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首页> 外文期刊>Therapeutic advances in chronic disease. >Topical, systemic and biologic therapies in hidradenitis suppurativa: pathogenic insights by examining therapeutic mechanisms
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Topical, systemic and biologic therapies in hidradenitis suppurativa: pathogenic insights by examining therapeutic mechanisms

机译：Hidradenitisupturativa的局部，系统性和生物疗法：通过检查治疗机制的致病性见解

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摘要

Hidradenitis suppurativa (HS) is a chronic inflammatory disease of the skin, manifesting in chronic, recurrent painful pustules, nodules, boils and purulent draining abscesses. Our current understanding of the pathogenesis of the disease is incomplete. This review aims to identify available treatment options in HS and discuss the pharmacological mechanisms through which such agents function. Identifying common pathways may inform our understanding of the pathogenesis of HS as well as identify future therapeutic targets. The pharmacological mechanisms implicated in topical therapies, antibiotic, hormonal, systemic immunomodulatory and biologic therapies for HS are discussed. Significant differences exist between agents and implicated pathways in therapy for mild and severe disease. This is an expression of the possible dichotomy in inflammatory pathways (and treatment responses) in HS. Studies involving monoclonal antibodies provide the greatest insight into what these specific mechanisms may be. Their variable levels of clinical efficacy compared with placebo bolsters the suggestion that differential inflammatory pathways may be involved in different presentations and severity of disease. Nuclear factor kappa B (NF-κB), tumor necrosis factor (TNF)-α and other innate immune mechanisms are strongly represented in treatments which are effective in mild to moderate disease in the absence of scarring or draining fistulae, however complex feed-forward mechanisms in severe disease respond to interleukin (IL)-1 inhibition but are less likely to respond to innate immune inhibition (through NF-κB or TNF-α) alone. It is unclear whether IL-17 inhibition will parallel TNF-α or IL-1 inhibition in effect, however it is plausible that small molecule targets (Janus kinase1 and phosphodiesterase 4) may provide effective new strategies for treatment of HS.
机译：HIDradenitisupturativa（HS）是皮肤的慢性炎症疾病，表现为慢性，复发性痛苦的脓疱，结节，沸腾和脓性排出的脓肿。我们目前对疾病发病机制的理解是不完整的。该审查旨在识别HS中的可用治疗方案，并讨论这种药物功能的药理学机制。鉴定常见途径可以告知我们对HS的发病机制以及识别未来治疗目标的理解。讨论了局部疗法，抗生素，激素，全身免疫调节和HS的生物疗法的药理学机制。药剂与疗法治疗中的药物与患者患者患者之间存在显着差异。这是HS中炎性途径（和治疗反应）中可能的二分法的表达。涉及单克隆抗体的研究提供了最大的洞察，对这些具体机制可以是什么。与安慰剂止血剂相比，它们可变临床疗效的水平这一建议可以参与不同介绍和疾病的严重程度。核因子Kappa B（NF-κB），肿瘤坏死因子（TNF）-α和其他先天免疫机制在治疗中强烈地表示，在没有瘢痕或排水的瘘管的情况下有效地在轻度至中度疾病中有效，但复杂的前馈严重疾病的机制应对白细胞介素（IL）-1抑制，但不太可能仅对单独的INNATE免疫抑制（通过NF-κB或TNF-α）响应。目前尚不清楚IL-17抑制是否将平行于TNF-α或IL-1抑制作用，然而，它是合理的，小分子靶标（Janus激酶1和磷酸二酯酶4）可以提供有效的治疗HS的新策略。

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