AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Acne vulgaris is a common skin disease that affects 85-100% of people at some time during their lives. It is characterized by noninflammatory follicular papules or comedones and by inflammatory papules, pustules, and nodules in its more severe forms. Acne vulgaris 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.

The following are other eMedicine articles on acne:

• Acne Conglobata
• Acne Fulminans
• Acne Keloidalis Nuchae
• Acneiform Eruptions

Additionally, the news article Acne Treatment Linked to Depression and the Medscape Acne Resource Center may be helpful.

Pathophysiology

The pathogenesis of acne vulgaris is multifactorial. Four key factors are responsible for the development of an acne lesion. These factors are follicular epidermal hyperproliferation with subsequent plugging of the follicle, excess sebum, the presence and activity of Propionibacterium acnes, and inflammation.

Follicular epidermal hyperproliferation is the first recognized event in the development of acne. The exact underlying cause of this hyperproliferation is not known. Currently, the 3 leading hypotheses have been proposed to explain why the follicular epithelium is hyperproliferative in individuals with acne.

First, androgen hormones have been implicated as the initial trigger. Comedones, the clinical lesion that results from follicular plugging, begin to appear around adrenarche in persons with acne. Furthermore, the degree of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S). Additionally, androgen hormone receptors are present in the portion of the follicle where the comedone forms; individuals with malfunctioning androgen receptors do not develop acne.

Second, changes in lipid composition have been implicated in the development of acne vulgaris. Persons with acne frequently have excess sebum production and oily skin. This excess sebum may dilute the normal epidermal lipids and result in a change in the relative concentrations of the various lipids. Diminished concentrations of linoleic acid have been demonstrated in individuals with acne and, interestingly, these levels normalize after successful treatment with isotretinoin. This relative decrease in linoleic acid may be what initiates comedone formation.

Inflammation is the third hypothesized factor incriminated in comedone formation.¹ Interleukin (IL)–1–alpha is a proinflammatory cytokine. It has been used in a tissue model to induce follicular epidermal hyperproliferation and comedone formation. Although inflammation is not apparent microscopically or clinically in early lesions of acne, it may still play a pivotal role in the development of acne vulgaris and the comedones.

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. Androgen hormones, in particular, promote sebum production and release. Still, most men and women with acne have normal circulating levels of androgen hormones. An end-organ hyperresponsiveness to androgen hormones has been hypothesized. Androgen hormones are not the only regulators of the human sebaceous gland. Numerous other agents, including growth hormone and insulinlike growth factor, also regulate the sebaceous gland and may contribute to the development of acne.

P acnes is a microaerophilic organism present in many acne lesions. Although, it has not been shown to be present in the earliest lesions of acne, the microcomedo, its presence in later lesions is almost certain. 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. Recent studies have shown that P acnes activates the toll-like receptor 2 on monocytes and neutrophils.² Activation of the toll-like receptor 2 then leads to the production of multiple proinflammatory cytokines, including IL-12, IL-8, and tumor necrosis factor. Hypersensitivity to P acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not.³

Inflammation may be a primary phenomenon or a secondary phenomenon. Most of the evidence to date suggests a secondary inflammatory response to P acnes as mentioned above. However, IL-1-alpha expression has been identified in the microcomedone, and it may play a role in the development of acne.⁴

Frequency

United States

Acne vulgaris affects 85-100% of people at some time during their lives.

Mortality/Morbidity

• Acne can cause physical pain and psychosocial suffering.
• Acne can lead to scarring.
• A severe inflammatory variant of acne, acne fulminans, can be associated with fever, arthritis, and other systemic symptoms.

Race

• The prevalence of acne in North Americans of African ancestry and whites is similar.

Sex

• Acne vulgaris is more common in males than in females during adolescence.
• It is more common in women than in men during adulthood.

Age

• Acne vulgaris 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. This neonatal acne resolves spontaneously.
• Adolescent acne usually begins prior to the onset of puberty, when the adrenal gland begins to produce and release more androgen hormone.
• Acne is not limited to adolescence. Twelve percent of women and 5% of men at age 25 years have acne. By age 45 years, 5% of both men and women still have acne.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Local symptoms may include pain or tenderness.
• Systemic symptoms are most often absent in acne vulgaris.
• Severe acne with associated systemic signs and symptoms is referred to as acne fulminans.
• Acne may have a psychological impact on any patient, regardless of the severity or the grade of the disease.

Physical

Acne vulgaris is characterized by comedones, papules, pustules, and nodules in a sebaceous distribution. A comedone is a whitehead (closed comedone) or a blackhead (open comedone) without any clinical signs of inflammation. Papules and pustules are raised bumps with obvious inflammation. The face may be the only involved skin surface, but the chest, the back, and the upper arms are often involved.

• In comedonal acne, no inflammatory lesions are present. Comedonal lesions are the earliest lesions of acne, and closed comedones are the precursor lesion of inflammatory lesions.
• Mild inflammatory acne is characterized by inflammatory papules and comedones.
• Moderate inflammatory acne has comedones, inflammatory papules, and pustules. Greater numbers of lesions are present than in milder inflammatory acne.
• Nodulocystic acne is characterized by comedones, inflammatory lesions, and large nodules greater than 5 mm in diameter. Scarring is often evident.

Causes

An external cause is seldom identifiable in acne vulgaris.

• Some cosmetic agents and hair pomades may worsen acne.
• Medications that can promote acne include steroids, lithium, some antiepileptics, and iodides.
• Congenital adrenal hyperplasia, polycystic ovary syndrome, and other endocrine disorders with excess androgens may trigger the development of acne vulgaris.
• Acne vulgaris may also be influenced by genetic factors.⁵

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Demodex folliculitis
Bacterial folliculitis
Papular sarcoidosis

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• The diagnosis of acne vulgaris is a clinical diagnosis.
• • In a female patient with dysmenorrhea or hirsutism, a hormonal evaluation should be considered. Patients with evidence of virilization must have their total testosterone levels measured. Many authorities would also measure free testosterone, DHEA-S, leuteinizing hormone, and follicle-stimulating hormone levels.
  • Skin lesion cultures to rule out gram-negative folliculitis are warranted when no response to treatment occurs or when improvement is not maintained.

Histologic Findings

The microcomedo is characterized by a dilated follicle with a plug of loosely arranged keratin. With progression of the disease, the follicular opening becomes dilated, and an open comedo results. The follicular wall thins, and it may rupture. Inflammation and bacteria may be evident, with or without follicular rupture. Follicular rupture is accompanied by a foreign body reaction. Dense inflammation into and throughout the dermis may be associated with fibrosis and scarring.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Treatment should be directed toward the known pathogenic factors involved in acne. These include follicular hyperproliferation, excess sebum, P acnes, and inflammation. The grade and the severity of the acne help in determining which of the following treatments, alone or in combination, is most appropriate. When a topical or systemic antibiotic is used, it should be used in conjunction with benzoyl peroxide to reduce the emergence of resistance.

• Topical treatments
• • Topical retinoids are comedolytic and anti-inflammatory. They cause epidermal differentiation and, thus, normalize follicular hyperproliferation and hyperkeratinization. Topical retinoids reduce the numbers of microcomedones, comedones, and inflammatory lesions. They may be used alone or in combination with other acne medications. The most commonly prescribed topical retinoids include adapalene, tazarotene, and tretinoin. These retinoids should be applied once daily to clean, dry skin, but they may need to be applied less frequently if irritation occurs. Skin irritation with peeling and redness may be associated with the use of topical retinoids. The use of mild, nondrying cleansers and noncomedogenic moisturizers may help reduce this irritation. Alternate-day dosing may be used if irritation persists. Topical retinoids thin the stratum corneum, and they have been associated with sun sensitivity. Instruct patients about sun protection.
  • Topical antibiotics are mainly used for their role against P acnes. They may also have anti-inflammatory properties. Topical antibiotics are not comedolytic, and bacterial resistance may develop to any of these agents. The development of resistance is lessened if topical antibiotics are used in combination with benzoyl peroxide.⁶ Commonly prescribed topical antibiotics include erythromycin and clindamycin alone or in combination with benzoyl peroxide. Clindamycin and erythromycin are available in a variety of topical agents. They may be applied once or twice a day. Gels and solutions may be more irritating than creams or lotions.
  • Benzoyl peroxide products are also effective against P acnes, and bacterial resistance to benzoyl peroxide has not been reported.⁷ Benzoyl peroxides are available over the counter and by prescription in a variety of topical forms, including soaps, washes, lotions, creams, and gels. Benzoyl peroxides may be used once or twice a day. These agents may cause a true allergic contact dermatitis. More often, an irritant contact dermatitis develops especially if used with tretinoin or when accompanied by aggressive washing methods.
• Systemic treatments
• • Systemic antibiotics are a mainstay in the treatment of acne vulgaris. These agents have anti-inflammatory properties, and they are effective against P acnes. The tetracycline group of antibiotics is commonly prescribed for acne. The more lipophilic antibiotics, such as doxycycline and minocycline, are generally more effective than tetracycline. Greater efficacy may also be due to less P acnes resistance to minocycline. However, P acnes resistance is becoming more common with all classes of antibiotics currently used to treat acne vulgaris.⁸ P acnes resistance to erythromycin has greatly reduced its usefulness in the treatment of acne. Subantimicrobial therapy or concurrent treatment with topical benzoyl peroxide may reduce the emergence of resistant strains.
  • Other antibiotics, including trimethoprim, alone or in combination with sulfamethoxazole, and azithromycin, are reportedly helpful.^{9, 10}
  • Some hormonal therapies may be effective in the treatment of acne vulgaris. Oral contraceptives increase sex hormone binding globulin, resulting in an overall decrease in circulating free testosterone. Combination birth control pills have shown efficacy in the treatment of acne vulgaris.^{11, 12, 13, 14} Spironolactone may also be used in the treatment of acne vulgaris.¹⁵ Spironolactone binds the androgen receptor and reduces androgen production. Adverse effects include dizziness, breast tenderness, and dysmenorrhea. Dysmenorrhea may be lessened by coadministration with an oral contraceptive. Periodic evaluation of blood pressure and potassium levels is appropriate. Pregnancy must be avoided while on spironolactone because of the risk of feminization of the male fetus.
  • Isotretinoin is a systemic retinoid that is highly effective in the treatment of severe, recalcitrant acne vulgaris. It causes normalization of epidermal differentiation, depresses sebum excretion by 70%, is anti-inflammatory, and even reduces the presence of P acnes. Isotretinoin therapy should be initiated at a dose of 0.5 mg/kg/d for 4 weeks and increased as tolerated until a cumulative dose of 120-150 mg/kg is achieved. Coadministration with steroids at the onset of therapy may be useful in severe cases to prevent initial worsening.
  • • Isotretinoin is a teratogen, and pregnancy must be avoided. Contraception counseling is mandatory, and 2 negative pregnancy test results are required prior to the initiation of therapy. Baseline laboratory examination should also include cholesterol and triglyceride assessment, hepatic transaminases, and a CBC count. Pregnancy tests and laboratory examinations should be repeated monthly during treatment.
    • Associated mood changes and depression have been reported during treatment. Although the cause is not clear, patients should be informed of this potential effect and must sign a consent form acknowledging they are aware of this potential risk.^{16, 17}
    • A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.
    • The patient is considered at high risk for abnormal healing and development of excessive granulation tissue following procedures. Many dermatologists delay elective procedures, such as dermabrasion or laser resurfacing, for up to a year after completion of therapy. Other procedures to be avoided during therapy include tattoos, piercings, leg waxing, and other epilation procedures.

Surgical Care

• Procedural treatments include manual extraction of comedones and intralesional steroid injections.
• Additionally, some patients may benefit from superficial peels that use glycolic or salicylic acid.
• Phototherapy using red light or blue light and photodynamic therapy are being assessed as potential treatments for acne.^{18, 19}
• The usefulness of some laser treatments in the management of acne is also being evaluated.

MEDICATION

Section 7 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Drug Category: Retinoids

These agents decrease the cohesiveness of abnormal hyperproliferative keratinocytes, and they may reduce the potential for malignant degeneration. They also modulate keratinocyte differentiation.

Drug Category: Antibiotics

Topical and systemic antibiotics used in the treatment of acne vulgaris are directed at P acnes. They also have anti-inflammatory properties.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Appropriate laboratory examinations (electrolytes with particular attention to potassium levels and, when appropriate, pregnancy tests) should be ordered as baseline and in follow up when spironolactone is prescribed.
• CBC counts should be obtained and monitored in patients on trimethoprim or trimethoprim/sulfamethoxazole.
• Baseline assessment of antinuclear antibody levels and hepatic transaminases has been recommended for patients expected to be on minocycline for more than 1 year.²⁰

Complications

• Acne lesions may lead to permanent scarring.

Prognosis

• In male patients, acne generally clears by early adulthood.
  Five percent of men still have acne at the age of twenty-five.
• 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.
• The overall prognosis for persons with acne is good. However, acne can result in long-lasting psychosocial impairment and physical scarring.

Patient Education

• Patients should be instructed to treat their skin gently. Mild, nonabrasive cleansers and noncomedogenic moisturizers and cosmetics are preferred.
• Prescriptions should be accompanied by a discussion of the potential adverse effects.
• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center and Teen Health Center. Also, see eMedicine's patient education articles Acne.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Careful prescribing of isotretinoin is mandatory. Aggressive pregnancy prevention in female patients and monthly follow-up of all patients on isotretinoin are necessary. Some patients develop a significant flare of acne at the outset of isotretinoin therapy, resulting in scar formation. This potential risk may be lessened by starting therapy at 0.5 mg/kg/d or less and by the coadministration of systemic steroids.

Special Concerns

• Treating acne during pregnancy is a challenge. Many of the most commonly prescribed acne medications are not safe during pregnancy. A safer approach incorporates topical or systemic erythromycin or clindamycin.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Inflammatory papules and pustules in a patient with acne vulgaris. Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.
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Media type:  Photo

Media file 2:  Inflammatory papules and pustules in a patient with acne vulgaris. Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.
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Media type:  Photo

Media file 3:  Close-up view of inflammatory papules and pustules. Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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3. Webster GF. Inflammatory acne represents hypersensitivity to Propionibacterium acnes. Dermatology. 1998;196(1):80-1. [Medline].
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11. Koulianos GT. Treatment of acne with oral contraceptives: criteria for pill selection. Cutis. Oct 2000;66(4):281-6. [Medline].
12. Redmond GP. Effectiveness of oral contraceptives in the treatment of acne. Contraception. Sep 1998;58(3 Suppl):29S-33S; quiz 68S. [Medline].
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15. Shaw JC. Low-dose adjunctive spironolactone in the treatment of acne in women: a retrospective analysis of 85 consecutively treated patients. J Am Acad Dermatol. Sep 2000;43(3):498-502. [Medline].
16. Jacobs DG, Deutsch NL, Brewer M. Suicide, depression, and isotretinoin: is there a causal link?. J Am Acad Dermatol. Nov 2001;45(5):S168-75. [Medline].
17. Jick SS, Kremers HM, Vasilakis-Scaramozza C. Isotretinoin use and risk of depression, psychotic symptoms, suicide, and attempted suicide. Arch Dermatol. Oct 2000;136(10):1231-6. [Medline].
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19. Papageorgiou P, Katsambas A, Chu A. Phototherapy with blue (415 nm) and red (660 nm) light in the treatment of acne vulgaris. Br J Dermatol. May 2000;142(5):973-8. [Medline].
20. Knowles SR, Shapiro L, Shear NH. Serious adverse reactions induced by minocycline. Report of 13 patients and review of the literature. Arch Dermatol. Aug 1996;132(8):934-9. [Medline].
21. Cunliffe WJ, Holland DB, Clark SM, Stables GI. Comedogenesis: some new aetiological, clinical and therapeutic strategies. Br J Dermatol. Jun 2000;142(6):1084-91. [Medline].
22. Eady EA, Ingham E, Walters CE, Cove JH, Cunliffe WJ. Modulation of comedonal levels of interleukin-1 in acne patients treated with tetracyclines. J Invest Dermatol. Jul 1993;101(1):86-91. [Medline].
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24. Gollnick H, Cunliffe W, Berson D, Dreno B, Finlay A, Leyden JJ, et al. Management of acne: a report from a Global Alliance to Improve Outcomes in Acne. J Am Acad Dermatol. Jul 2003;49(1 Suppl):S1-37. [Medline].
25. Gollnick H, Schramm M. Topical drug treatment in acne. Dermatology. 1998;196(1):119-25. [Medline].
26. Goulden V, Stables GI, Cunliffe WJ. Prevalence of facial acne in adults. J Am Acad Dermatol. Oct 1999;41(4):577-80. [Medline].
27. Holland DB, Cunliffe WJ, Norris JF. Differential response of sebaceous glands to exogenous testosterone. Br J Dermatol. Jul 1998;139(1):102-3. [Medline].
28. Kellett SC, Gawkrodger DJ. The psychological and emotional impact of acne and the effect of treatment with isotretinoin. Br J Dermatol. Feb 1999;140(2):273-82. [Medline].
29. Kligman AM. Postadolescent acne in women. Cutis. Jul 1991;48(1):75-7. [Medline].
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32. Mango D, Ricci S, Manna P, Miggiano GA, Serra GB. Clinical and hormonal effects of ethinylestradiol combined with gestodene and desogestrel in young women with acne vulgaris. Contraception. Mar 1996;53(3):163-70. [Medline].
33. Mulder MM, Sigurdsson V, van Zuuren EJ, Klaassen EJ, Faber JA, de Wit JB, et al. Psychosocial impact of acne vulgaris. evaluation of the relation between a change in clinical acne severity and psychosocial state. Dermatology. 2001;203(2):124-30. [Medline].
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36. Ross JI, Snelling AM, Eady EA, Cove JH, Cunliffe WJ, Leyden JJ, et al. Phenotypic and genotypic characterization of antibiotic-resistant Propionibacterium acnes isolated from acne patients attending dermatology clinics in Europe, the U.S.A., Japan and Australia. Br J Dermatol. Feb 2001;144(2):339-46. [Medline].
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Article Last Updated: Jul 15, 2008