Šperl J
Klinika hepatogastroenterologie IKEM Praha.
Vnitr Lek. 2013 Jul;59(7):591-6.
Hepatitis B (HBV) is a DNA virus, which cannot be eradicated completely from the organism by treatment, only its replication can be suppressed to low levels. The pathogenesis of liver damage due to HBV is immune mediated, the infected hepatocytes represent the target structures of immune reaction. In individuals who spontaneously achieved the state of inactive carriage of the virus or even achieved HBsAg negativity, we deal only with immune control of viral replication. Chemotherapy or immunosuppressive treatment disrupt the immune control of HBV infection, the virus replication substantially increases and hepatitis B reactivates. HBV reactivation manifests as further flareup of chronic inflammation with rapid progression of liver cirrhosis or even as a fulminant hepatitis with liver failure. The risk of reactivation increases with degree of induced immunosuppression, the highest risk is associated with corticosteroid and rituximab therapy. HBV reactivation threatens patients during solid tumours treatment as well as haemato oncological malignancies, patients treated with immunosuppressive and bio-logical therapies for systemic inflammatory diseases and inflammatory bowel diseases, as well as patients on maintenance haemodialysis, after kidney transplantation and patients with HBV/ HIV co infection. HBV reactivation increases both morbidity and mortality in listed groups of patients. The patients threatened by HBV reactivation can be identified easily based on HBV serological markers assessment. Preemptive therapy with nucleos(t)ide analogues significantly reduces the risk of HBV reactivation, the effect of longterm antiviral therapy is described in detail in kidney transplant recipients in whom the 3rd generation antivirals (entecavir and tenofovir) completely obviate the negative impact of HBV on longterm survival. In oncological patients who are treated for a determined time period, we can use lamivudine, which is not suitable for longterm treatment due to high risk of resistance emergence.
乙型肝炎病毒(HBV)是一种DNA病毒,治疗无法将其从机体中完全清除,只能将其复制抑制到低水平。HBV所致肝损伤的发病机制是免疫介导的,被感染的肝细胞是免疫反应的靶结构。在自发达到病毒非活动携带状态甚至实现HBsAg阴性的个体中,我们仅应对病毒复制的免疫控制。化疗或免疫抑制治疗会破坏HBV感染的免疫控制,病毒复制大幅增加,乙型肝炎复发。HBV复发表现为慢性炎症进一步加剧,肝硬化迅速进展,甚至表现为暴发性肝炎伴肝衰竭。复发风险随诱导的免疫抑制程度增加而增加,最高风险与皮质类固醇和利妥昔单抗治疗相关。HBV复发在实体瘤治疗以及血液肿瘤恶性肿瘤患者、接受免疫抑制和生物疗法治疗全身性炎症性疾病和炎症性肠病的患者、维持性血液透析患者、肾移植后患者以及HBV/HIV合并感染患者中均对患者构成威胁。HBV复发会增加上述患者群体的发病率和死亡率。根据HBV血清学标志物评估,可轻松识别受HBV复发威胁的患者。核苷(酸)类似物的抢先治疗可显著降低HBV复发风险,长期抗病毒治疗的效果在肾移植受者中有详细描述,其中第三代抗病毒药物(恩替卡韦和替诺福韦)完全消除了HBV对长期生存的负面影响。在接受特定时间段治疗的肿瘤患者中,我们可以使用拉米夫定,但由于出现耐药的风险较高,它不适合长期治疗。