Acne Vulgaris
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.
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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. 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. 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.
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.
Frequency
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.
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
Other Problems to Be Considered
Demodex folliculitis
Bacterial folliculitis
Papular sarcoidosis
Laboratory 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.
Source - http://emedicine.medscape.com/
