Notified viral hepatitis in Auckland

One hundred and forty-nine patients notified in Auckland health district as suffering from hepatitis A or B during the period July 1978-June 1979 were investigated by health inspectors. The results were analysed by age, sex, ethnic group, potential source of infection and immunoglobulin prophylaxis of the contacts, and have increased the understanding of the epidemiology of these types of viral hepatitis in Auckland.     

Fulminant viral hepatitis

In the United Kingdom and United States of America, fulminant viral hepatitis is due mainly to sporadic (non-parenteral) non-A, non-B hepatitis and hepatitis B whereas that caused by hepatitis A virus is very uncommon and by the herpes viruses remains rare. Recent advances in fulminant non-A, non-B hepatitis have come with the identification and cloning of a virus (27-34 nm) in the enteral variety (hepatitis E) which is prevalent in the Indian sub-continent, North Africa and elsewhere, especially in pregnant women. Virus-like particles (50-70 nm) with ultrastructural features similar to the togaviridae and flaviviridae have been identified in some patients with fulminant non-A, non-B hepatitis in the United Kingdom. The relation to hepatitis C virus, recently identified as a major cause of chronic post-transfusion (parenteral) non-A, non-B hepatitis, awaits serological analysis. The recent demonstration that persistence of active viral replication can occur in some cases of fulminant hepatitis types A and B using monoclonal antibody and molecular biology techniques challenges the classical views on the pathogenesis of these varieties of fulminant viral hepatitis.     

复方卡尼汀治疗慢性病毒性肝炎

目的 :评估复方卡尼汀治疗慢性病毒性肝炎的作用。方法 :91例慢性病毒性肝炎病人分为 2组。对照组 30例 (男性 2 0例 ,女性 10例 ,年龄 4 1a±s 17a) ,给予甘草酸单铵 80mL加入 10 %葡萄糖注射液 50 0mL中iv ,gtt ,qd ,疗程 30d。治疗组61例 (男性 4 9例 ,女性 12例 ,年龄 4 0a± 13a) ,在甘草酸单铵治疗基础上 ,给予复方卡尼汀 2支加入10 %葡萄糖注射液 50 0mL中iv ,gtt ,qd ,疗程 30d。结果 :治疗组对改善病人乏力、纳差、降低ALT的总有效率分别为 93% ,10 0 % ,92 % ,均明显优于对照组 75% ,84 % ,70 % (P <0 .0 5)。对 2组部分病人治疗 6mo时的随访表明治疗组的ALT复常率为83% ,明显高于对照组 54% (P <0 .0 5) ,无明显不良反应。结论 :复方卡尼汀是一种有效的治疗慢性病毒性肝炎的药物     

Notified viral hepatitis in New Zealand

23 760 cases of hepatitis A and 1042 cases of hepatitis B notified in New Zealand between 1971-1978 were analysed by health district, age and sex. There appear to be important regional differences, and statistics will be incomplete until specific hepatitis B tests are performed in all cases of viral hepatitis, and all cases are notified.     

Treatment of viral hepatitis in pregnancy

Viral hepatitis can be caused by the hepatitis A, B, C, D and E viruses. In the Western world, hepatitis A, B or C do not seem to influence the course of pregnancy, whereas hepatitis E infection, when contracted during the second or third trimester, seems to have a higher risk of developing into a fulminant hepatitis. Mother-to-infant transmission of hepatitis A seems to be very uncommon. The majority of HBsAg-positive and HBeAg-positive mothers can transmit the disease vertically. The timing of transmission is predominantly peripartum, and newborns of HBsAg-positive mothers should receive hepatitis B immunoglobulins within 12 h of birth, with HBV vaccine at birth and 1 and 6 months later. Hepatitis C is more often a chronic disease. Vertical transmission of hepatitis C is considered to be relatively rare but high viraemia or coinfection with HIV can increase this risk. There is currently no treatment to prevent this vertical transmission and pregnancies among HCV-positive mothers should not be discouraged. Infants should be tested for anti-HCV at 1 year and followed for the development of hepatitis. Breast feeding does not seem to play an important role in the transmission of hepatitis B and C.     

Liver transplantation for viral hepatitis

Current one year survival rates of 73-83% for elective transplantation, and 55-70% for emergency transplantation, render liver transplantation an appropriate treatment for both end-stage chronic liver disease and acute liver failure. Candidates for transplantation for acute liver failure need to be identified as early as possible, and a model for selection using clinical criteria is described. Recurrent viral infection after transplantation is either a possible or proven problem in all patient subgroups, but the clearest manifestation is in patients with chronic hepatitis B infection. In our series of 29 patients surviving at least 60 days after transplantation, 41% died as a consequence of recurrent infection at 3-13 months. Delta virus infection appears to confer some protection in this regard, and the role of long-term immunoprophylaxis in preventing this serious complication remains to be established.     

The ABC of viral hepatitis

Viral hepatitis has long been under-diagnosed. Hepatitis A is an acute disease, while patients infected by hepatitis B and hepatitis C viruses are likely to develop chronical infections and severe complications (cancer, cirrhosis). The current treatment of hepatitis B and C consists in alpha interferon (preferably under its pegylated form), in combination with ribavirin for hepatitis C. The frequent and severe adverse effects of interferon-based therapy constitute, however, a major limiting factor (reactions at the injection site, flu-like syndrome, neurological disorders, ...). For hepatitis B, two alternatives are available so far, namely lamivudine and adefovir (used as a prodrug with highe oral bioavailability).     

Genetic susceptibility in chronic viral hepatitis.

Infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) may result in a number of different clinical outcomes. There is strong evidence in HBV infection that host genetic factors play a major role in determining the outcome of infection. A number of approaches may be used to determine the specific genetic factors involved but the principal method which has been used to date is the disease association study. Disease association studies have a number of drawbacks but trials with well-constructed designs and large numbers of cases have recently produced compelling and reproducible results. In particular alleles in the MHC class II loci and interleukin 10 promoter have been demonstrated to influence the outcome of these infections.     

Treatment of viral hepatitis B in children

Importance of the field: Treatment of chronic hepatitis B (CHB) in children is aimed at reducing viral replication and at minimizing liver injury and related consequences in children with chronic active viral liver infection.

Areas covered in this review: In this review, treatment options available for both adults and children are summarized, together with suggestions from our own experience. The most relevant works published between 1982 and 2009 on PubMed/Medline database search were used.

What the reader will gain: At present, standardized treatment is available in only a few therapeutic options, such as IFN-α and lamivudine; it is hoped that these will be complemented in the future by new, encouraging drugs still under study in pediatric age patients. Moreover, current treatment approaches have their limitations: although IFN-α has been shown to be effective in patients with non-vertically-transmitted infection, HBeAg clearance while on treatment is similar to spontaneous seroconversion after long-term follow-up. IFN-α-induced side effects are frequent rarely severe in children. Lamivudine achieves similar results in children with active viral replication. However, despite good compliance to oral administration, this treatment can lead to the development of drug-resistant mutations.

Take home message: In conclusion, the decision to treat CHB in children demands that the possibility of favorable spontaneous viral clearance has been considered and must be made on the bases of the extent of liver damage.     

Notified viral hepatitis in New Zealand.

Statistical analysis of notified cases of viral hepatits in New Zealand for an 18-month period is used first to demonstrate and then to consider a geographical gradient across the country with implications warranting further epidemiologic enquiry.     

Cyclophilin inhibitors in hepatitis C viral infection

Cyclophilins (Cyps) are proteins that are ubiquitously present with peptidyl-prolyl cis-trans isomerase activity and play an important role in de novo protein folding and in isomerization of native proteins in several cellular systems. There is growing evidence that indicates CypB is a positive modulator of the HCV RNA-dependent RNA polymerase in the replication complex. Early in vitro and animal data with selective Cyp inhibitors show a potent anti-HCV effect. This anti-HCV effect was confirmed in the first patient study with the selective Cyp inhibitor Debio-025. Preclinical data suggest that Cyp inhibitors may present a higher barrier to the selection of resistance than protease and polymerase inhibitors and that a combination of Cyp inhibitors with either of these drugs or interferon results in additive or synergistic anti-HCV activity. By interfering at the level of host-viral interaction, Cyp inhibition may open the way for a novel approach to anti-HCV treatment that could be complementary, not only to interferon-based treatment, but also to future treatments that directly target HCV replication enzymes such as protease and polymerase inhibitors.     

Cyclophilin inhibitors in hepatitis C viral infection

Cyclophilins (Cyps) are proteins that are ubiquitously present with peptidyl-prolyl cis-trans isomerase activity and play an important role in de novo protein folding and in isomerization of native proteins in several cellular systems. There is growing evidence that indicates CypB is a positive modulator of the HCV RNA-dependent RNA polymerase in the replication complex. Early in vitro and animal data with selective Cyp inhibitors show a potent anti-HCV effect. This anti-HCV effect was confirmed in the first patient study with the selective Cyp inhibitor Debio-025. Preclinical data suggest that Cyp inhibitors may present a higher barrier to the selection of resistance than protease and polymerase inhibitors and that a combination of Cyp inhibitors with either of these drugs or interferon results in additive or synergistic anti-HCV activity. By interfering at the level of host–viral interaction, Cyp inhibition may open the way for a novel approach to anti-HCV treatment that could be complementary, not only to interferon-based treatment, but also to future treatments that directly target HCV replication enzymes such as protease and polymerase inhibitors.