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This publication contains information from a conference titled "Individual Perspectives on the Silent Epidemic of Viral Hepatitis in Hawai'i" held in October of 2007 with updates and additional contributions from annual conferences in 2008 and 2009. These conferences were sponsored by the Hepatitis Support Network of Hawai'i and held in Honolulu, Hawai'i at the Queen's Conference Center. The primary objectives of the conferences have been to heighten awareness of viral hepatitis in Hawai'i and to bring together health care professionals to learn about these infections and to help them respond to the challenges they bring to the people of Hawai'i. The initial conference was oriented to present the unique and individual perspectives of patients, physicians, and other healthcare providers specific to the complex issues of hepatitis in an effort to help them understand their role in the context of others and to develop a team approach in responding to this epidemic.

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BACKGROUND: Hepatic encephalopathy is a chronically debilitating complication of hepatic cirrhosis. The efficacy of rifaximin, a minimally absorbed antibiotic, is well documented in the treatment of acute hepatic encephalopathy, but its efficacy for prevention of the disease has not been established. METHODS: In this randomized, double-blind, placebo-controlled trial, we randomly assigned 299 patients who were in remission from recurrent hepatic encephalopathy resulting from chronic liver disease to receive either rifaximin, at a dose of 550 mg twice daily (140 patients), or placebo (159 patients) for 6 months. The primary efficacy end point was the time to the first breakthrough episode of hepatic encephalopathy. The key secondary end point was the time to the first hospitalization involving hepatic encephalopathy. RESULTS: Rifaximin significantly reduced the risk of an episode of hepatic encephalopathy, as compared with placebo, over a 6-month period (hazard ratio with rifaximin, 0.42; 95% confidence interval [CI], 0.28 to 0.64; P<0.001). A breakthrough episode of hepatic encephalopathy occurred in 22.1% of patients in the rifaximin group, as compared with 45.9% of patients in the placebo group. A total of 13.6% of the patients in the rifaximin group had a hospitalization involving hepatic encephalopathy, as compared with 22.6% of patients in the placebo group, for a hazard ratio of 0.50 (95% CI, 0.29 to 0.87; P=0.01). More than 90% of patients received concomitant lactulose therapy. The incidence of adverse events reported during the study was similar in the two groups, as was the incidence of serious adverse events. CONCLUSIONS: Over a 6-month period, treatment with rifaximin maintained remission from hepatic encephalopathy more effectively than did placebo. Rifaximin treatment also significantly reduced the risk of hospitalization involving hepatic encephalopathy. (ClinicalTrials.gov number, NCT00298038.)

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Recent studies suggest that consensus interferon and ribavirin is effective in retreating patients with chronic hepatitis C who failed therapy with interferon alfa and ribavirin. The objective of the present study was to assess the efficacy, safety, and tolerability of consensus interferon and ribavirin in patients who did not respond to pegylated interferon alfa-2b and ribavirin. We retrospectively identified 137 consecutive nonresponders to pegylated interferon alfa-2b and ribavirin and initiated patients on daily treatment with consensus interferon 15 mug subcutaneously and weight-based ribavirin for 48 weeks. If patients were HCV RNA negative at 12 weeks, the dose was reduced to 15 mug three times weekly for the remaining 36 weeks. The sustained virologic response rate was 37%. Daily consensus interferon therapy was safe and well tolerated in all patients. No dose reductions were required, and no patient discontinued therapy. Further studies of consensus interferon and ribavirin in nonresponders are warranted.

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We sought to compare frequency and duration of hepatic encephalopathy-related hospitalizations during rifaximin versus lactulose treatment. Hospitalizations, clinical efficacy data, and adverse events obtained from charts of 145 patients with hepatic encephalopathy who received lactulose (30 cc twice daily) for > or = 6 months and then rifaximin (400 mg 3 times a day) for > or = 6 months compared last 6 months on lactulose (lactulose period) to first 6 months on rifaximin (rifaximin period). Fewer hospitalizations (0.5 versus 1.6; P < .001), fewer days hospitalized (2.5 versus 7.3; P < .001), fewer total weeks hospitalized (0.4 versus 1.8; P < .001), and lower hospitalization charges per patient ($14,222 versus $56,635) were reported during the rifaximin period. More patients had asterixis, diarrhea, flatulence, and abdominal pain during the lactulose period (P < .001). Treatment of hepatic encephalopathy with rifaximin was associated with lower hospitalization frequency and duration, lower hospital charges, better clinical status, and fewer adverse events.

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Alcohol-induced liver injury is a reflection of the immunologic response of the liver to this stimulus. Reported studies of immunologic abnormalities in alcoholic liver disease (ALD) patients suggest that immunologic response plays a key role in the pathogenesis of chronic liver disease in alcoholics, and have contributed to the understanding of how some patients with ALD progress into alcoholic liver cirrhosis. The immunologic response of the liver is reflected in alcoholic fatty liver disease, hyaline necrosis, and cirrhosis, promoted by the role of neutrophils in damaging liver cells through cytotoxicity, and lymphocytes through cytotoxicity, inducing fibrogenesis of the liver and formation of immune complexes responsible for immune complex-mediated cytotoxicity, in addition to the role of different chemokines in attracting leucocytes, inducing fibrogenesis and liver cell apoptosis, with the established mechanism by which Mallory bodies evoke both cellular and humoral immunity contributing to the process of alcoholic liver cirrhosis, which plays a key role in transformation of alcoholic hepatitis to cirrhosis. At present, research is underway to find modalities to correct the induced immunologic changes, so at this time, it is necessary to avoid alcoholism, with the use of social and educational programs to stop alcoholism.

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Development of ethanol-induced fatty liver, alcoholic hepatitis, and cirrhosis has been attributed in part to nutritional deficiencies for many years. Special attention must be focused on treating alcohol-induced liver disease while providing replacement of deficient amino acids, vitamins, minerals, and other nutrients. Avoidance of alcohol intake is required to eliminate progressive liver disease in alcoholics. This is best achieved by using educational and social programs to convince patients and their caretakers of the great necessity to eliminate alcohol intake.

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