Faculty Bibliography

OBJECTIVE: The purpose of this study was to evaluate our preliminary experience using diffusion-weighted MRI for quantification of liver fibrosis. SUBJECTS AND METHODS: Diffusion-weighted MRI with single-shot echo-planar technique at b values of 50, 300, 500, 700, and 1,000 s/mm2 was prospectively performed on 23 patients with chronic hepatitis and on seven healthy volunteers. The apparent diffusion coefficient (ADC) was measured in four locations in the liver. Liver biopsy results (n = 19) were retrospectively reviewed by two hepatopathologists in consensus to determine stage of fibrosis and grade of inflammation. A Mann-Whitney test was used to compare the ADCs between patients classified with respect to having stage 2 or greater versus stage 1 or less fibrosis and stage 3 or greater versus stage or less 2 fibrosis. Receiver operating characteristics analysis was used to assess the performance of ADC in prediction of the presence of stage 2 or greater and stage 3 or greater fibrosis. RESULTS: Using a b value of 500 s/mm2 and all combined b values, we found significantly lower hepatic ADCs in stage 2 or greater versus stage 1 or less fibrosis and stage 3 or greater versus stage 2 or less fibrosis. The mean ADCs (x 10(-3) mm2/s) with all b values were 1.47 +/- 0.11 (SD) versus 1.65 +/- 0.10 for stage 2 or greater versus stage 1 or less fibrosis (p < 0.001) and 1.44 +/- 0.07 versus 1.66 +/- 0.10 for stage 3 or greater versus stage 2 or less fibrosis (p <0.001). Hepatic ADC was a significant predictor of stage 2 or greater and stage 3 or greater fibrosis, with areas under the curve of 0.896 and 0.896, sensitivity of 83.3% and 88.9%, and specificity of 83.3% and 80.0% (ADC with all b values, 1.54-1.53 x 10(-3) mm2/s or less). CONCLUSION: Diffusion-weighted MRI can be used for prediction of the presence of moderate and advanced liver fibrosis

Chronic hepatitis B (CHB) is an important public health problem worldwide and in the United States, with approximately 25% of patients infected as neonates dying prematurely from cirrhosis or liver cancer. A treatment algorithm for CHB previously developed and published by a panel of United States hepatologists was revised based on new developments in the understanding of CHB, the availability of more sensitive molecular diagnostic testing, the addition of new treatments, and better understanding of the advantages and disadvantages of approved therapies. This updated algorithm is based on available evidence using a systematic review of the scientific literature. Where data are lacking, the panel relied on clinical experience and consensus expert opinion. Serum HBV DNA can be detected at levels as low as 10 IU/mL using molecular assays and should be determined to establish a baseline level before treatment, monitor response to antiviral therapy, and survey for the development of drug resistance. The primary aim of antiviral therapy is durable suppression of serum HBV DNA to the lowest levels possible. The threshold level of HBV DNA for determination of candidacy for therapy is 20,000 IU/mL or more for patients with hepatitis B e antigen-positive CHB. A lower serum HBV DNA threshold of 2000 IU/mL or more is recommended for patients with hepatitis B e antigen-negative CHB, and 200 IU/mL or more for those with decompensated cirrhosis. Interferon alfa-2b, lamivudine, adefovir, entecavir, and peginterferon alfa-2a all are approved as initial therapy for CHB and have certain advantages and disadvantages. Issues for consideration include efficacy, safety, incidence of resistance, method of administration, and cost