Owczarczyk-Saczonek Agnieszka, Placek Waldemar
Klinika Dermatologii, Chorób Przenoszonych Drogą Płciową i Immunologii Klinicznej Uniwersytetu Warmińsko-Mazurskiego, Miejski Szpital Zespolony w Olsztynie.
Postepy Hig Med Dosw (Online). 2017 Aug 24;71(1):761-772. doi: 10.5604/01.3001.0010.3854.
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.
许多流行病学研究已证实肥胖与银屑病之间的关系，并且人们认为肥胖是银屑病发生发展的独立危险因素，且与预后较差相关。此外，采用低热量饮食结合运动来减轻体重，可降低银屑病的严重程度。内脏脂肪组织是最大的内分泌器官，可产生促炎细胞因子（肿瘤坏死因子-α、白细胞介素-6、白细胞介素-17）和脂肪因子（脂联素、网膜素、趋化素）。它们参与血脂异常、胰岛素抵抗、糖尿病以及心血管疾病的发生发展。内脏脂肪组织中的巨噬细胞具有特殊作用，在肥胖状态下其数量会显著增加。它们负责脂肪组织炎症的发生，并产生炎性细胞因子（肿瘤坏死因子-α、白细胞介素-6、白细胞介素-8、白细胞介素-17、白细胞介素-18、单核细胞趋化蛋白-1）和其他脂肪因子：抵抗素、内脂素、视黄醇结合蛋白4。这解释了“银屑病进展”的概念以及银屑病与肥胖常同时存在的现象。由内脏脂肪组织产生的促炎细胞因子和脂肪因子引发的与全身性疾病相关的炎症，会导致胰岛素抵抗、内皮细胞损伤。内皮功能障碍易引发动脉粥样硬化斑块的形成以及心血管事件的更快发展。肥胖的并发症是非酒精性脂肪性肝病（NAFLD）的发生，斑块状银屑病患者患NAFLD的可能性是正常人的两倍，且与疾病严重程度相关。另一个后果是抑郁症的发生。可能促炎细胞因子会与神经递质的代谢相互作用。肥胖对银屑病的治疗也有重大影响，增加了全身性药物不良反应的风险，降低了生物制剂的疗效，而生物制剂的剂量应根据患者体重进行调整。肥胖是导致药物分布容积增加以及药物浓度滴度降低的一个因素。
