Evaluation of the Quantitative and Qualitative Alterations in the Fatty Acid Contents of the Sebum of Patients with Inflammatory Acne during Treatment with Systemic Lymecycline and/or Oral Fatty Acid Supplementation
Background. Acne is a dermatosis that involves an altered sebum pattern. Objectives. (1) To evaluate if a treatment based on antibiotics (lymecycline) can alter fatty acids contents of the sebum of patients with acne; (2) to evaluate if oral supplementation of fatty acids can interfere with fatty acids contents of the sebum of patients with acne; (3) to evaluate if there is any interaction in fatty acids contents of the sebum of patients with acne when they use both antibiotics and oral supplementation of fatty acids. Methods. Forty-five male volunteers with inflammatory acne vulgaris were treated with 300?mg of lymecycline per day, with 540?mg of -linolenic acid, 1,200?mg of linoleic acid, and 510?mg of oleic acid per day, or with both regimens for 90 days. Every 30 days, a sample of sebum from the forehead was collected for fatty acids’ chromatographic analysis. Results. Twelve fatty acids studied exhibited some kind of pattern changes during the study: C12:0, C14:0, C15:0, C16:1, C18:0, C18:1n9c+C18:1n9t, C18:2n6t, C18:3n6, C18:3n3, C20:1, C22:0, and C24:0. Conclusions. The daily administration of lymecycline and/or specific fatty acids may slightly influence some fatty acids levels present in the sebum of patients with inflammatory acne vulgaris. 1. Introduction Acne is a chronic dermatosis that affects the pilosebaceous follicles. The physiopathogenesis of this condition involves periglandular dermal inflammation mechanisms, sebum hyperproduction, follicular hyperkeratosis, an increase of colonization of Propionibacterium acnes (P. acnes), and hormones [1–3]. We have observed that many of these pathogenic mechanisms are governed by a bio-immuno-molecular phenomenon that serves as the basis for research on and the future development of possible individual treatments for this dermatosis [4]. Fatty acids (FAs) constitute an essential part of corporeal lipids, especially FAs with chains composed of 12 to 24 carbons and 0 to 6 double bonds [5]. Essential fatty acids (EFAs) are FAs that the body is not capable of producing, such as linoleic acid (LA, 18:2n-6) and -linolenic acid (ALA, 18:3n-3), which cannot be produced due to lack of Δ12- and Δ15-desaturases [5]. In the human body, EFAs are primarily found in phospholipids and in the triglycerides (TGs) which participate in sebum (SB) formation [6]. SB of patients with AV is different from those without this condition. One of the main characteristics is the lower concentration of LA, and this low AL concentration facilitates follicular hyperkeratosis [7–9], SB hyperproduction [3, 10, 11], and
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