Practice Essentials

Acne vulgaris is a common chronic skin disease involving blockage and/or inflammation
of pilosebaceous units (hair follicles and their accompanying sebaceous gland). Acne can
present as noninflammatory lesions, inflammatory lesions, or a mixture of both, affecting
mostly the face but also the back and chest.[1]See the image below.

Acne, grade I; multiple open comedones.

Acne vulgaris has a multifactorial pathogenesis, of which the key factor is genetics.[2]
Acne develops as a result of an interplay of the following four factors: (1) follicular
epidermal hyperproliferation with subsequent plugging of the follicle, (2) excess sebum
production, (3) the presence and activity of the commensal bacteriaPropionibacterium
acnes, and (4) inflammation.[3]

Signs and symptoms

Acne vulgaris is characterized by noninflammatory, open or closed comedones and by
inflammatory papules, pustules, and nodules. Acne vulgaris typically affects the areas of
skin with the densest population of sebaceous follicles (eg, face, upper chest, back). Local
symptoms of acne vulgaris may include pain, tenderness, or erythema.
Systemic symptoms are most often absent in acne vulgaris. Severe acne with associated
systemic signs and symptoms, such as fever, is referred to as acne fulminans. Severe
acne, characterized by multiple comedones, without the presence of systemic symptoms,
is known as acne conglobata. This severe form of acne frequently heals with disfiguring
scars. Additionally, acne vulgaris may have a psychological impact on any patient,
regardless of the severity or the grade of the disease.[4]
See Clinical Presentation for more detail.

Diagnosis
Examination in patients with acne vulgaris includes the following features:

Comedonal acne: Presence of open and closed comedones but usually no inflammatory papules or
nodules

Mild acne: Presence of comedones and a few papulopustules

Moderate acne: Presence of comedones, inflammatory papules, and pustules; a greater number of
lesions are present than in milder inflammatory acne

Nodulocystic acne: Presence of comedones, inflammatory lesions, and large nodules greater than 5
mm in diameter; scarring is often evident

Laboratory tests
Acne vulgaris is a clinical diagnosis. However, laboratory testing may be indicated in the
following situations:

Female patients with dysmenorrhea or hirsutism: Consider a hormonal evaluation with levels of total
and/or free testosterone, dehydroepiandrosterone sulfate, luteinizing hormone, and folliclestimulating hormone

Cases refractory to treatment or when improvement is not maintained: Culture skin lesions to rule
out gram-negative folliculitis

See Workup for more detail.

Management
Treatment of acne vulgaris should be directed toward the known pathogenic factors,
including follicular hyperproliferation, excess sebum, P acnes, and inflammation. The
most appropriate treatment is based on the grade and severity of the acne.
Pharmacotherapy
The following medications are used in the treatment of Propionibacterium acne vulgaris:

Retinoid-like agents (eg, topical tretinoin, adapalene, tazarotene, isotretinoin)

Antibiotics (eg, tetracycline, minocycline, doxycycline, trimethoprim/sulfamethoxazole,

clindamycin, topical clindamycin, topical erythromycin, daptomycin)

Selective aldosterone antagonists (eg, spironolactone)

Estrogen/progestin combination oral contraceptive pills (eg, ethinyl estradiol, drospirenone, and
levomefolate; ethinyl estradiol and norethindrone; ethinyl estradiol and norgestimate; ethinyl
estradiol and drospirenone)

Acne products (eg, erythromycin and benzoyl peroxide, clindamycin and tretinoin, clindamycin and
benzoyl peroxide, azelaic acid, benzoyl peroxide)

When a topical or systemic antibiotic is used, it should be used in conjunction with

benzoyl peroxide or topical retinoid to reduce the emergence of resistance.
Nonpharmacotherapy
Diet therapy, such as a low-glycemic diet and avoidance of junk foods, has been
suggested as a nonpharmacologic measure to manage acne vulgaris.
Procedures
Procedural treatments for acne vulgaris include the following:

Manual extraction of comedones

Intralesional steroid injections

Superficial peels that use glycolic or salicylic acid

See Treatment, Guidelines, and Medication for more detail.

Background
Acne vulgaris is characterized by noninflammatory, open or closed comedones and by
inflammatory papules, pustules, and nodules. Acne vulgaris typically affects the areas of
skin with the densest population of sebaceous follicles; these areas include the face, the
upper part of the chest, and the back.
Acne vulgaris is the most common skin disease in the United States; it affects an
estimated 80% of Americans at some time during their lives.[5]Twenty percent have
severe acne, which can result in permanent physical and mental scarring.
Medscape Reference articles on acne include Acne Conglobata,Acne Fulminans,Acne
Keloidalis Nuchae, and Acneiform Eruptions. Also see the Medscape Acne Resource
Center.

Pathophysiology

The pathogenesis of acne vulgaris is multifactorial. The key factor is genetics.[2]Acne

develops as a result of an interplay of the following four factors[3]:

Release of inflammatory mediators into the skin

Follicular hyperkeratinization with subsequent plugging of the follicle

Propionibacterium acnes follicular colonization

Excess sebum production

Research has shown that inflammatory responses actually occur before

hyperkeratinization. Cytokines produced by CD4+ T cells and macrophages activate local
endothelial cells to up-regulate inflammatory mediators such as vascular cell adhesion
molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and human
leukocyte antigen (HLA)DR in the vessels around the pilosebaceous follicle.[6]
Follicular hyperkeratinization involves increased keratinocyte proliferation and decreased
desquamation, leading to sebum- and keratin-filled microcomedones.[7]
P acnes is an anaerobic organism present in acne lesions. The presence of P
acnes promotes inflammation through a variety of mechanisms. P acnes stimulates
inflammation by producing proinflammatory mediators that diffuse through the follicle
wall. Studies have shown that P acnes activates the toll-like receptor 2 on monocytes and
neutrophils.[8]Activation of the toll-like receptor 2 then leads to the production of
multiple proinflammatory cytokines, including interleukins 12 and 8 and tumor necrosis
factor. Hypersensitivity to P acnes may also explain why some individuals develop
inflammatory acne vulgaris while others do not.[9]
Excess sebum is another key factor in the development of acne vulgaris. Sebum
production and excretion are regulated by a number of different hormones and mediators.
In particular, androgen hormones promote sebum production and release.[10]The degree
of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal
androgen dehydroepiandrosterone sulfate (DHEA-S).[11]
Numerous other mediators and receptors, including growth hormone and insulinlike
growth factor, as well as peroxisome proliferator-activated receptors also regulate the
sebaceous gland and may contribute to the development of acne.[12, 13]Furthermore, the
sebaceous gland acts a neuroendocrine-inflammatory organ that is activated via
corticotrophin-releasing hormones in response to stress and normal functions.[14]

Epidemiology
United States

Acne vulgaris affects 80% of Americans at some time during their lives.[5]Twenty percent
have severe acne, which can result in permanent physical and mental scarring.

International
Persons of some races are affected more than others. Cystic acne is prevalent in the
Mediterranean region from Spain to Iran.[15]

Race
Acne is common in North American whites. African Americans have a higher prevalence
of pomade acne, likely stemming from the use of hair pomades. Ethnicities with darker
skin are also more prone to postinflammatory hyperpigmentation.[16]

Sex
During adolescence, acne vulgaris is more common in males than in females. In
adulthood, acne vulgaris is more common in women than in men.[17]

Age
Acne or acneform lesions, such as in neonatal cephalic pustulosis, may be present in the
first few weeks and months of life, when a newborn is still under the influence of
maternal hormones and when the androgen-producing portion of the adrenal gland is
disproportionately large.[18]This neonatal acne tends to resolve spontaneously. However,
some neonates may require therapy (eg, topical retinoids).[18]
Adolescent acne usually begins with the onset of puberty, when the gonads begin to
produce and release more androgen hormone.
Acne is not limited to adolescence. Twelve percent of women and 5% of men at aged 25
years have acne. By age 45 years, 5% of both men and women still have acne.[19]

Prognosis
Acne may cause long-lasting and detrimental psychosocial and physical effects. It is
associated with depression and anxiety, regardless of disease severity, although the
psychological effects usually improve with treatment. Furthermore, acne may cause
permanent scarring that is difficult to correct.[20]
In male patients, acne generally clears by early adulthood. Five percent of men still have
acne at age 25 years. Female patients frequently have adult acne. Twelve percent of
women still have acne at age 25 years. Five percent of women still have acne at age 45
years.[19]
The overall prognosis for persons with acne is good.

Patient Education
Patients should be instructed on their morning and evening treatment programs. Retinoid
dermatitis may develop at approximately day 10 of therapy. Patients must be informed of
this in advance so they will not consider this exfoliation an allergy. By skipping a day or
2 and restarting the program slowly, the skin can adapt to this irritation.

Prescriptions should be accompanied by a discussion of the potential adverse effects.

For patient education resources, see the Skin Conditions and Beauty Center as well as the
patient education article Acne. Also see the Medscape Acne Resource Center.