Department of Physiological Sciences, Faculty of Science, Stellenbosch University, Stellenbosch, South Africa.
Division of Rheumatology, Institute of Orthopaedics and Rheumatology, Winelands Mediclinic Orthopaedic Hospital, Stellenbosch, South Africa.
Front Immunol. 2021 Jul 16;12:688861. doi: 10.3389/fimmu.2021.688861. eCollection 2021.
Psoriasis (PsO) is a common T cell-mediated inflammatory disorder of the skin with an estimated prevalence of 2%. The condition manifests most commonly as erythematous plaques covered with scales. The aetiology of PsO is multifactorial and disease initiation involves interactions between environmental factors, susceptibility genes, and innate and adaptive immune responses. The underlying pathology is mainly driven by interleukin-17. In addition, various inflammatory mediators from specific T helper (T) cell subsets, namely T1, T17, and T22, are overexpressed in cutaneous lesions and may also be detected in the peripheral blood of psoriatic patients. Moreover, these individuals are also at greater risk, compared to the general population, of developing multiple comorbid conditions. Cardiovascular disease (CVD) has been recognised as a prominent comorbidity of PsO. A potential mechanism contributing to this association may be the presence of a hypercoagulable state in these individuals. Inflammation and coagulation are closely related. The presence of chronic, low-grade systemic inflammation may promote thrombosis - one of the major determinants of CVD. A pro-inflammatory milieu may induce the expression of tissue factor, augment platelet activity, and perturb the vascular endothelium. Altogether, these changes will result in a prothrombotic state. In this review, we describe the aetiology of PsO, as well as the pathophysiology of the condition. We also consider its relationship to CVD. Given the systemic inflammatory nature of PsO, we evaluate the potential contribution of prominent inflammatory mediators (implicated in PsO pathogenesis) to establishing a prothrombotic state in psoriatic patients.
银屑病（PsO）是一种常见的 T 细胞介导的炎症性皮肤病，估计患病率为 2%。这种疾病最常见的表现是红斑覆盖着鳞片。银屑病的病因是多因素的，疾病的发生涉及环境因素、易感基因和先天及适应性免疫反应之间的相互作用。潜在的病理学主要由白细胞介素-17 驱动。此外，在皮肤损伤中过度表达了各种来自特定 T 辅助（T）细胞亚群的炎症介质，即 T1、T17 和 T22，也可以在银屑病患者的外周血中检测到。此外，与普通人群相比，这些个体患多种合并症的风险更高。心血管疾病（CVD）已被认为是银屑病的一种主要合并症。导致这种关联的一个潜在机制可能是这些个体存在高凝状态。炎症和凝血密切相关。慢性、低度全身炎症的存在可能促进血栓形成——这是 CVD 的主要决定因素之一。促炎环境可能诱导组织因子的表达，增强血小板活性，并扰乱血管内皮。总的来说，这些变化将导致血栓形成状态。在这篇综述中，我们描述了银屑病的病因，以及该病的病理生理学。我们还考虑了它与 CVD 的关系。鉴于银屑病具有全身性炎症性质，我们评估了（参与银屑病发病机制）的主要炎症介质对银屑病患者形成血栓形成状态的潜在贡献。
