Rheumatology service and Medical and Surgical Sciences Department, Maimonides Biomedical Research Institute of Cordoba (IMIBIC)/University of Cordoba/Reina Sofia University Hospital, Cordoba, Spain.
Front Immunol. 2022 Sep 23;13:997270. doi: 10.3389/fimmu.2022.997270. eCollection 2022.
Liver disease is one of the most important causes of morbidity and mortality worldwide whose prevalence is dramatically increasing. The first sign of hepatic damage is inflammation which could be accompanied by the accumulation of fat called non-alcoholic fatty liver disease (NAFLD), causing damage in the hepatocytes. This stage can progress to fibrosis where the accumulation of fibrotic tissue replaces healthy tissue reducing liver function. The next stage is cirrhosis, a late phase of fibrosis where a high percentage of liver tissue has been replaced by fibrotic tissue and liver functionality is substantially impaired. There is a close interplay of cardiovascular disease (CVD) and hepatic alterations, where different mechanisms mediating this relation between the liver and systemic vasculature have been described. In chronic inflammatory diseases such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA), in which the CVD risk is high, hepatic alterations seem to be more prevalent compared to the general population and other rheumatic disorders. The pathogenic mechanisms involved in the development of this comorbidity are still unraveled, although chronic inflammation, autoimmunity, treatments, and metabolic deregulation seem to have an important role. In this review, we will discuss the involvement of liver disease in the cardiovascular risk associated with inflammatory arthritis, the pathogenic mechanisms, and the recognized factors involved. Likewise, monitoring of the liver disease risk in routine clinical practice through both, classical and novel techniques and indexes will be exposed. Finally, we will examine the latest controversies that have been raised about the effects of the current therapies used to control the inflammation in RA and PsA, in the liver damage of those patients, such as methotrexate, leflunomide or biologics.
肝脏疾病是全球发病率和死亡率最高的疾病之一,其患病率正在显著上升。肝脏损伤的最初迹象是炎症,炎症可能伴随着脂肪的积累,即非酒精性脂肪性肝病 (NAFLD),导致肝细胞损伤。这个阶段可以进展为纤维化,其中纤维组织的积累取代了健康组织,从而降低了肝功能。下一个阶段是肝硬化,这是纤维化的晚期阶段,大量的肝组织已被纤维组织取代,肝脏功能严重受损。心血管疾病 (CVD) 和肝脏改变之间存在密切的相互作用,其中已经描述了介导肝脏和全身脉管系统之间这种关系的不同机制。在慢性炎症性疾病如类风湿关节炎 (RA) 和银屑病关节炎 (PsA) 中,心血管疾病风险较高,与普通人群和其他风湿性疾病相比,肝脏改变似乎更为普遍。尽管慢性炎症、自身免疫、治疗和代谢失调似乎起着重要作用,但这种合并症发展的发病机制仍在研究中。在这篇综述中,我们将讨论肝脏疾病在与炎症性关节炎相关的心血管风险中的作用、发病机制以及已识别的相关因素。同样,通过经典和新型技术和指标,在常规临床实践中监测肝脏疾病风险也将被揭示。最后,我们将研究目前用于控制 RA 和 PsA 炎症的治疗方法对这些患者的肝脏损伤的最新争议,如甲氨蝶呤、来氟米特或生物制剂。