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Compounds of psoriasis with obesity and overweight

机译:肥胖和超重的牛皮癣患者

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Many epidemiological studies have confirmed the relationship of obesity and psoriasis, and it is believed that obesity is an independent risk factor for its development and is associated with a worse prognosis. Furthermore, the reduction of body weight, using low-calorie diet combined with exercise, reduces the severity of psoriasis.Visceral adipose tissue is the largest endocrine organ, producing proinflammatory cytokines (TNF-α, IL-6, IL-17) and adipokines (adiponectin, omentin, chemerin). They participate in the development of dyslipidemia, insulin resistance, diabetes, and consequently of the cardiovascular diseases. Macrophages of visceral adipose tissue have a special role and they increase significantly in obesity. They are responsible for the development of inflammation in adipose tissue and produce inflammatory cytokines (TNF alpha, IL-6, Il-8, Il-17, Il-18, MCP-1) and other adipokines: resistin, visfatin, retinol-binding protein 4. This explains the concept of ?psoriatic march ?and observations of the frequent coexistence of psoriasis with obesity. Inflammation associated with systemic disease, fanned by pro-inflammatory cytokines and adipokines produced by the visceral adipose tissue lead to the development of insulin resistance, endothelial cell damage. Endothelial dysfunction predisposes to the formation of atherosclerotic plaques and faster development of cardiovascular events. Complication of obesity is the development of non-alcoholic fatty liver disease (NAFLD), which states twice as likely in patients with plaque psoriasis and is associated with the severity of the disease. Another consequence is the development of depression. Probably the proinflammatory cytokines can interact with metabolism of neurotransmitters. Obesity also has a significant impact on the treatment of psoriasis, increasing the risk of adverse effects of systemic drugs, reducing the efficacy of biological agents which dose should be adjusted to the weight of the patient. It is a factor responsible for the increased volume of distribution and it causes low titter of drug concentration.
机译:许多流行病学研究已经证实肥胖与牛皮癣之间的关系,并且认为肥胖是肥胖症发展的独立危险因素,并且与预后较差有关。此外,通过低热量饮食和运动相结合来减轻体重可减轻牛皮癣的严重程度。内脏脂肪组织是最大的内分泌器官,可产生促炎细胞因子(TNF-α,IL-6,IL-17)和脂肪因子。 (脂联素,omentin,chemerin)。它们参与血脂异常,胰岛素抵抗,糖尿病的发展,并因此参与心血管疾病的发展。内脏脂肪组织的巨噬细胞具有特殊作用,并且在肥胖中会明显增加。它们负责脂肪组织中炎症的发展,并产生炎性细胞因子(TNFα,IL-6,II-8,II-17,II-18,MCP-1)和其他脂肪因子:抵抗素,visfatin,视黄醇结合蛋白质4。这解释了牛皮癣行军的概念,并观察到牛皮癣与肥胖症并存。内脏脂肪组织产生的促炎性细胞因子和脂肪因子激起了与全身性疾病相关的炎症,导致胰岛素抵抗,内皮细胞损伤。内皮功能障碍易导致动脉粥样硬化斑块的形成和心血管事件的更快发展。肥胖症的并发症是非酒精性脂肪肝疾病(NAFLD)的发展,这种疾病在斑块状牛皮癣患者中的发病率是其两倍,并且与疾病的严重程度有关。另一个后果是抑郁症的发展。促炎细胞因子可能与神经递质的代谢相互作用。肥胖症对牛皮癣的治疗也有重大影响,增加了全身药物不良反应的风险,降低了应根据患者体重调整剂量的生物制剂的功效。这是导致分配体积增加的原因,并且导致药物浓度的低滴度。

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