1,721,180 research outputs found

    Lack of hepatitis C transmission among institutionalized psychiatric patients

    No full text
    Prevalence studies have shown low rates of hepatitis C virus (HCV) infection in psychiatric inpatient population [1], [2] and [3]. A recent survey [4] in two psychiatric institutions in northern Italy has shown a 6.7% anti-HCV prevalence rate, which most likely reflects the relatively old median age (55 years) of the subjects studied. In fact there is evidence that anti-HCV prevalence in the Italian general population increases with age, suggesting a cohort effect, i.e. decreased risk of infection along generations as a consequence of improved sanitary and socio-economic conditions over time [5]. In the above-mentioned study [4] logistic regression analysis showed that length of hospitalization was not associated with the likelihood of HCV seropositivity, while a diagnosis of psychosis and a history of trauma both were independent predictors of infection. However, prevalence data, reflecting a cumulative incidence of infection over time, cannot establish exactly the temporal relationship between an exposure and the acquisition of infection. To our knowledge, no prospective study, the best tool to assess directly the risk of infection, has been so far performed on this subject. Therefore, we have conducted in one of these two previously studied institutions a prospective survey to evaluate the risk of acquiring HCV infection. Although the overall clinical features the inpatient population studied was the same, demographics were not exactly identical because three deaths and five new admissions occurred between the period of our study and that of the previous one. In 1993, 526 subjects (409 with mental retardation, 117 psychotic and three with dementia) were tested for anti-HCV by a commercially available ELISA (Ortho HCV II, Ortho Diagnostic Systems, Raritan, NJ, USA). Anti-HCV positivity was detected in 27 (5.1%) subjects; HCV RNA, examined by reverse transcription–polymerase chain reaction, was present in 24 (88.9%) of these subjects. The 499 anti-HCV negative subjects (133 females and 366 males) were followed up with anti-HCV test at yearly intervals. No subject seroconverted to anti-HCV during a mean follow-up of 7.4 years. Clearance of anti-HCV was observed in three subjects initially anti-HCV positive, but HCV RNA-negative. Our findings confirm and extend those of a previous survey [4] which reported low or absent risk of HCV in this setting despite violent behavior, with associated biting and scratching, poor sanitation and presence of not negligible proportion of HCV viremic subjects among the inmates of this institution

    Hepatocellular carcinoma in cirrhosis:incidence and risk factors

    No full text
    Emerging data indicate that the mortality rate of hepatocellular carcinoma (HCC) associated with cirrhosis is rising in some developed countries, whereas mortality from non- HCC complications of cirrhosis is decreasing or is stable. Cohort studies indicate that HCC is currently the major cause of liver-related death in patients with compensated cirrhosis. Hepatitis C virus (HCV) infection is associated with the highest HCC incidence in persons with cirrhosis, occurring twice as commonly in Japan than in the West (5-year cumulative incidence, 30% and 17%, respectively), followed by hereditary hemochromatosis (5-year cumulative incidence, 21%). In hepatitis B virus (HBV)-related cirrhosis, the 5-year cumulative HCC risk is 15% in high endemic areas and 10% in the West. In the absence of HCV and HBV infection, the HCC incidence is lower in alcoholic cirrhotics (5-year cumulative risk, 8%) and subjects with advanced biliary cirrhosis (5-year cumulative risk, 4%). There are limited data on HCC risk in cirrhosis of other causes. Older age, male sex, severity of compensated cirrhosis at presentation, and sustained activity of liver disease are important predictors of HCC, independent of etiology of cirrhosis. In viral-related cirrhosis, HBV/HCV and HBV/HDV coinfections increase the HCC risk (2- to 6-fold relative to each infection alone) as does alcohol abuse (2- to 4-fold relative to alcohol abstinence). Sustained reduction of HBV replication lowers the risk of HCC in HBV-related cirrhosis. Further studies are needed to investigate other viral factors (eg, HBV genotype/mutant, occult HBV, HIV coinfection) and preventable or treatable comorbidities (eg, obesity, diabetes) in the HCC risk in cirrhosis
    corecore