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Abstract AV is one of the most prevalent skin disease, affecting about 85% of the population aged 11 to 30 years old .It is not a life threatening condition, yet it lasts for years and causes physical and emotional scarring, The presentation of acne vulgaris has both non-inflammatory lesions (comedones) and inflammatory lesions (papules, pustules, and/or cystic lesions) (Davidovici and Wolf, 2010). Acne is a disease of the pilo-sebaceous unit with a complex pathophysiology. Four main pathogenic factors are known to lead to the development of acne: follicular epidermal hyperproliferation;excess sebum production; inflammation and the presence and activity of Propionibacterium acnes (Katsambas and Dessinioti, 2010). Androgen is one of the main factor in acne pathogenesis because it enhances follicular keratosis and influence sebum production As androgens are the major sebotropic hormones. The increased sebum production in acne patients may be due to increased circulating androgens or a hyper-responsiveness of the target organ (the pilo-sebaceous unit) to androgens, or both (Strauss et al., 2007). Most acne patients do not have endocrinologic abnormalities, however, persistent or severe acne can be the only clinical sign of androgen excess in women. Hormonal treatments are effective in acne by lowering circulating and local androgens levels, and opposing their effects on the sebaceous gland and probably on the follicular keratinocytes as well (Katsambas and Papakonstantinou, 2004). Androgen is produced by the gonads and the adrenal gland (testosterone and DHEA-S). Testosterone can also be produced locally within the sebaceous gland from the adrenal precursor hormone, DHEA-S (Thiboutot D, 2001). |