Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disulfiram alone or in combination with ethanol was administered orally for six weeks. Disulfiram significantly elevated the triglyceride level in the blood serum and hepatic tissue and cholesterol level in the blood serum, and depressed the content of free fatty acids in the hepatic tissue. Given together with ethanol, disulfiram increased the concentration of triglycerides and cholesterol in the blood serum and depressed the cholesterol level in the hepatic tissue. Given separately or in combination with ethanol, disulfiram disturbed the lipid metabolism. The results may indicate that chronically given disulfiram may produce in man similar disturbance and owing to that may aggravate hepatic steatosis present in 60--90% of alcoholics, in this way intensifying the damage of this organ.
Pol J Pharmacol Pharm
PMID:The effect of prolonged administration of disulfiram alone or in combination with ethanol on some indices of lipid metabolism in the blood serum and hepatic tissue of the rat. 727 93

The aim of this study was to evaluate selected diagnostic and clinical aspects of chronic hepatitis C (CH-C) in the group of 80 patients: 68 males aged 24-65 (mean 39.8 +/- 10,5) and 12 females aged 35-66 (mean 48.7 +/- 12.6). The epidemiological data allowed to divide the basic group into 3 subgroups: patients with transfusion-associated CH-C (subgroup I: 12 males, mean age 38 +/- 6.7 and 2 females aged 40 and 46), CH-C patients with parenteral hepatitis C virus exposure-other than blood transfusion (subgroup II: 25 males, mean age 40.6 +/- 8.2 and 5 females aged 43 +/- 15.1) and sporadic cases with unknown HCV exposure (subgroup III: 31 males, mean age 38.2 +/- 11.2 and 5 females, mean age 50.5 +/- 10.3). The duration of the disease (CH-C) was calculated from the incident of acute viral hepatitis or the first signs of liver damage caused by HCV to the confirmation of CH-C by liver biopsy. The following data were analyzed: a frequency of acute viral hepatitis with jaundice at the beginning of the disease, ALT flare-ups, mean highest activities of ALP and GGT, frequency of hypergammaglobulinaemia and sings of fatty liver in ultrasonographic finding (USG). In all patients but one anti-HCV antibodies (ELISA 2nd generation test by Abbott) were detected. In 64/80 subjects antibodies to HCV antigens: 5-1-1, C 100-3, C 33c and C 22 were determined by RIBA-2 test (Ortho). In 62/80 patients HCV-RNA in serum was determined by RT PCR. Liver biopsy was performed in 71/80 patients. Other co-existent liver diseases were excluded. The similarity between 3 subgroups was shown: similar percentage of males and females, similar patients mean age and the duration of the disease. It was shown that the acute beginning of the disease with jaundice has been observed twice as frequent in subgroups I and II compared with subgroup III. The same frequency of ALT flare-ups in all subgroups was observed (25-28.6%). No differences in mean highest ALP and GGT activities in 3 subgroups were observed. It was shown, however, that hypergammaglobulinaemia was detected more frequently in subgroup III (30.5%) compared with subgroup I (7.1%) and II (16.7%). The signs of fatty liver in ultrasonographic findings were also observed more frequently in subgroup III (30.5%) than in subgroup I (14.3%) or II (16.7%). In all patient but one, in which anti-HCV antibodies by ELISA test were detected, anti-C 33c and anti-C 22 antibodies by RIBA were present. HCV-RNA in serum was detected in 77.8% subjects from subgroup I. 73.9%-from subgroup II and 66.7%-from subgroup III. In all HCV-RNA positive patients anti-HCV antibodies were detected. The evidence of chronic active hepatitis confirmed by liver biopsy was shown in 63.6%, 67.8% and 71.8% of patients from subgroup I, II and III, respectively. In no case normal liver morphology was present. Authors concluded the distressing fact of the high incidence of chronic active hepatitis in patients unaware of HCV infection, without the incident of acute hepatitis at the beginning of the disease (over 1/3 of all described subjects). The differences of the clinical course of the disease between subgroups 1 + II and subgroup III suggest two different routes of HCV infection or the presence of two different HCV mutants in Polish population. Authors emphasise the necessity of HCV gene typing in CH-C patients, which might explain the surprisingly high incidence of chronic active hepatitis in the reported group. The use of the presented data for the general practitcioner making the diagnosis of crytogenetic liver disease is also accentuated.
Pol Arch Med Wewn 1996 Apr
PMID:[Selected diagnostic and clinical aspects of chronic viral hepatitis type C]. 875 40

Two cases of acute fatty liver of pregnancy (AFLP) are described. The liver function abnormalities have been ignored in the both cases. The review literature on this rare clinical entity unique to pregnancy is presented. The importance of clinical and biochemical findings in the diagnosis of disease is emphasized. Although etiology is unknown, deficiency of fatty acid beta-oxidation has been suggested.
Ginekol Pol 1999 Apr
PMID:[Acute fatty liver of pregnancy: underestimated complication of the third trimester?]. 1058 6

Increasing number of patients with inborn errors of metabolism (IEM) are now reaching adulthood and are in position to reproduce. Because of the rarity of individual disorders our knowledge of risks factors associated with pregnancy is limited. Obstetrics problems in IEM can be divided into two categories: pregnancy effects on maternal metabolic disorders and relation between mother and fetus related to who of them is affected. Detrimental effects upon the fetus may be directly caused by maternal disease, as it occurs in PKU, or indirectly by maternal supplementation with harmful substrate, as occurs in galactosemia. Less commonly, fetal inborn error of metabolism may affect the mother's health. Pregnancies in which the fetus had long-chain hydroxyacyl-CoA dehydrogenase deficiency have been complicated by life-threatening HELLP syndrome (haemolysis, elevated liver enzymes and low platelets) or AFL (acute fatty liver of pregnancy) during third trimester. The management of labor and the postpartum period (for women and newborns) has to be carefully planned to avoid significant metabolic decompensation.
Ginekol Pol 2003 Jun
PMID:[Pregnancy and inborn errors of metabolism]. 1293 56

Serum interleukin-6 concentrations in patients with alcoholic liver disease Pathogenesis of alcoholic liver disease (ALD) is not well defined, but immune mediated hepatic injury is thought to be important. The main aim of this study was estimation of serum concentrations of IL-6 in patients with chronic alcoholic liver disease and determination of correlations between IL-6 serum concentration and occurrence of clinical manifestations, biochemical parameters and a stage of ALD. 85 patients with the diagnosis of chronic ALD and 35 healthy subjects (mached for age and sex) were enrolled into the study. Serum concentration of IL-6 was measured with ELISA. Serum IL-6 concentrations were markedly elevated in the all analyzed groups of patients with ALD when compared with healthy controls. When compared in groups, patients with alcoholic cirrhosis and chronic alcoholic hepatitis had the highest and patients with fatty liver had the lowest serum IL-6 concentrations. In addition, IL-6 concentrations were higher in patients with hepatic encephalopathy than in those without liver failure. Furthermore, we found statistically significant correlation between serum IL-6 and albumin concentrations. High IL-6 concentrations were associated with high mortality in patients with ALD. These findings suggest that IL-6 is an important immunological factor associated with alcoholic liver disease.
Pol Merkur Lekarski 2004 Sep
PMID:[Serum interleukin-6 concentrations in patients with alcoholic liver disease]. 1562 53

RNA interference (RNAi) has been used increasingly for reverse genetics in invertebrates and mammalian cells, and has the potential to become an alternative to gene knockout technology in mammals. Thus far, only RNA polymerase III (Pol III)-expressed short hairpin RNA (shRNA) has been used to make shRNA-expressing transgenic mice. However, widespread knockdown and induction of phenotypes of gene knockout in postnatal mice have not been demonstrated. Previous studies have shown that Pol II synthesizes micro RNAs (miRNAs)-the endogenous shRNAs that carry out gene silencing function. To achieve efficient gene knockdown in mammals and to generate phenotypes of gene knockout, we designed a construct in which a Pol II (ubiquitin C) promoter drove the expression of an shRNA with a structure that mimics human miRNA miR-30a. Two transgenic lines showed widespread and sustained shRNA expression, and efficient knockdown of the target gene Sod2. These mice were viable but with phenotypes of SOD2 deficiency. Bigenic heterozygous mice generated by crossing these two lines showed nearly undetectable target gene expression and phenotypes consistent with the target gene knockout, including slow growth, fatty liver, dilated cardiomyopathy, and premature death. This approach opens the door of RNAi to a wide array of well-established Pol II transgenic strategies and offers a technically simpler, cheaper, and quicker alternative to gene knockout by homologous recombination for reverse genetics in mice and other mammalian species.
 ...
PMID:Pol II-expressed shRNA knocks down Sod2 gene expression and causes phenotypes of the gene knockout in mice. 1645 9

In patients without substantial alcohol use, triglyceride accumulation in the liver can lead to nonalcoholic fatty liver disease (NAFLD) that may progress to nonalcoholic steatohepatitis (NASH). The differential diagnosis between NAFLD and NASH can be accomplished only by morphological examination. Although the relationship between mitochondrial dysfunction and the progression of liver pathologic changes has been described, the exact mechanisms initiating primary liver steatosis and its progression to NASH are unknown. We selected 16 genes encoding mitochondrial proteins which expression was compared by quantitative RT-PCR in liver tissue samples taken from patients with NAFLD and NASH. We found that 6 of the 16 examined genes were differentially expressed in NAFLD versus NASH patients. The expression of hepatic HK1, UCP2, ME2, and ME3 appeared to be higher in NASH than in NAFLD patients, whereas HMGCS2 and hnRNPK expression was lower in NASH patients. Although the severity of liver morphological injury in the spectrum of NAFLD-NASH may be defined at the molecular level, expression of these selected 6 genes cannot be used as a molecular marker aiding histological examination. Moreover, it is still unclear whether these differences in hepatic gene expression profiles truly reflect the progression of morphological abnormalities or rather indicate various metabolic and hormonal states in patients with different degrees of fatty liver disease.
Acta Biochim Pol 2007
PMID:Expression of genes encoding mitochondrial proteins can distinguish nonalcoholic steatosis from steatohepatitis. 1750 23

Severe liver function disorders in late pregnancy are relatively rare but extremely dangerous, as they may quickly develop into a fulminant disease and become a life-threatening disorder for the mother and the fetus. In the following study we have reported a case of a previously healthy woman with severe liver disorder in the third trimester of pregnancy. On the basis of anamnesis, differential diagnosis, typical course and complications of the disease, and proper response to intensive supportive medical therapy, we diagnosed an acute fatty liver of pregnancy. The diagnosis was based on clinical presentation and laboratory abnormalities. Owing to timely intervention and adequate supportive care management, this severe complication of a pregnancy has had a successful outcome for both the mother and the child.
Ginekol Pol 2008 Mar
PMID:[Acute fatty liver of pregnancy--case report]. 1859 56

Non-alcoholic fatty liver disease (NAFLD) covers a wide spectrum of liver pathology--from steatosis alone, through the necroinflammatory disorder of non-alcoholic steatohepatitis (NASH) to cirrhosis and liver cancer. NAFLD/NASH is mostly related with visceral adiposity, obesity, type 2 diabetes melitus (DM t.2) and metabolic syndrome. Pathogenetic concepts of NAFLD include overnutrition and underactivity, insulin resistance (IR) and genetic factor. The prevalence of NAFLD has been estimated to be 17-33% in some countries, NASH may be present in about 1/3 of such cases, while 20-25% of NASH cases could progress to cirrhosis. NAFLD is now recognized as one of the most frequent reason of liver tests elevation without clinical symptoms. Insulin resistance is considering as having a central role in NAFLD pathogenesis. In hepatocytes, IR is related to hyperglycaemia and hyperinsulinaemia, formation of advanced glycation end-products, increased free fatty acids and their metabolites, oxidative stress and altered profiles of adipocytokines. Early stages of fatty liver are clinically silent and include elevation of ALT and GGTP, hyperechogenic liver in USG and/or hepatomegaly. Among clinical symptoms, abdominal discomfort is relatively common as well as chronic fatigue. NAFLD/NASH is not a benign disease, progressive liver biopsy have shown histological progression of fibrosis in 32%, the estimated rate of cirrhosis development is 20% and a liver--related death is 12% over 10 years. No treatment has scientifically proved to ameliorate NAFLD or to avoid its progression. The various therapeutic alternatives are aimed at interfering with the risk factors involved in the pathogenesis of the disorder in order to prevent the progression to end-stage liver disease. The most important therapeutic measure is increasing insulin sensitivity by an attempt to change a lifestyle mostly by dieting and physical activity in order to loose weight. The most used agent is metformin, the others are under controlled trials or their effectiveness is low. NASH is not a common indication for liver transplantation because of the older age distribution of patients and high prevalence of comorbidity, related to metabolic syndrome. Recurence of NASH in the grafted liver is also a relatively frequent complication.
Pol Merkur Lekarski 2008 Jun
PMID:[Non-alcoholic fatty liver disease--new view]. 1870 46

Non-alcoholic steatohepatitis (NASH) is a part of the spectrum of non-alcoholic fatty liver disease (NAFLD), which can progress to hepatic cirrhosis and end-stage liver disease or hepatocellular carcinoma (HCC). Its pathogenesis is associated with insulin resistance (IR) and the metabolic syndrome. Hepatic steatosis has also been considered an early marker of IR. It is now accepted that NASH is a multistep process with a prominent role for IR, where oxidative stress and cytokines retain a central role. Markers for predicting NAFLD with advanced fibrosis are needed. Once considered irreversible, liver fibrosis is now recognized a dynamic process with significant prospects for remission. The liver biopsy is still a gold standard in assessment of liver fibro-inflammatory activity in the injured liver, but has its own limitations: invasiveness, small tissue sample and inter- and intra-observer error. The lack of non-invasive tests limits the ability of monitoring progression of hepatic fibrosis and response to treatment. Therefore, clinical trials focused on finding of new non-invasive diagnostic tools giving possibilities of frequent, more accurate and reproducible assessment of hepatic fibrosis are constantly conducted.
Pol Merkur Lekarski 2008 Aug
PMID:[Non invasive markers of non-alcoholic steatohepatitis]. 1894 40


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