Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty four CAH type B patients were studied, they were simultaneously treated with corticosteroids and azathioprine for an average period of 52 months. The patients were classified into two groups: CAH without cirrhosis (45) and CAH with cirrhosis (19). Patients were initially treated with doses of 40 mg prednisone and 50 mg azathioprine. The reduction of steroids was done according to ASAT level; medication being discontinued when there were not signs of activity in liver biopsy. Therapy was readministered due to elevation of ASAT (5 fold) and the liver biopsy shown pattern of CAH. 49% of CAH patients without cirrhosis improve histology and discontinue treatment; half of them had to resume therapy because of relapse. 14% of the patients died (4); three of them belonging to the group who continued taking the drugs. In the CAH group with cirrhosis, 6 were in remission and withdrawn-from treatment, but 5 had to resume it. The mortality rate of this group was of 69% (13), all patients belonging to the group where were not able to discontinue medication. In both groups ASAT was a good parameter of activity. Complications were more frequent in the group with cirrhosis (42%) than in the one without cirrhosis (17%) (p less than 0.01). In patients with CAH type B, the best therapeutic response was associated to those cases without cirrhosis. Mortality rate is high in patients with cirrhosis at onset of therapy.
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PMID:[Immunosuppressive treatment of patients with chronic active HBsAg positive hepatitis]. 718 30

Fasting and postprandial serum concentrations of conjugates of cholic (CCA) and chenodeoxycholic (CCDA) acid measured by radioimmunoassay were compared with morphological changes in percutaneous liver biopsies from 49 patients with alcohol abuse. Sulfobromophthalein (BSP) and galactose elimination tests were also performed, and serum levels of aminotransferases (ASAT, ALAT), glutamyltransferase, alkaline phosphatase, and bilirubin were determined. Raised fasting serum concentrations of CCDA were found in 29 patients (59%), whereas elevated fasting serum levels of CCA were found in 19 patients (39%). The mean fasting and postprandial serum bile acid concentrations were significantly higher in patients with hepatofibrosis and cirrhosis than in those with only fatty changes. The extent of the postprandial rise, however, was variable and not significantly different among the various groups. The BSP elimination test was abnormal in 12 patients (25%) but gave normal results in 2 of the 3 patients with cirrhosis of the liver. The galactose elimination rates differed only between patients with normal liver biopsies and patients with cirrhosis of the liver. The serum enzyme levels were not significantly different between the various morphological groups. It is concluded that determinations of fasting serum bile acids, especially CCDA, give more reliable and sensitive information on the degree of liver damage in alcoholic liver disease than BSP and galactose elimination tests or serum enzyme assays.
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PMID:Serum cholic and chenodeoxycholic acid conjugates and standard liver function tests in various morphological stages of alcoholic liver disease. 720 76

The reliability of serum aminotransferase (ASAT and ALAT) levels, currently used in deciding on performing liver biopsy and to assess interferon therapy in chronic hepatitis C has been questioned. In Belgium, interferon therapy is actually only reimbursed for treatment of chronic hepatitis C when serum aminotransferase levels are more than twice the upper limit of normal. The aim of the present study was to assess the relationship between serum aminotransferase levels and histological severity of chronic hepatitis C. Sixty-seven liver biopsies from 51 different patients with chronic hepatitis C and presenting with elevated ASAT and/or ALAT levels, were retrospectively evaluated using the original terminology (minimal hepatitis, chronic persistent hepatitis, chronic active hepatitis, cirrhosis), the Knodell score and the components of the Bianchi-Gudat score, where grading (portal inflammation, piecemeal necrosis, intra-acinar necrosis and inflammation) and staging components (fibrosis/ cirrhosis) are quantitated separately. The correlation between amino-transferase levels measured at or near to the biopsy date and histological criteria were evaluated using Spearman's rank correlation. About one third of the patients, including patients with chronic active hepatitis and cirrhosis, presented with ASAT and ALAT levels less than twice the upper limit of normal. ASAT levels correlated with originally determined histological severity, the numerical Knodell score and the numerical scores for piecemeal necrosis, for intra-acinar necrosis and inflammation and for fibrosis in the Bianchi-Gudat score. ALAT levels correlated only with intra-acinar necrosis and inflammation. It is concluded that limiting interferon therapy to patients with aminotransferase levels over twice the upper limit of normal excludes a large proportion of patients from potentially curative treatment. ASAT levels are more useful than ALAT to assess the histological severity of the disease, probably because this mitochondrial enzyme is present in higher quantities in the liver as compared to the cytosolic ALAT, and is more released when tissue damage is more severe.
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PMID:Serum aminotransferase levels and histological disease in chronic hepatitis C. 914 72

The term 'non-alcoholic fatty liver disease' (NAFLD) includes cases with steatosis alone and those with non-alcoholic steatohepatitis (NASH). Usually there are no signs or symptoms, sometimes fatigue or pain, and apart from hepatomegaly the condition is revealed by abnormal liver biochemistry or by abdominal ultrasound. Most cases are associated with overweight or diabetes. Liver enzymes are usually elevated, especially GGT, ASAT and ALAT. Other conditions, including alcohol abuse and autoimmune hepatitis, have to be excluded. The diagnosis of steatosis can be made with ultrasound or CT scan. A liver biopsy is often needed to exclude other disease and to assess inflammation and fibrosis. Cirrhosis can develop. NAFLD is usually caused by two 'hits': the 'first hit' is peripheral insulin resistance, causing steatosis. The 'second hit' is caused by reactive oxygen species, inducing vicious cycles leading to inflammation. Weight loss, metformin or thiazolidinediones can improve NAFLD by increasing insulin sensitivity. Radical scavengers such as vitamin E, betaine and perhaps also urodeoxycholic acid may improve the hepatitis component. Further studies on treatment are needed.
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PMID:Non-alcoholic fatty liver disease: a brief review. 1569 51

Liver cancer is one of the leading causes of cancer death in Mongolia. Since 1982-1986 , when HCC became the most frequent cancer among the Mongolian population, the rate has been increasing continuously. In the period 2000-2005 years 35.3%of all newly registered cancer cases were liver cancers, with an incidence rate of 51.3 per 100,000 population. Compared to the previous 5 year period, the rate increased by 11%. The objective here was to analyze hepatitis B (HBV) and C virus (HCV)-related HCC cases and to evaluate the possibility of tumor marker (AFP) testing for early detection in Mongolia. Sera from a total of 513 patients with chronic liver diseases, liver cirrhosis and HCC were analyzed for liver function (ALAT, ASAT) and hepatitis virus markers (HBsAg, anti-HCV). Sera from 316 patients were also examined for alpha-fetoprotein (AFP) levels. The overall incidence of HBsAg or anti-HCV were very high ( 95.3%) among all patients. Some 33.5% (66/197) of patients with HCC were positive for HBsAg and 45.2% (89/197) for anti-HCV. Moreover, 17.3% ( 34/197) of HCC patients demonstrated co-infection with HBV and HCV. AFP levels were elevated in 4.6% (11/238) and 29.5% (23/78) of chronic hepatitis and cirrhosis patients, respectively. In HCC cases, 84.3% (166) of patients had increased level of AFP ranging from 32 ng/ml to more than 400 ng/ml. We conclude that HBV/HCV infection is the main factor related to development of HCC in Mongolia and that testing for AFP serum levels is a useful tool for early detection and diagnosis.
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PMID:Hepatocellular carcinoma and its early detection by AFP testing in Mongolia. 1705 45

Alcohol abuse is a major cause of liver cirrhosis as well as chronic liver disease. The aim of the present study was to investigate the possible correlation, between liver dysfunction biological markers and vitamin B12, with interleukin-6, in the serum of alcohol-dependent individuals without liver disease (AWLD). In a sample of 43 alcohol abusing/dependent subjects (33 males and 10 females) treated on an inpatient basis according to a standard detoxification protocol, the serum activities of the hepatic enzymes (ASAT, ALAT, gamma-GT), as well as the concentration of B12 and IL-6, were determined on admission. A strong positive correlation has been observed between IL-6 and B12, ASAT, ALAT, and gamma-GT at the beginning of the detoxification period. The results confirmed that in alcohol-dependent individuals, the median serum concentration of IL-6, before the beginning of the treatment, had a significant positive correlation with the liver dysfunction biological markers and B12. In conclusion, IL-6 might be used as an additional diagnostic marker for the degree of liver dysfunction in alcohol dependent individuals.
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PMID:Vitamin B12 and hepatic enzyme serum levels correlate with interleukin-6 in alcohol-dependent individuals without liver disease. 1744 94

This report correlates the clinical and biological findings, liver hemodynamics and histological features of focal INL in an infant with BA cirrhosis. An eight month old boy with BA, with previous successful porto-enterostomy, was admitted with signs of cholangitis and ascites. He was treated with antibiotics and diuretics with subsequent clinical improvement. Eight days later, while being fed with hyper-osmolar milk, he became febrile again: ASAT/ALAT climbed (9000/2300 IU/L), liver function deteriorated. Infectious work-up was negative. Liver-ultrasound showed reversed portal flow and a negative arterial diastolic flow. The patient recovered within five days under supportive treatment. A similar event recurred five days later. INL was suspected and semi-urgent living-related liver transplantation was performed, with uneventful post-operative course. Histology of the explanted liver showed extensive foci of INL of different ages. This report illustrates how the association of reversed portal and arterial diastolic flows, with subsequent liver hypoperfusion, may repeatedly cause foci of INL in BA cirrhosis, and lead to rapid progression to liver failure. Because of precarious hepatic blood supply in such patients, close monitoring of portal and diastolic arterial flows is recommended.
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PMID:Focal ischemic necrosis in advanced biliary atresia cirrhosis. 1833 37

A 58-year-old female patient was transferred by her general practitioner with fatigue, nausea and icterus which had begun 2 weeks prior to admission. Laboratory results revealed acute hepatitis (ALAT [alanine aminotransferase] 3,871 U/l, ASAT [aspartate aminotransferase] 2,004 U/l, bilirubin 6.7 mg/dl, gamma-GT [gamma-glutamyl transferase] 503 U/l). The patient's medical history included genetic hemochromatosis (without cirrhosis). Hepatitis A to C, infection with herpesviruses or Leptospira interrogans were excluded by serologic and molecular biological tests. There was no diagnostic evidence for underlying autoimmune or additional metabolic liver disease. Due to a trip to Africa 5 months earlier, the patient was tested for hepatitis E, leading to positive anti-hepatitis E-IgM and negative anti-hepatitis E-IgG. PCR (polymerase chain reaction) detection of hepatitis E virus (HEV) was positive as well. In conclusion, acute HEV infection was diagnosed. After close reconsideration, the nonfitting incubation period precluded a travel-associated infection. Additionally, there was no evidence for current HEV infections within the patient's social environment, so that a zoonotic origin has to be discussed.
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PMID:[Rare acute hepatitis in a female patient with hemochromatosis: a zoonosis?]. 2045 55

Noninvasive tests are utilized in chronic liver diseases to assess excessive connective tissue. Blood tests such as the N-terminal peptide of procollagen (PIIINP) and APRI (ASAT/platelet count) measure the formation and degradation of connective tissue or liver function. Elastography (Fibroscan) is based on the propagation of ultrasound in liver tissue, accelerated by fibrosis: the results are more sensitive and accurate than those based on blood tests. Reliable detection of severe fibrosis and cirrhosis is possible with Fibroscan along with determining normal liver tissue.
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PMID:Diagnosis for liver fibrosis - noninvasively. 2918 50

Nonalcoholic fatty liver disease (NAFLD) is a metabolic disorder due to increased accumulation of fat in the liver and in many cases to enhanced inflammation. Although the contribution of inflammation in the pathogenesis of NAFLD is well established, the cytokines that are involved and how they influence liver transformation are still poorly characterized. In addition, with other modifiers, inflammation influences NAFLD progression to liver cirrhosis and hepatocellular carcinoma, demonstrating the need to find new molecular targets with potential future therapeutic applications. We investigated gene signatures in 38 liver biopsies from patients with NAFLD and obesity who had received bariatric surgery and compared these to 10 control patients who had received a cholecystectomy, using DNA microarray technology. A subset of differentially expressed genes was then validated on a larger cohort of 103 patients who had received bariatric surgery for obesity; data were thoroughly analyzed in terms of correlations with NAFLD pathophysiological parameters. Finally, the impact of a specific cytokine, interleukin-32 (IL32), was addressed on primary human hepatocytes (PHHs). Transcript analysis revealed an up-regulation of proinflammatory cytokines IL32, chemokine (C-X-C motif) ligand 9 (CXCL9), and CXCL10 and of ubiquitin D (UBD), whereas down-regulation of insulin-like growth factor-binding protein 2 (IGFBP2) and hypoxanthine phosphoribosyltransferase 1 (HPRT1) was reported in patients with NAFLD. Moreover, IL32, which is the major deregulated gene, correlated with body mass index (BMI), waist circumference, NAFLD activity score (NAS), aminotransferases (alanine aminotransferase [ALAT] and aspartate aminotransferase [ASAT]), and homeostasis model assessment of insulin resistance (HOMA-IR) index in patients. Consistent with an instrumental role in the pathophysiology of NAFLD, treatment of control human hepatocytes with recombinant IL32 leads to insulin resistance, a hallmark metabolic deregulation in NAFLD hepatocytes. Conclusion: IL32 has a critical role in the pathogenesis of NAFLD and could be considered as a therapeutic target in patients.
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PMID:Interleukin-32 Contributes to Human Nonalcoholic Fatty Liver Disease and Insulin Resistance. 3149 42


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