less than 5 mm in diameter are generally considered papules and pustules; nodular lesions are greater than 5 mm [36]. Nodular acne is sometimes inaccurately referred to as "cystic" or "nodulocystic" acne (picture 6 and picture 7). In reality, true cysts are rare. 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 [36]. 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 [33,37]. 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 8). 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 have been treated with systemic glucocorticoids (0.5 to 1 mg/kg) plus oral isotretinoin or oral antibiotics [38]. 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 [38]. 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 acne fulminans.
Acne conglobata — Acne conglobata is a severe form of nodular acne that is most commonly seen in young males (picture 9 and picture 10). 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 [37]. Patients can respond well to isotretinoin, although they may experience severe flares at the start of isotretinoin therapy. Lower doses of isotretinoin (0.5 mg/kd/day or less) plus systemic glucocorticoids before or during isotretinoin therapy are often required [37].
SAPHO syndrome — The SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) is another rare disorder (picture 11). This diagnosis also requires systemic therapy [39]. (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/or nodules typically appear on perinasal skin and the central face. A culture of lesions will yield gram-negative organisms, such as Enterobacter, Klebsiella, or Escherichia species. Patients are treated with antibiotics with gram negative coverage. Recalcitrant cases are managed with oral isotretinoin for four to five months [33].
Neonatal acne and infantile acne — Neonatal acne and infantile acne are distinct conditions. Neonatal acne appears within the first few weeks of life; infantile acne can appear as early as three 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'.)
Acne excoriée des jeunes filles — This scarring acne condition is primarily seen in young women, in whom relatively mild acne comedones or inflammatory papules are chronically self-excoriated, leading to erosions and scarring (picture 12). 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 [37].
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 13). (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 [40]. 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/or hormonal evaluation. Referral to an endocrinologist should be considered in these cases. (See "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 late-onset 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.
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) [41]. 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 14 and picture 15), and postinflammatory pigmentary changes (picture 16) 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 section on Overview of treatment.)
Hirsutism or virilization should prompt further laboratory and imaging studies or referral. (See "Evaluation of 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 (picture 17). (See "Rosacea".)
- Perioral dermatitis — Perioral dermatitis is characterized by small, grouped, erythematous papules in a perioral (or occasionally perinasal or periorbital) distribution (picture 18). In perioral dermatitis, a rim of spared skin is usually seen around the vermilion border of the lip. Fine scale may be seen in some cases. (See "Approach to the patient with pustular skin lesions", section on 'Perioral dermatitis'.)
- Sebaceous hyperplasia — In sebaceous hyperplasia, umbilicated yellowish papules are most commonly found on the forehead and cheeks (picture 19). This condition is seen in adults and may also occur in the neonatal period.
- Pseudofolliculitis barbae/Acne keloidalis nuchae — These two conditions occur most commonly in blacks, and are likely related to prevalence of tightly curled hair in this population. 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 20 and picture 21). 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 22 and picture 23). 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 follicularly based small papules on the extensor upper arms and/or thighs (picture 24). 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. Comedones are found in areas of photodamage, usually on the lateral upper cheeks (picture 25).
- Nevus comedonicus — A lesion presenting at birth or in childhood, in which grouped or a linear arrangement of comedones are noted.
- Adnexal tumors — Follicular benign 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 26).
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 27). 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.
EGFR inhibitor acneiform eruption — Epidermal growth factor receptor (EGFR) inhibitors are known to cause an inflammatory acneiform eruption involving the upper body in the majority of patients receiving these medications (picture 28). (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 head and neck, axillae, and scrotal areas, 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) is an autosomal dominant disorder associated with synostoses of bone in the hands, feet, cranium, and vertebral bodies. A diffuse acneiform eruption on 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 — Educational materials on this topic are available for patients. (See "Patient information: Acne".) We encourage you to print or e-mail this topic review, or to refer patients to our public web site, www.uptodate.com/patients, which includes this and other topics.
SUMMARY
- Acne vulgaris is a common condition in adolescents that may also affect 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. The accumulation of sebum and keratinous material contribute to the formation of comedones. P. acnes proliferation contributes to the inflammatory response seen in acne vulgaris. Follicular rupture, which releases proinflammatory lipids and keratin into the dermis, is also associated with inflammation. (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. Exacerbations of acne during periods of stress have been reported. (See 'Diet' above and 'Stress' above.)
- Typically, acne vulgaris occurs on areas of the body with high numbers of 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 are 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.)
ACKNOWLEDGMENT — UpToDate acknowledges Dr. Fern A Wirth, who contributed to earlier versions of this topic review.
