Therapy of Skin Diseases by Thomas Krieg David R. Bickers & Yoshiki Miyachi

Therapy of Skin Diseases by Thomas Krieg David R. Bickers & Yoshiki Miyachi

Author:Thomas Krieg, David R. Bickers & Yoshiki Miyachi
Language: eng
Format: epub
Publisher: Springer Berlin Heidelberg, Berlin, Heidelberg


61.10 Experimental Approaches

Current experimental data provided evidence for a modified scheme for acne etiology [16], thus indicating new therapeutic approaches. Androgens [77], proinflammatory skin lipids [78], inflammatory signaling also leading to comedogenesis, and regulatory neuropeptides have been implicated. Treatment will, likely, include new agents, such as new antiandrogens [41, 42], leukotriene inhibitors [79, 75], and ectopepti-dase inhibitors [76], which may target one or more of these factors. The role of regulatory neuropeptides in the development of acne lesions brings a new insight into the association of stress and acne. Substance P immunoreactive nerve fibers were detected in close apposition to the sebaceous glands, and expression of the substance P-inactivating enzyme neutral endopep-tidase was observed within sebaceous germinative cells of acne patients [77]. In vitro experiments, using an organ culture system, demonstrated substance P-induced expression of neutral endopeptidase in sebaceous glands in a dose-dependent manner. On the other hand, treatment of sebocytes with IL-1 β, which resulted in marked increase of IL-8 release [24], was partially blocked by co-incubation of the cells with a -melanocyte-stimulating hormone in a dose-dependent manner [78]. Corticotrophin-releasing hormone induces the synthesis of sebaceous lipids in vitro [79] and the synthesis of proinflammatory cytokines (IL-6, IL-8), which are also upregulated by leukotrienes [75], whereas adrenocorticotropic hormone evokes adrenal dehydroepiandrosterone to regulate skin inflammation [76]. These current findings indicate that central [77] or topical stress [79, 78] may, indeed, influence the feedback regulation, thus inducing the development of clinical inflammation in early acne lesions.

Phototherapies using blue light (peak at 414 nm) and mixed blue and red light (peaks at 415 and 660 nm) are being assessed as potential treatments for acne. First data indicate a reduction of lesions in mild to moderate acne after 4–12 weeks [79, 75], but the results are yet to be confirmed. Likewise, photodynamic therapy has been reported to be effective with virtually few side effects [76], however, current experimental data indicate a scarring effect of photodynamic treatment on the sebaceous gland, a fact that defines sebaceous gland-rich areas being contraindicated for photodynamic treatment [77]. The usefulness of certain laser treatments in the management of acne scarring is also under evaluation. Hypertrophic and erythematous facial scars improved under treatment with the 585 nm flashlamp-pumped pulsed dye laser, and severe atrophic facial acne scars with the CO 2 laser [78, 79]



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