Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0239946 (liver fibrosis)
 8,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in 78 Italian patients with hereditary hemochromatosis as well as the relation between HCV antibody (anti-HCV) status, hepatitis B surface antigen (HBsAg) and liver histology. None of the patients had been transfused or ever consumed more than 60 g of alcohol per day. Eighteen showed histological signs of chronic hepatitis, active cirrhosis was present in 12, chronic active hepatitis in 4 and chronic persistent hepatitis in 2. Liver fibrosis or cirrhosis without inflammatory activity was observed in 31 subjects, whereas liver histology was normal except for iron overload in 18. The prevalence of HBsAg in the whole series was 5% and of anti-HCV was 20.5%. The prevalence of HBsAg and anti-HCV was significantly higher in the chronic hepatitis group than in the fibrosis/cirrhosis (p = 0.01) and the normal groups (p < 0.01). Fourteen of 18 hereditary hemochromatosis patients with chronic hepatitis were HBsAg (4) or anti-HCV (10) positive and all the latter subgroup had HCV-RNA in their serum as shown by the polymerase chain reaction. Although most of the patients with associated chronic hepatitis had cirrhosis, their serum ferritin levels and amount of mobilizable iron were significantly lower than those of the fibrosis/cirrhosis group (p < 0.01). This indicates that hepatitis viral infection acts synergistically with iron in accelerating the development of liver damage.
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PMID:Liver damage in Italian patients with hereditary hemochromatosis is highly influenced by hepatitis B and C virus infection. 148 15

Serum levels of several markers for liver fibrosis were measured utilizing three groups of human subjects related with schistosomiasis mansoni in northeast Brazil; (1) 20 Schistosoma mansoni egg-positives, who have never been administered with anti-schistosomal drugs, (2) 29 egg-negative inhabitants in the endemic area of schistosomiasis, and (3) 23 egg-negative Japanese immigrants in the non-endemic area. None of these sera were positive for antibody to the surface antigen of human hepatitis B (HBs) and circulating HBs antigen. There was no significant difference in the serum levels of N-terminal peptide of procollagen type-III between the egg-positive subjects and either of the egg-negative Brazilian or Japanese immigrants, whereas the mean value of serum laminin significantly increased in the egg-positive subjects. A significantly higher concentration of serum immunoreactive beta-subunit of prolyl 4-hydroxylase (IR beta PH) was also observed in the egg-positive subjects only in comparison with that of the egg-negative Brazilian. Serum laminin and IR beta PH concentrations of the egg-positive subjects did not correlate with the absorbance of enzyme-linked immunosorbent assay (ELISA) which utilized crude antigens isolated from schistosome adults or eggs. No significant difference in these two parameters was observed between two subgroups of the egg-negative Brazilian or Japanese immigrants divided according to the serological data by ELISA. These findings suggest that serum laminin and IR beta PH levels are worth further evaluation for their usefulness as the marker for liver fibrosis in schistosomiasis.
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PMID:Elevation of laminin and beta-subunit of prolyl 4-hydroxylase in the sera of human subjects with Schistosomiasis mansoni. 255 32

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

A histopathological study was conducted on alcoholic liver fibrosis with fatty change (21 cases) and alcoholic liver fibrosis without fatty change (18 cases) in comparison with nutritional fatty liver (27 cases). The diagnoses of alcoholic liver fibrosis groups were clinically fulfilled according to the criteria established by the Alcohol and Liver Research Group (Chief: Professor Takeuchi) of the Ministry of Education of Japan. Histological diagnosis of alcoholic liver fibrosis with fatty change was based on moderate and/or greater fatty metamorphosis of the hepatic lobules, alcoholic liver fibrosis without fatty change on a lesser degree of fatty metamorphosis than alcoholic liver fibrosis with fatty change, and nutritional fatty liver on clinicopathological features. All 66 cases were negative for viral markers of hepatitis B surface antigen and anti-hepatitis C virus in serum. Intrasinusoidal neutrophil infiltrations were significant in cases of alcoholic liver fibrosis groups more often than in cases of nutritional fatty liver. The degree of intrasinusoidal neutrophil infiltration in cases of alcoholic liver fibrosis groups was higher in cases who had last consumed alcohol recently, compared with those with longer abstinence. In alcoholic liver fibrosis with fatty change and nutritional fatty liver groups, mild-to-moderate degrees of ceroid-lipofuscinosis were recognized, but both fatty change and ceroid-lipofuscinosis were decreased according to the deterioration of fibrotic changes in alcoholic liver fibrosis with fatty change cases. On the other hand, it is significant that the frequency of ceroid-lipofuscinosis in alcoholic liver fibrosis without the fatty change group was lower than those of the alcoholic liver fibrosis with fatty change and nutritional fatty liver groups. Distribution of ceroid-lipofuscinosis has a tendency to be recognized around the central zone (zone III) of alcoholic liver fibrosis with fatty change cases with mild fibrosis, as in nutritional fatty liver cases, and the ceroid-lipofuscinosis disperses with the progression of fibrosis. These results suggest that fibrosis and fatty droplet deposition lead to microvascular heterogeneity. Therefore, the degree and distribution of fatty droplets, ceroid-lipofuscinosis, and intrasinusoidal neutrophil infiltration differ, depending on the etiology of fatty liver, and are an important histopathological barometer in cases of alcoholic liver fibrosis with fatty change and alcoholic liver fibrosis without fatty change, thus indicating the degree of fibrosis and the period since last alcohol intake.
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PMID:Correlation between intrasinusoidal neutrophilic infiltration and ceroid-lipofuscinosis in alcoholic liver fibrosis with or without fatty change: clinicopathological comparison with nutritional fatty liver. 898 40

The influence of hepatitis G virus (HGV) infection on disease activity in hepatitis C related and unrelated liver disease was investigated in 254 individuals using an EIA polymerase chain reaction assay for HGV. One hundred patients had chronic hepatitis C, 26 primary biliary cirrhosis, and 30 alcoholic liver cirrhosis. In addition, 51 hepatitis B surface antigen (HBsAg)-positive and 47 anti-hepatitis C virus (HCV)-positive blood donors were screened. Hepatitis G virus was detected in 18% of patients with chronic hepatitis C, 13% of patients with alcoholic liver cirrhosis, 11% of patients with primary biliary cirrhosis, 10% of anti-HCV-positive blood donors, and 2% of HBsAg-positive blood donors. Virus load and alanine aminotransferase (ALT) levels did not differ significantly in patients with HCV alone versus patients coinfected with HCV and HGV. However, mild liver fibrosis correlated with HGV coinfection. Hepatitis G virus did not influence ALT levels or liver damage in liver disease unrelated to viral infection.
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PMID:Influence of hepatitis G virus infection on liver disease. 949 73

Increased concentrations of serum hyaluronan, a polysaccharide widely distributed in the extracellular space, have been demonstrated in liver disease of various aetiologies and proposed as a useful marker of liver fibrosis. The aim of the present study was to evaluate the association of serum hyaluronan with the extent of hepatic fibrosis in asymptomatic cases of chronic hepatitis B viral infection. The study was conducted in a consecutive sample of 111 asymptomatic chronic carriers of hepatitis B surface antigen. Liver function tests, alcohol consumption and cigarette smoking were determined and, for 84 subjects, liver biopsy was performed and degrees of inflammation and fibrosis were scored. Hyaluronan was measured using a radiometric assay. Mean serum hyaluronan increased with increasing fibrosis score (from 22.2 +/- 4.8 to 50.6 +/- 12.7 microg/l, p = 0.058) or pathological severity (from 18.8 +/- 5.9 to 50.6 +/- 12.5 microg/l, p = 0.048), even after adjusting for the effect of age. No such correlation was found with portal inflammation. The study showed that, in asymptomatic chronic carriers of hepatitis B, serum hyaluronan concentration correlates with hepatic fibrosis, a known marker of disease prognosis. This finding supports the hypothesis that hyaluronan might be of use in assessing and monitoring time trends in liver disease, substituting for repeated biopsies.
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PMID:Serum hyaluronan as a marker of liver fibrosis in asymptomatic chronic viral hepatitis B. 1053 46

The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognised. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. The nature and degree of liver involvement are reported on the basis of hospital based studies in patients who consumed arsenic contaminated drinking water for one to 15 years. Two hundred forty-eight patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examination including liver function tests and hepatitis B surface antigen (HBsAg) status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. Hepatomegaly was present in 190 of 248 patients (76.6%). Non-cirrhotic portal fibrosis was the predominant lesion (91.3%) in liver histology. The maximum arsenic content in liver was 6 mg/kg (mean 1.46 [0.42], control value 0.16 [0.04]; p <0.001); it was undetected in 6 of 29 samples studied. The largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic contaminated water are reported. Non-cirrhotic portal fibrosis is the predominant lesion in this population. Hepatic fibrosis has also been demonstrated due to long term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferases elevated at 12 months and hepatic fibrosis at 15 months.
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PMID:Arsenic and liver disease. 1167 19

To assess whether extended treatment with interferon improves the outcome of hepatitis B e antigen (HBeAg)-negative chronic hepatitis B, 101 consecutive patients were treated with 6 MU of interferon alfa 2b 3 times weekly for 24 months. During the 68-month study, 30 patients (30%) had a sustained response (i.e., normal serum transaminase levels and undetectable hepatitis B virus DNA by non-polymerase chain reaction [PCR] assays), and 15 cleared serum surface antigen. Twenty-five nonresponders, 16 relapsers, and 30 who discontinued treatment were considered treatment failures. Multivariate analysis predicted a sustained response for young age (odds ratio, 0.94; 95% confidence interval, 0.89-0.99; P =.041) and high pretreatment serum levels of immunoglobulin M (IgM) anti-hepatitis B core antigen (HBc) (odds ratio, 4.52; 95% confidence interval, 1.63-12.5; P =.004). Liver disease progressed in none of the sustained responders but in 16 with treatment failure (0% vs. 22%, P =.002); hepatocellular carcinoma (HCC) developed with similar frequency in both groups (7%). Overall, estimated 8-year complication-free survival was longer for the 30 sustained responders than the 71 patients with treatment failure (90% vs. 60%, P <.001), but 8-year patient survival was similar in the 2 groups (100% and 90%). Short complication-free survival was predicted by failure to respond to interferon (hazard ratio, 7.8; 95% confidence interval, 1.8-34.0; P =.006) and high scores for liver fibrosis (hazard ratio, 1.71; 95% confidence interval, 1.17-2.50; P =.005). In conclusion, 24 months of treatment with interferon alfa 2b led to sustained disease suppression in a significant proportion of patients with HBeAg-negative chronic hepatitis B.
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PMID:Long-term suppression of hepatitis B e antigen-negative chronic hepatitis B by 24-month interferon therapy. 1293 9

The long-term impact of acute self-limited hepatitis B on the liver is unknown. Fourteen patients were recalled at a median of 4.2 years (range, 1.8-9.5 years) after the onset of acute hepatitis B. All showed clinical and serologic recovery with circulating hepatitis B surface antigen (HBsAg) clearance. Antibody to HBsAg (anti-HBs) had developed in 12 patients. Nine underwent liver biopsies at a median of 7.2 years, and histologic findings were evaluated using Ishak scores. Serum samples and frozen liver tissue were subjected to real-time detection polymerase chain reaction (PCR) to quantify the surface and X regions of the hepatitis B virus (HBV) genome and qualitative PCR to detect the covalently closed circular (ccc) HBV DNA replicative intermediate. Three patients had low levels of circulating HBV DNA up to 8.9 years after the onset, whereas both HBV DNA surface and X regions were found in the liver of all 9 patients examined, including 7 negative for serum HBV DNA. Liver viral loads assessed by the 2 regions showed a significant correlation (r = 0.946; P =.008), and all patients tested positive for ccc HBV DNA. Liver fibrosis and mild inflammation persisted in 8 patients. The fibrosis stage had relation to peak serum HBV DNA in the acute phase (P =.046) but not to liver viral loads in the late convalescent phase. In conclusion, occult HBV infection persists in the liver and is accompanied by abnormal liver histology for a decade after complete clinical recovery from acute self-limited hepatitis B.
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PMID:Long-term histologic and virologic outcomes of acute self-limited hepatitis B. 1271 99

In a 65-year-old patient with ascites, jaundice and positive hepatitis B surface antigen (HBsAg), the histological diagnosis of cirrhosis with knodell total score 13 was made in 1995. The patient was followed up for 8 years. Spontaneous seroconversion of HBsAg appeared. Except for slight hyperbilirubinemia, all pathologic, clinical laboratory data remained normal from the second year of diagnosis till 8 years of follow-up. In the last follow up, the markers of liver fibrosis were all normal. The portal vein diameter was decreased and the esophageal varices disappeared. The imaging of liver by sonography and CT-scan did not reveal any abnormality.
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PMID:Clinical, biochemical and imaging-verified regression of hepatitis B-induced cirrhosis. 1507 73


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