Acne is a multifactorial dermatosis with a polymorphous clinical appearance. Particularly in severe forms of acne, comedones, papules, pustules and deep inflammatory lesions (nodules and cysts) can be present simultaneously.
The therapy of acne is oriented to the four known pathogenetic factors of the disease: Follicular hyperkeratosis, increased sebaceous gland activity with hyperseborrhoea, microbial hypercolonisation with Propionibacterium acnes, inflammation and immunological host reaction.
Azelaic acid (AzA), an aliphatic nine-carbon saturated and linear dicarboxylic acid (nonanedioic acid). [HOOC-(CH2)7-COOH], has been employed as a 20% cream in topical acne therapy since 1989. It is an effective and well-tolerated monotherapy in mild and moderate forms of acne vulgaris which is comparable in its efficacy to other established topical acne treatments such as benzoyl peroxide, erythromycin, and tretinoin.
Activity of AzA is exerted through the interference with the major events triggering the onset of acne lesions. The cytostatic action exerted on proliferative keratinocytes, the antimicrobial properties against different bacteria, including Propiontibacterium acnes, and the interference with sebum secretion, account for the effects of AzA on follicular hyperkeratosis, P. acnes colonization and seborrhoea, respectively, in acne. Moreover, AzA has been shown to be effective in the treatment of inflammatory acne resulting in the reduction in inflammatory papules and pustules. Application of AzA has been recently extended to the treatment of rosacea as an innovative formulation contributed to the improvement of its therapeutic efficacy in this disease.
Combined treatments with systemic antibiotics, topical antibiotics and benzoyl peroxide have proven to be efficacious and the treatment of acne and as alternative to oral isotretinoin use.
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2. Mastrofrancesco A, Ottaviani M, Aspite N, Cardinali G, Izzo E, Graupe K, Zouboulis CC, Camera E, Picardo M . Azelaic acid modulates the inflammatory response in normal human keratinocytes through PPARgamma activation. Exp Dermatol. 2010 Sep;19(9):813-20. doi: 10.1111/j.1600-0625.2010.01107.x. Epub 2010 Jul.