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Abstract Acne vulgaris (AV) is a chronic inflammatory disorder of sebaceous follicles, found primarily on the face and upper trunk (chest and back). It is considered the most common skin disease, estimated to affect approximately 80% of individuals between ages of 11 and 30 years. It is a pleomrphic disorder with multifactorial pathogenesis There are four primary pathogenic factors which interact in a complex manner to produce acne lesions, these factors are follicular hyperkeratinization, excessive sebum production, hypercolonization of the duct by Propionibacterium acnes and direct or indirect inflammation. Another fifth factor included in the pathogenesis, is matrix metalloproteinases. Propionibacterium acnes (P. acnes) are gram positive, anaerobic diphtheroids that are part of the normal skin flora. It plays an important role in the pathogenesis of acne vulgaris by triggering proinflammatory mediators through activation of Toll-like receptors 2 (TLR2). Homocysteine is a sulfur containing amino acid derived from methionine. Once synthesized, it can be converted back to methionine by 5-methyltetrahydrofolate reductase and methionine synthase using cofactors such as vitamin B12 and folic acid. Normal range of serum homocysteine is 10μmol/L and hyperhomocysteinemia is characterized by an abnormaly high level of homocysteine in the blood conventionally described as above 15 μmol/L. |