Chronic liver disease in Peru: Role of viral hepatitis

Barham, William B.; Figueroa, Roig; Phillips, Irving A.; Hyams, Kenneth C.

doi:10.1002/jmv.1890420206

Cited by 12 publications

(6 citation statements)

References 26 publications

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“…We found an anti-HCV-positivity prevalence of 39% in cirrhotics and 5% in hospital controls without significant differences between the examined areas. Although these figures are positioned within the range of prevalences reported in the literature (11%-73% in cirrhotics [45][46][47][48][49][50][51][52][53][54] and 0.8%-11% in hospital controls [46][47][48]54,55 ), we cannot exclude an overestimated prevalence because of the use of frozen sera. 56 However, under the assumption that the probability of false positive results is independent of alcohol consumption, this potential bias should not have affected the validity of the results on the joint effect of alcohol and HCV positivity.…”

Section: Discussionmentioning

confidence: 47%

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Corrao¹,

Aricò²

1998

European Journal of Gastroenterology & Hepatology

100

119

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Although alcohol intake and hepatitis C virus (HCV) infection are the major determinants of liver cirrhosis (LC)in Western countries, the joint effect of these two factors on LC risk has not yet been adequately studied. We used data from two hospital-based case-control studies performed in Italy. Cases were 285 cirrhotic patients admitted for the first time to district hospitals for liver decompensation. Controls were 417 patients admitted during the same period, and in the same hospitals as the cases, for acute diseases unrelated to alcohol. Alcohol consumption was expressed as lifetime daily alcohol intake (LDAI). Serum HCV antibodies (anti-HCV) were detected using a secondgeneration test and recombinant immunoblotting assay. We found a dose-effect relationship between LDAI and the risk of LC in both anti-HCV-negative and -positive subjects. Considering the extreme LDAI categories (LDAI ‫؍‬ 0 g, lifetime teetotalers, and LDAI ‫؍‬ 175 g), the LC odds ratios increased from 1.0 (reference category) to 15.0 (95% CI, 7.1-31.7) and from 9.2 (95% CI, 2.0-43.2) to 147.2 (95% CI, 42.1-514.3) in anti-HCV-negative and -positive patients respectively. The interaction between LDAI and HCV showed an additive structure for LDAI F50 g/day and a multiplicative structure for consumption G125 g/day. Alcohol intake and HCV infection are independent risk factors for symptomatic liver cirrhosis, each being sufficient to induce the disease. In subjects with high alcohol intake, the coexistence of HCV infection multiplies the alcohol-associated risk of cirrhosis. In subjects with low alcohol intake, other factors could be involved. (HEPATOLOGY 1998;27:914-919.)Alcohol intake represents the main determinant of liver cirrhosis in Italy 1,2 and other Western countries. 3 Evidence in this respect has been given by ecological, 3-5 prevalence, 6-9 case-control, 10-15 and cohort 16,17 studies. However, several observations suggest that other factors should interact with alcohol consumption in causing liver damage. [18][19][20] In alcoholics, liver histology is normal in 5% to 25% of biopsies and 18% of autopsy findings, 21 and cirrhosis develops at a low yearly incidence rate of around 2%. 16 Thus, only 10% to 25% of alcoholics will suffer from cirrhosis during their life. 22 Among these interacting factors, the role of chronic infection with hepatitis B virus is still debated. [23][24][25][26] Similarly, despite the initial suggestion that chronic infection with hepatitis C virus (HCV) may multiplicatively interact with alcohol intake in determining cirrhosis, 27 recent evidence suggests that these two factors act independently. 28 The aim of the present study was to assess, using a case-control design, the risk of developing liver cirrhosis associated with alcohol intake, HCV infection, and the combined action of these factors. PATIENTS AND METHODS Selection of Cases and Controls.We used the data from two hospitalbased case-control studies performed with the same design in two different periods and in two different Italian areas.The design...

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Section: Discussionmentioning

confidence: 47%

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Corrao¹,

Aricò²

1998

European Journal of Gastroenterology & Hepatology

100

119

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show abstract

“…Although these figures are positioned within the range of prevalences reported in the literature (11%-73% in cirrhotics [45][46][47][48][49][50][51][52][53][54] and 0.8%-11% in hospital controls [46][47][48]54,55 ), we cannot exclude an overestimated prevalence because of the use of frozen sera. 56 However, under the assumption that the probability of false positive results is independent of alcohol consumption, this potential bias should not have affected the validity of the results on the joint effect of alcohol and HCV positivity.…”

Section: Discussionmentioning

confidence: 47%

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Corrao

Aricò²

1998

Hepatology

302

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Although alcohol intake and hepatitis C virus (HCV) infection are the major determinants of liver cirrhosis (LC) in Western countries, the joint effect of these two factors on LC risk has not yet been adequately studied. We used data from two hospital-based case-control studies performed in Italy. Cases were 285 cirrhotic patients admitted for the first time to district hospitals for liver decompensation. Controls were 417 patients admitted during the same period, and in the same hospitals as the cases, for acute diseases unrelated to alcohol. Alcohol consumption was expressed as lifetime daily alcohol intake (LDAI). Serum HCV antibodies (anti-HCV) were detected using a secondgeneration test and recombinant immunoblotting assay. We found a dose-effect relationship between LDAI and the risk of LC in both anti-HCV-negative and -positive subjects. Considering the extreme LDAI categories (LDAI ‫؍‬ 0 g, lifetime teetotalers, and LDAI ‫؍‬ 175 g), the LC odds ratios increased from 1.0 (reference category) to 15.0 (95% CI, 7.1-31.7) and from 9.2 (95% CI, 2.0-43.2) to 147.2 (95% CI, 42.1-514.3) in anti-HCV-negative and -positive patients respectively. The interaction between LDAI and HCV showed an additive structure for LDAI F50 g/day and a multiplicative structure for consumption G125 g/day. Alcohol intake and HCV infection are independent risk factors for symptomatic liver cirrhosis, each being sufficient to induce the disease. In subjects with high alcohol intake, the coexistence of HCV infection multiplies the alcohol-associated risk of cirrhosis. In subjects with low alcohol intake, other factors could be involved. (HEPATOLOGY 1998;27:914-919.)Alcohol intake represents the main determinant of liver cirrhosis in Italy 1,2 and other Western countries. 3 Evidence in this respect has been given by ecological, 3-5 prevalence, 6-9 case-control, 10-15 and cohort 16,17 studies. However, several observations suggest that other factors should interact with alcohol consumption in causing liver damage. [18][19][20] In alcoholics, liver histology is normal in 5% to 25% of biopsies and 18% of autopsy findings, 21 and cirrhosis develops at a low yearly incidence rate of around 2%. 16 Thus, only 10% to 25% of alcoholics will suffer from cirrhosis during their life. 22 Among these interacting factors, the role of chronic infection with hepatitis B virus is still debated. [23][24][25][26] Similarly, despite the initial suggestion that chronic infection with hepatitis C virus (HCV) may multiplicatively interact with alcohol intake in determining cirrhosis, 27 recent evidence suggests that these two factors act independently. 28 The aim of the present study was to assess, using a case-control design, the risk of developing liver cirrhosis associated with alcohol intake, HCV infection, and the combined action of these factors. PATIENTS AND METHODS Selection of Cases and Controls.We used the data from two hospitalbased case-control studies performed with the same design in two different periods and in two different Italian areas.The desi...

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“…In the healthcare setting, patients may serve as a reservoir for transmission, and the prevalence among patients in hospital-related (inpatient and outpatient) settings has been reported to range from 2 to 18% [96][97][98][99] and in chronic hemodialysis settings to average 20%. 82 The few reported episodes of HCV transmission from patient to patient in hospital-related settings have mostly involved unsafe injection practices resulting in contamination of equipment used for phlebotomy or flushing intravenous lines or of multiple dose medication vials.…”

Section: Unsafe Injections and Other Healthcare-related Proceduresmentioning

confidence: 99%

Epidemiology of Hepatitis C: Geographic Differences and Temporal Trends

Wasley

Alter²

2000

Semin Liver Dis

865

611

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Hepatitis C Virus (HCV) infection appears to be endemic in most parts of the world, with an estimated overall prevalence of 3%. However, there is considerable geographic and temporal variation in the incidence and prevalence of HCV infection. Using age-specific prevalence data, at least three distinct transmission patterns can be identified. In countries with the first pattern (e.g., United States, Australia), most infections are found among persons 30-49 years old, indicating that the risk for HCV infection was greatest in the relatively recent past (10-30 years ago) and primarily affected young adults. In countries with the second pattern (e.g., Japan, Italy), most infections are found among older persons, consistent with the risk for HCV infection having been greatest in the distant past. In countries with the third pattern (e.g., Egypt), high rates of infection are observed in all age groups, indicating an ongoing high risk for acquiring HCV infection. In countries with the first pattern, injection drug use has been the predominant risk factor for HCV infection, whereas in those with the second or third patterns, unsafe injections and contaminated equipment used in healthcare-related procedures appear to have played a predominant role in transmission. Much of the variability between regions can be explained by the frequency and extent to which different risk factors have contributed to the transmission of HCV. Because different strategies are required to interrupt different patterns of HCV transmission, determining the epidemiology of HCV infection in areas where that information has not yet been assessed is critical for developing appropriate prevention programs.

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Chronic liver disease in Peru: Role of viral hepatitis

Cited by 12 publications

References 26 publications

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Epidemiology of Hepatitis C: Geographic Differences and Temporal Trends

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