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Practice EssentialsAcne 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 !ee the image belo".
Acne, grade #$ multiple open comedones.
Acne vulgaris has a multifactorial pathogenesis, of "hich the key factor is genetics.
[%
Acne develops as a result of an interplay of the follo"ing four factors& (1) follicular
epidermal hyperproliferation "ith subse'uent plugging of the follicle, (%) excess sebum
production, () the presence and activity of the commensal bacteriaropionibacterium
acnes, and (*) inflammation.[
Signs and symptoms
Acne vulgaris is characteri+ed by noninflammatory, open or closed comedones and by
inflammatory papules, pustules, and nodules. Acne vulgaris typically affects the areas of
skin "ith the densest population of sebaceous follicles (eg, face, upper chest, back). ocal
symptoms of acne vulgaris may include pain, tenderness, or erythema.
!ystemic symptoms are most often absent in acne vulgaris. !evere acne "ith associatedsystemic signs and symptoms, such as fever, is referred to as acne fulminans. !evere
acne, characteri+ed by multiple comedones, "ithout the presence of systemic symptoms,
is kno"n as acne conglobata. -his severe form of acne fre'uently heals "ith disfiguringscars. Additionally, acne vulgaris may have a psychological impact on any patient,
regardless of the severity or the grade of the disease.[*
!ee linical resentation for more detail.
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Diagnosis
xamination in patients "ith acne vulgaris includes the follo"ing features&
•
omedonal acne& resence of open and closed comedones but usually no inflammatory papules or
nodules
•
•
0ild acne& resence of comedones and a fe" papulopustules
•
•
0oderate acne& resence of comedones, inflammatory papules, and pustules$ a greater number of
lesions are present than in milder inflammatory acne
•
•
odulocystic acne& resence of comedones, inflammatory lesions, and large nodules greater than 2
mm in diameter$ scarring is often evident
•
aboratory tests
Acne vulgaris is a clinical diagnosis. 3o"ever, laboratory testing may be indicated in thefollo"ing situations&
•
4emale patients "ith dysmenorrhea or hirsutism& onsider a hormonal evaluation "ith levels of total
and/or free testosterone, dehydroepiandrosterone sulfate, luteini+ing hormone, and follicle5
stimulating hormone
•
•
ases refractory to treatment or "hen improvement is not maintained& ulture skin lesions to rule
out gram5negative folliculitis•
!ee 6orkup for more detail.
Management
-reatment of acne vulgaris should be directed to"ard the kno"n pathogenic factors,
including follicular hyperproliferation, excess sebum, acnes, and inflammation. -hemost appropriate treatment is based on the grade and severity of the acne.
harmacotherapy
-he follo"ing medications are used in the treatment of ropionibacterium acne vulgaris&
•
7etinoid5like agents (eg, topical tretinoin, adapalene, ta+arotene, isotretinoin)
•
•
Antibiotics (eg, tetracycline, minocycline, doxycycline, trimethoprim/sulfamethoxa+ole,
clindamycin, topical clindamycin, topical erythromycin, daptomycin)
•
•
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!elective aldosterone antagonists (eg, spironolactone)
•
•
strogen/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 ben+oyl peroxide, clindamycin and tretinoin, clindamycin and
ben+oyl peroxide, a+elaic acid, ben+oyl peroxide)
•
6hen a topical or systemic antibiotic is used, it should be used in con8unction "ith
ben+oyl peroxide or topical retinoid to reduce the emergence of resistance.
onpharmacotherapy
9iet therapy, such as a lo"5glycemic diet and avoidance of “ 8unk foods,” has been
suggested as a nonpharmacologic measure to manage acne vulgaris.
rocedures
rocedural treatments for acne vulgaris include the follo"ing&
•
0anual extraction of comedones
•
•
#ntralesional steroid in8ections
•
•
!uperficial peels that use glycolic or salicylic acid
•
!ee -reatment, :uidelines, and 0edication for more detail.
BackgroundAcne vulgaris is characteri+ed by noninflammatory, open or closed comedones and byinflammatory papules, pustules, and nodules. Acne vulgaris typically affects the areas of
skin "ith 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 ;nited !tates$ it affects an
estimated <=> of Americans at some time during their lives.[2 -"enty percent have
severe acne, "hich can result in permanent physical and mental scarring.
0edscape 7eference articles on acne include Acne onglobata,Acne 4ulminans,Acne
?eloidalis uchae, and Acneiform ruptions. Also see the 0edscape Acne 7esource
enter .
Pathophysiology
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-he pathogenesis of acne vulgaris is multifactorial. -he key factor is genetics.[%Acne
develops as a result of an interplay of the follo"ing four factors[ &
•
7elease of inflammatory mediators into the skin
•
•
4ollicular hyperkeratini+ation "ith subse'uent plugging of the follicle
•
•
ropionibacterium acnes follicular coloni+ation
•
•
xcess sebum production
•
7esearch has sho"n that inflammatory responses actually occur before
hyperkeratini+ation. ytokines produced by 9*@ - cells and macrophages activate localendothelial cells to up5regulate inflammatory mediators such as vascular cell adhesion
molecule51 (A051), intercellular adhesion molecule51 (#A051), and human
leukocyte antigen (3A)–97 in the vessels around the pilosebaceous follicle.[B
4ollicular hyperkeratini+ation involves increased keratinocyte proliferation and decreaseddes'uamation, leading to sebum5 and keratin5filled microcomedones.[C
acnes is an anaerobic organism present in acne lesions. -he presence of
acnes promotes inflammation through a variety of mechanisms. acnes stimulates
inflammation by producing proinflammatory mediators that diffuse through the follicle
"all. !tudies have sho"n that acnes activates the toll5like receptor % on monocytes andneutrophils.[<
Activation of the toll5like receptor % then leads to the production of
multiple proinflammatory cytokines, including interleukins 1% and < and tumor necrosisfactor. 3ypersensitivity to acnes may also explain "hy some individuals developinflammatory acne vulgaris "hile others do not.[D
xcess sebum is another key factor in the development of acne vulgaris. !ebum
production and excretion are regulated by a number of different hormones and mediators.
#n particular, androgen hormones promote sebum production and release.[1= -he degree
of comedonal acne in prepubertal girls correlates "ith circulating levels of the adrenal
androgen dehydroepiandrosterone sulfate (93A5!).[11
umerous other mediators and receptors, including gro"th hormone and insulinlike
gro"th factor, as "ell as peroxisome proliferator5activated receptors also regulate the
sebaceous gland and may contribute to the development of acne.[1%, 1
4urthermore, thesebaceous gland acts a neuroendocrine5inflammatory organ that is activated via
corticotrophin5releasing hormones in response to stress and normal functions.[1*
EpidemiologyUnited States
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Acne vulgaris affects <=> of Americans at some time during their lives.[2 -"enty percent
have severe acne, "hich can result in permanent physical and mental scarring.
Inte national
ersons of some races are affected more than others. ystic acne is prevalent in the
0editerranean region from !pain to #ran.[12
Race
Acne is common in orth American "hites. African Americans have a higher prevalenceof pomade acne, likely stemming from the use of hair pomades. thnicities "ith darker
skin are also more prone to postinflammatory hyperpigmentation.[1B
Se
9uring adolescence, acne vulgaris is more common in males than in females. #n
adulthood, acne vulgaris is more common in "omen than in men.[1C
!ge
Acne or acneform lesions, such as in neonatal cephalic pustulosis, may be present in thefirst fe" "eeks and months of life, "hen a ne"born is still under the influence of
maternal hormones and "hen the androgen5producing portion of the adrenal gland is
disproportionately large.[1< -his neonatal acne tends to resolve spontaneously. 3o"ever,
some neonates may re'uire therapy (eg, topical retinoids).[1<
Adolescent acne usually begins "ith the onset of puberty, "hen the gonads begin to produce and release more androgen hormone.
Acne is not limited to adolescence. -"elve percent of "omen and 2> of men at aged %2
years have acne. Ey age *2 years, 2> of both men and "omen still have acne.[1D
PrognosisAcne may cause long5lasting and detrimental psychosocial and physical effects. #t is
associated "ith depression and anxiety, regardless of disease severity, although the
psychological effects usually improve "ith treatment. 4urthermore, acne may cause permanent scarring that is difficult to correct.[%=
#n male patients, acne generally clears by early adulthood. 4ive percent of men still have
acne at age %2 years. 4emale patients fre'uently have adult acne. -"elve percent of
"omen still have acne at age %2 years. 4ive percent of "omen still have acne at age *2years.[1D
-he overall prognosis for persons "ith acne is good.
Patient Educationatients should be instructed on their morning and evening treatment programs. 7etinoiddermatitis may develop at approximately day 1= of therapy. atients must be informed of
this in advance so they "ill not consider this exfoliation an allergy. Ey skipping a day or
% and restarting the program slo"ly, the skin can adapt to this irritation.
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rescriptions should be accompanied by a discussion of the potential adverse effects.
4or patient education resources, see the !kin onditions and Eeauty enter as "ell as the
patient education article Acne. Also see the 0edscape Acne 7esource enter .