OBJECTIVE:To determine the level of a single transverse scan of intra-abdominal fat between L1 and L5 vertebrae that best predicts intra-abdominal fat volumes. SUBJECTS: Sixteen male and seven female patients with non-insulin-dependent diabetes mellitus, aged 44±74 y. OUTCOME MEASURES: Volumes and areas from single scans of intra-abdominal fat measured by magnetic resonance imaging with a 1.5 Tesla magnetic ®eld strength. RESULTS: Intra-abdominal fat volumes and masses were calculated from fat areas from eight cross-sectional transverse single scans (nine scans in eight men) of 20 mm thickness. Men and women, respectively, had mean body mass index (BMI) of 27.9 (s.d. 3.0) and 31.6 (s.d. 4.7) kgam 2 , and intra-abdominal fat of 2.3 (s.d. 0.5) and 2.5 (s.d. 0.6) kg. Intra-abdominal fat area of the fourth scan (in the direction of L1 to L5) gave the highest prediction of total intra-abdominal fat both in men (r 0.959, P`0.001) and in women (r 0.973, P`0.001). The intra-abdominal fat area of the third scan gave almost as good a prediction. These third and fourth scans corresponded to L2 and L3 vertebrae. The intra-abdominal fat areas from the sixth and seventh scans, corresponded to the frequently used L4±L5 and had lower correlations with intra-abdominal fat. There were no gender differences in the prediction of volumes from areas of intra-abdominal fat. Intra-abdominal fat areas of the fourth scan explained 93% of variance (SEE 0.14 kg) of total intra-abdominal fat for both genders: intra-abdominal fat (kg) 0.0108 6 intra-abdominal fat area of the fourth scan (cm 2 ) 0.244. CONCLUSIONS: In large studies of intra-abdominal fat, using magnetic resonance imaging (MRI) or computerised tomography scanning, a single intra-abdominal fat area at the intervertebral disc between L2 and L3 vertebrae offers a cheaper, faster and safer method, with high prediction of total intra-abdominal fat volumes and masses.

Fibrosing cholestatic hepatitis (FCH) is a severe clinical and histological variant of hepatitis B virus (HBV) infection seen most commonly in the HBV infected allograft after liver transplantation. Without treatment, FCH is fatal, rapidly and universally. Remission has been reported with lamivudine but is associated with evolving resistance to lamivudine. Adefovir dipivoxil has recently been reported to be a potent and highly eVective inhibitor of HBV replication in both wild-type and lamivudine resistant HBV infection. We report a case of FCH 15 months after liver transplantation for HBV related cirrhosis despite therapy with lamivudine and hepatitis B immunoglobulin (HBIg). Within two weeks of commencing treatment with adefovir dipivoxil 10 mg once daily, the patient had made a remarkable recovery with resolution of jaundice and normalisation of liver biochemistry. HBV DNA and hepatitis B e antigen were lost from serum subsequently and liver histology had improved at four months. This case report suggests firstly, that advanced FCH can be reversed and secondly, that addition of adefovir dipivoxil to lamivudine and HBIg may be an eVective antiviral strategy. (Gut 2001;49:436-440)

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Many recent and significant advances in the field of chronic viral hepatitis, including therapy, suggest that an update on chronic hepatitis is timely.Chronic hepatitis B virus infection remains a significant worldwide cause of liver cirrhosis and hepatocellular carcinoma, despite the wide availability of a long established and eVective vaccine. Transmission occurs via perinatal, sexual, and parenteral routes (particularly intravenous drug abuse and although blood products still carry a risk, this is now extremely low in Western countries). Only a minority of infected adult cases develop chronic hepatitis but in children under 1 year, 90% develop chronic hepatitis. The clinical spectrum of chronic liver injury ranges from mild inflammation to end stage liver cirrhosis. Interferon alfa has been the mainstay of treatment for patients with active disease but nucleoside analogues (lamivudine and adefovir) are now available with similar eYcacy. Patients with end stage liver disease and hepatocellular carcinoma can be oVered transplantation but infection in the graft is commonplace. The combination of hepatitis B immunoglobulin and newer antiviral drugs reduce the incidence and severity of graft infection significantly.The hepatitis C virus epidemic of the latter half of the 20th century now aVects more than 1% of populations worldwide. This RNA virus is spread parenterally and is becoming the leading indication for liver transplantation. The majority of patients develop chronic hepatitis, which may be progressive, evolving to significant liver disease (cirrhosis or hepatocellular carcinoma) in about 20% cases after decades. Treatment with the combination of interferon alfa and ribavirin is successful in up to 40% cases. Liver transplantation is a therapeutic option for some but graft infection is universal and often complicated by progressive liver fibrosis. A vaccine remains a remote prospect so that prevention is crucial.Hepatitis D virus infection occurs on a background of hepatitis B virus infection and can also cause liver damage. The response to antiviral therapy is poor.The newer "hepatitis" viruses G and TT do not cause significant liver injury. (Postgrad Med J 2001;77:498-505) Keywords: hepatitis A number of viruses are known to cause chronic hepatitis. These include hepatitis B and D viruses identified in the 1960s and 1970s respectively and hepatitis C virus isolated in 1989. More recently, newer "hepatitis" viruses such as hepatitis G and TTV have been described, although their role in chronic hepatitis is in doubt. Hepatitis A virus does not cause chronic infection. Hepatitis B virusEPIDEMIOLOGY Chronic hepatitis B virus (HBV) infection accounts for 5%-10% of cases of chronic liver disease and cirrhosis in the United States.1 It aVects 350 million people worldwide. The major modes of transmission of HBV are perinatal, sexual (via semen and vaginal secretions), via blood products, and via contaminated needles in intravenous drug addicts. A recent US study found that the prevalence of HBV infect...

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SUMMARYBoth hepatitis B and hepatitis C are spread parenterally. Chronic hepatitis C is fast becoming the leading indication for liver transplantation. Most infected patients go on to develop chronic hepatitis, with approximately 20% developing liver cirrhosis or hepatocellular carcinoma after 20 years. Standard treatment now is with a combination of alpha‐interferon and ribavirin, which is successful in up to 40% of patients. A vaccine is still a remote possibility and prevention remains all‐important. Despite having a successful vaccine, chronic hepatitis B remains an important cause of liver cirrhosis and hepatocellular carcinoma. Treatments for active hepatitis include alpha‐interferon and the newer nucleoside analogues such as lamivudine and adefovir. In patients undergoing liver transplantation, recurrence of hepatitis B in the graft can be reduced with a combination of hepatitis B immunoglobulin and these nucleoside analogues.

Aims/Buckground: Response rates to alpha-interferon therapy for chronic hepatitis C are poor. An early indication of efficacy would reduce the need for prolonged therapy, leading to significant cost savings. It was established that a change in quantitative hepatitis C virus RNA (HCV-RNA) titre at 4 weeks could predict the outcome of alpha-interferon therapy in chronic hepatitis C. Methods: Serum HCV-RNA titres were quantified using branched chain DNA (bDNA) assay in 26 patients who responded to alpha-interferon (serum HCV-RNA negative after 12 weeks therapy) and 11 age and sex matched non-responders. Quantitative bDNA and qualitative RT-PCR assays for HCV-RNA were measured pretreatment and at 4 weeks. The change in quantitative HCV-RNA titre between pre-therapy and after 4 weeks was compared in the two groups. Results: Seventeen of the 37 patients had become RT-PCR negative at 4 weeks (early responders) and had an undetectable HCV-RNA titre on bDNA assay. Nine patients were RT-PCR positive at 4 weeks but negative by 12 weeks (delayed responders), and of these, 8 had an undetectable viral titre at 4 weeks on bDNA assay. The patient with a detectable HCV titre did become RT-PCR negative after 12 weeks, but subsequently became RT-PCR positive again at 24 weeks. All the non-responders had a detectable bDNA titre (>0.2 Meq/ml) at 4 weeks. Conclusions: Change in quantitative HCV-RNA titre measured by bDNA assay at 4 weeks predicts response to alpha interferon. If HCV-RNA remains detectable on bDNA assay at 4 weeks, no sustained response to treatment is found and 1 alpha-interferon can be discontinued.to