Chronic viral hepatitis in kidney transplantation

Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection in potential kidney transplant candidates-once considered absolute contraindications to kidney transplantation-no longer creates overt barriers to transplantation. Advances in the medical management of HBV and HCV infection have created opportunities for a substantial number of patients to be effectively treated with antiviral therapy before transplantation. For HBV infection, a number of new drugs enable clearance of the virus with minimal adverse effects and drug resistance. Pretransplantation antiviral therapy is advisable for patients with HCV infection, but adverse effects are common and viral eradication remains challenging. Regardless of viral clearance, pretransplant patients without bridging fibrosis (as confirmed by liver biopsy) or clinical stigmata of cirrhosis should be considered for kidney transplantation as survival is superior when compared to treatment with dialysis, and progression of liver disease is unlikely. For patients with advanced liver disease, simultaneous liver-kidney transplantation is an important consideration. These treatment advances further increase the burden of organ donor shortage; however, organs from deceased donors with chronic HBV or HCV infection could be efficiently allocated to certain individuals with a viral infection of the same type to increase the pool of available transplant organs.     

Chronic viral hepatitis and TNF-alpha blockade

SIR, We read with interest the article by Roux et al. [1] regardingthe use of tumour necrosis factor- (TNF-) blocking agents inpatients with hepatitis B virus (HBV) and hepatitis C virus(HCV). The authors describe three patients with chronic HBVinfection (all surface antigen positive) who were successfullytreated with TNF- blockade, in conjunction with     

慢性病毒性肝炎与肝脂肪变性

慢性乙型、丙型肝炎是目前我国最为常见的两种病毒性肝炎类型.患者不仅表现为肝功能异常,肝脏影像学及病理检查还发现部分患者在肝细胞变性坏死同时伴有脂肪变性.目前认为,病毒和宿主代谢因素是导致肝脂肪变性的重要原因,而脂肪变性对于慢性病毒性肝炎患者肝纤维化进展和抗病毒疗效均产生重要影响.因此,对慢性病毒性肝炎患者发生肝脂肪变性机制的深入研究将为制定更为合理、有效的治疗方案提供重要理论依据.     

慢性丙型病毒性肝炎与铁代谢异常

铁是机体内一种重要的金属成分,它参与红细胞中血红蛋白的合成、各种细胞内的氧化还原反应、细胞增殖等过程。铁代谢异常不仅可以引起缺铁性贫血或铁沉积症,而且还与循环系统疾病以及肝炎等消化系统疾病有关[1]。本文将从体内铁代谢的分子机制、慢性丙型肝炎与铁代谢异常、肝细胞内铁离     

Chronic hepatitis in childhood: the spectrum of the disease

During a multicentre study of chronic hepatitis in childhood diagnosed by biopsy, the spectrum of the disease has been evaluated in 196 consecutive patients, including 157 from Northern Italy and 39 from Southern Italy. Only 31% of patients in the former group and 27% in the latter were symptomatic when first seen: the majority of cases being seen after familial screenings for hepatitis B virus (HBV) markers or during intercurrent infections, thus suggesting that the frequency of chronic hepatitis in childhood might be largely underestimated in our area. In Southern and Northern Italy 83% of symptomatic and 95% of asymptomatic patients were hepatitis B surface antigen (HBsAg) positive in serum; only 15 (8.3%) of these children were born to mothers known to be HBsAg positive at delivery, but a high circulation of HBV was found in their families: in fact more than 65% of household contacts in Northern Italy and more than 90% in Southern Italy had serological evidence of past or ongoing HBV infection. These data indicate that, although familial screenings for HBV could have enhanced the percentage of HBsAg positive asymptomatic cases, chronic hepatitis in Italian children is mainly caused by HBV infection acquired in the familial setting through horizontal transmission. Such findings also emphasise the importance of mass vaccination of infants as the most effective means to prevent chronic type B hepatitis in childhood in our area. Among HBsAg positive children 55% had histological features of chronic active hepatitis and 85% were hepatitis Be antigen (HBeAg) positive in serum. Anti-HBe positive hepatitis was significantly more frequent in Southern than in Northern Italy in parallel with the significantly higher prevalence (17%) of hepatitis delta virus infection in that area. Of the 16 HBsAg negative cases included in the study three had autoimmune hepatitis, three Wilson's disease, one alpha1 antitrypsin deficiency, and nine had cryptogenic hepatitis, often associated to mild liver lesions resembling those seen in our adult patients with chronic non-A, non-B hepatitis unrelated to percutaneous exposure.     

Chronic viral hepatitis as a public health issue in the world

Given the substantial global burden attributable to HBV- and HCV-related chronic liver disease, the reduction of global mortality and morbidity related to chronic viral hepatitis, particularly in those areas of our globe where resources are scarce, should be a public health concern and a priority for action. Hepatitis B and C prevention and control should seek to reduce both the incidence of new infections and the risk of chronic liver disease. Based on our current knowledge and on our existing preventive and therapeutic arsenal, primary, secondary and tertiary prevention activities should be implemented and monitored in each country, with precise targets to be reached. The elimination of hepatitis B and reducing the burden of hepatitis C by 50% are achievable goals for the first half of this century. The development of a vaccine against hepatitis C is a major public health requirement.

• About one third of the world population has been infected with hepatitis B, and 350 million people are chronic carriers of the virus

• 130–170 million people are chronic carriers of the hepatitis C virus

• Chronic viral hepatitis induces chronic liver diseas, cirrhosis, liver cancer and causes a substantial burden to society globally

• The reduction of global mortality and morbidity related to chronic viral hepatitis through implementation of primary, secondary and tertiary prevention activities is a public health priority

• Efficient public health prevention programme should be established and their effectiveness should be assessed

• Set clear and time limited goals for national targets to be achieved in prevention, detection, immunisation and treatment of viral hepatitis

• Develop a vaccine for hepatitis C

• Eliminate hepatitis B

• Determine the incidence and prevalence of viral hepatitis at the national level

• Implement surveillance of new viral hepatitis infections and of chronic HBV- and HCV- related liver disease

• Develop better treatments for chronic viral hepatitis that are cost-effective, exhibit fewer side effects and are easier to implement and monitor

• Evaluate and improve prevention activities, including behaviour modification

Conflict of interest

No conflict of interest declared.     

Chronic viral hepatitis C. Part 1. General considerations

Hepatitis C virus was identified in 1989 as the main causative agent of non-A, non-B and was followed by the recognition of a high prevalence of hepatitis C virus infection after transfusion of infected blood or blood products and in association with intravenous drug abuse. The availability of sensitive and reliable techniques to screen blood for hepatitis C virus has reduced the incidence of post-transfusion hepatitis. True healthy carriers of hepatitis C virus did not exist. Approximately 95% of hepatitis C virus infected individuals can be identified by third generation anti-hepatitis C virus testing. Retrospective studies of iatrogenic hepatitis C virus infection are the main source of the natural history of the disease. The distribution of different hepatitis C virus genotypes varies according to the geographic region. In South America, Europe, The United States and Japan hepatitis C virus genotypes 1, 2 and 3 account for the majority of the infections, being (sub)type 1b the most prevalent. Epidemiological parameters (age, risk factors and duration of infection) may be associated with hepatitis C virus genotypes (intravenous drug abuse with types 1-a and 3-a and 1-b with post-transfusion hepatitic C). Subtype 1-b, lead to a more severe course of viral infection, with ultrastructural alterations of the mitochondria, and greater impairment of the process of oxidative phosphorylation. No increased production of free radicals may influence the evolution of the liver disease by an enhancement of the cytopathic effect of hepatitis C virus. The clinical significance of intrahepatic hepatitis C virus level in patients with chronic hepatitis C virus infection is not determined by host factors (age of patient, mode or duration of infection) or by virus factors (hepatitis C virus genotypes) and, repeatedly negative RT-PCR for hepatitis C virus RNA in serum does not indicate absence of hepatitis C virus from the liver. The association between autoimmunity and hepatitis C virus is questioned. Markers of its does occur with high frequency in these patients. Modulation of immune responses to hepatitis C virus envelope E2 protein following injection of plasmid DNA, has been used for induction of specific response to hepatitis C virus. The spectrum of such responses could likely be broadened by combining plasmids, delivery routes, and other forms of encoded immunogens (peptide vaccines). These may be important to the development of a vaccine against the high mutable hepatitis C virus. The pathogenic role of novel DNA virus (TTV) is under spotlight. As with hepatitis G, however, the association of TTV with disease is far from clear.     

Chronic viral hepatitis: liver biopsy, yes or no?

LB increases costs and has--although minimal--potential risks; however, LB is: a) the gold standard to get to know lesion severity (grade and stage); b) the only method for the diagnosis of an F3 stage, which progresses to liver cirrhosis in approximately 10 years; c) the only method for the certain diagnosis of compensated liver cirrhosis, which requires early diagnosis programs for oesophageal varices and hepatocarcinoma; and d) the only method for the certain diagnosis of lesions predicting a good therapeutic response. On all these grounds--save for exceptions (contraindications, clinical and/or ultrasonographic cirrhosis)--liver biopsy should be carried out in the initial study of all patients. In non-responders to anti-viral therapy liver biopsy should be repeated once or twice with 5-10-year intervals to ascertain fibrosis growth rate and, according to this, plan a most appropriate follow-up. Assuming hepatitis progresses rapidly in all HIV co-infected patients, anti-viral therapy could be administered with no previous LB; such biopsy would be performed in non-responders to decide their course of therapy.     

丙氨酸氨基转移酶持续正常的慢性丙型肝炎病毒感染的研究进展

丙型肝炎病毒(HCV)感染极易慢性化,研究表明,约有20％~30％的HCV慢性感染患者丙氨酸氨基转移酶(ALT)持续正常,临床症状缺失或非常轻微。所谓ALT持续性正常,即为在6个月内间断1个月以上复查3次,ALT均在正常范围以内。对于此类患者是否进行抗病毒治疗一直存在争议。现就ALT持续性正常HCV感染的自然病史、肝脏病理变化、病毒载量、     

Chronic liver disease after acute non-A, non-B viral hepatitis.

We have analyzed the frequency of chronicity and its distribution according to epidemiologic background following acute non-A, non-B hepatitis. Eighteen of 45 cases (40%) developed chronic liver disease. The incidence of chronicity was significantly higher following transfusion and among drug addicts (54% and 58%) than among patients without obvious source of infection (20%). Chronic active hepatitis developed in 4 of 13 patients (31%) with posttransfusion hepatitis. This lesion was not observed among the addicts or the patients without obvious source for the acute hepatitis.