Therapeutic Targets and Acne Drugs

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Several clinical observations point to the importance of androgens in acne [23]. Androgens play an essential role in stimulating sebum production; androgen-insensitive subjects who lack functional androgen receptors do not produce sebum and do not develop acne. Moreover, systemic administration of testosterone and dehydro-epiandrosterone increases the size and secretion of sebaceous glands [24-27]. Sebosuppression, i.e. suppression of sebaceous gland hyperactivity, can classically be achieved by systemic administration of anti-androgens or isotreti-noin [19, 24-26, 28, 29] (table 2).

Abnormal keratinization of the infundibulum and the distal part of the sebaceous duct can be directly influenced through topical and systemic retinoids as well as through topical application of azelaic acid [30]. A number of further drugs can also secondarily induce keratolysis over their influence on other pathogenic factors [31]. Benzoyl peroxide and topical and systemic antibiotics primarily exhibit antimicrobial, but also anti-inflammatory activities [32, 33]. Various agents administered in acne treatment exhibit direct or indirect anti-inflammatory activi-

Table 2. Different action profile of systemic anti-acne drugs on the four major pathogenic factors of acne

Follicular Seborrhea hyperkeratosis

Bacterial Inflammation hypercolonization

+++ = Very strong, ++ = strong, + = moderate, + = indirect/weak.

ties in addition to their effects on further pathogenic factors of acne. However, solely anti-inflammatory agents have rarely been administered [13].

Bacterial hypercolonization is not involved at the onset of acne, but it plays a role in the maintenance of the disease [2, 3, 8]. Propionibacterium acnes (P. acnes), an anaerobic bacterium, is a normal constituent of the cutaneous flora; however, it is virtually absent in the skin before puberty. Sebaceous follicles turning to microcome-dones provide an anaerobic, lipid-rich environment for optimum bacterial proliferation. P. acnes produces li-pases which can split triglycerides into free fatty acids. The latter can irritate the follicular cells and may cause hyperproliferation and/or inflammation. Topical or systemic antibiotics administered successfully in acne patients exhibit a suppressive effect on P. acnes proliferation but also directly suppress inflammation by decreasing neutrophil chemotaxis and down-regulating the expression of pro-inflammatory mediators and the production of chemotactic factors [34]. The unique environment of the pilosebaceous follicle makes lipophilic compounds clinically more active than hydrophilic ones [35].

Inflammation in acne has been considered as secondary to bacterial hypercolonization and, consequently, neither has it been carefully investigated nor become the target of treatment. The major hypothesis was that early during development of acne lesions neutrophils accumulate around and in the follicles through chemoattractive substances which may originate from P. acnes [1-4]. Hydrolyt-ic enzymes and reactive oxygen species released by neutro-phils promote tissue damage, facilitating the occurrence of debris within the lumen. The latter is considered to trigger the inflammatory cascade [36]. This hypothesis has gained support because several anti-acne drugs have been shown to inhibit the generation or activity of chemotactic factors or the release of reactive oxygen species [37]. In addition, linoleic acid, which is deficient in acne comedones, inhibits neutrophil oxygen metabolism and phagocytosis.

Table 3. Indications for oral antibiotic therapy in acne

Patients with moderate to severe acne

Patients for whom topical antibiotic therapy has failed or cannot be tolerated

Patients with moderate acne with tendency for scarring or substantial post-inflammatory hyperpigmentation

Patients with involvement of the shoulders, back or chest (difficult for topical application)

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