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No inflammation? No cancer! Clear HBV early and live happily.
Full text linkCOMMENTARY ON: Clearance of Hepatitis B Surface Antigen and Risk of Hepatocellular Carcinoma in a cohort Chronically Infected with Hepatitis B Virus. Simonetti J, Bulkow L, McMahon BJ, Homan C, Snowball M, Negus S, Williams J, Livingston SE. Hepatology. 2009 Nov 30. [Epub ahead of print]. Copyright 2009. Reprinted with permission of John Wiley and Sons, Inc. Abstract: Some individuals who are chronically infected with hepatitis B virus (HBV) eventually lose hepatitis B surface antigen (HBsAg). Hepatocellular carcinoma (HCC) has been demonstrated to occur in a few patients after loss of HBsAg. Neither factors associated with loss of HBsAg nor the incidence of HCC thereafter have been clearly elucidated. We performed a prospective population-based cohort study in 1271 Alaska native persons with chronic HBV infection followed for an average of 19.6 years to determine factors associated with loss of HBsAg and risk of developing HCC thereafter. HBsAg loss occurred in 158 persons for a rate of HBsAg clearance of 0.7%/year. Older age, but not sex, was associated with clearance of HBsAg, and loss of HBsAg was not associated with any particular HBV genotypes (A-D, and F) found in this population. Participants were followed for an average of 108.9 months after HBsAg loss. Six patients, two with cirrhosis and four without, developed HCC a mean of 7.3 years after HBsAg clearance (range, 2.0-15.5 years). The incidence of HCC after clearance of HBsAg was 36.8 per 100,000 per year (95% CI 13.5-80.0) which was significantly lower than the rate in those who remained HBsAg-positive (195.7 cases per 100,000 person-years of follow-up [95% CI 141.1-264.5; P<0.001). After loss of HBsAg, HBV DNA was detected in the sera of 28 (18%) of those who cleared a median of 3.6 years after clearance. Conclusion: HCC can occur in persons with chronic hepatitis B who have lost HBsAg, even in the absence of cirrhosis. These persons should still be followed with periodic liver ultrasound to detect HCC earl
TERAPIA CON INTERFERON LINFOBLASTOIDE IN PAZIENTI CON EPATITE CRONICA DA HBV E POSITIVITA' SIERICA PER ANTI-HBe
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Natural history of chronic hepatitis B: special emphasis on disease progression and prognostic factors.
No full textThe natural history of chronic hepatitis B virus (HBV) infection and disease is complex and highly variable. We review
the natural history of chronic hepatitis B with emphasis on the rates of disease progression and factors influencing the
course of the liver disease. Chronic hepatitis B is characterized by an early replicative phase (HBeAg positive chronic hepatitis)
and a late low or non-replication phase with HBeAg seroconversion and liver disease remission (inactive carrier
state). Most patients become inactive carriers after spontaneous HBeAg seroconversion with good prognosis, but progression
to HBeAg negative chronic hepatitis due to HBV variants not expressing HBeAg occurs at a rate of 1–3 per 100 person
years following HBeAg seroconversion. The incidence of cirrhosis appears to be about 2-fold higher in HBeAg negative
compared to HBeAg positive chronic hepatitis. In the cirrhotic patient the 5-year cumulative risk of developing hepatocellular
carcinoma is 17% in East Asia and 10% in the Western Europe and the United States and the 5-year liver related
death rate is 15% in Europe and 14% in East Asia. There is a growing understanding of viral, host and environmental
factors influencing disease progression, which ultimately could improve the management of chronic hepatitis B
SOLUBLE INTERLEUKIN-2 RECEPTORS IN VIRAL HEPATITIS AND THE EFFECT OF ALFA-INTERFERON THERAPY
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Progression to cirrhosis, hepatocellular carcinoma and liver-related mortality in chronic hepatitis B patients in Italy.
No full textBACKGROUND: The natural history of chronic hepatitis B is variable. We evaluated some of the risk factors for cirrhosis, hepatocellular carcinoma and liver-related mortality in Italian patients with chronic hepatitis B.
METHODS: A cohort of 105 untreated patients with chronic hepatitis B without cirrhosis at diagnosis was followed prospectively for a mean period of 23 years.
Clinical, histological and ultrasound examinations, biochemical and virologicaltests, and causes of death were analyzed.
RESULTS: Forty-two (40%) patients became inactive carriers and 63 (60%) showed
persistent alanine aminotransferase elevation: 13 (13%) associated with HBeAg
persistence, 35 (33%) with detectable serum HBV-DNA but HBeAg-negative, 11 (10%)
with concurrent virus infection and 4 (4%) with non-alcoholic fatty liver disease. Cirrhosis incidence was 1.56/100 person-years. Older age and sustained HBV replication predicted cirrhosis occurrence independently. Hepatocellular
carcinoma incidence was 2.1/100 person-years in patients who developed cirrhosis and 0.06 in those who did not. Cirrhosis occurrence was associated with an increased risk of hepatocellular carcinoma (hazard ratio 20.4, 95% confidence
interval 2.54-167.5) and liver-related death (16.5, 2.0-138.8).
CONCLUSIONS: In Italian patients with chronic hepatitis B cirrhosis strongly predicts hepatocellular carcinoma occurrence and disease-related mortality, thus indicating that early antiviral treatment should be instituted before cirrhosis
occurrence
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