The main underlying cause of acne is a genetic predisposition. The condition is inherited in an autosomal dominant pattern with incomplete penetrance. For example, acne vulgaris may skip a generation. The following aggravating factors are recognized:
The diagnosis of acne vulgaris is clinical. Note the following:
* 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 also measure free testosterone, DHEA-S, leuteinizing hormone, and follicle-stimulating hormone levels.
* Skin lesion cultures to rule out gram-negative folliculitis are warranted if the patient does not respond to treatment or improvement is not maintained.
* Also see the Medscape Acne Resource Center.
Histologic Findings
The microcomedo is characterized by a dilated follicle with a plug of dense 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 dense inflammatory infiltrate throughout the dermis. Later, extensive fibrosis and scarring may develop.
Acne Vulgaris treatment should be directed toward the known pathogenic factors involved in acne. Acne treatments are discussed in part five of the Acne Vulgaris article.
Acne Vulgaris Article - TREATMENT - Part V is here
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