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)

APO A-1 and B HDL cholesterol in 15 cases of acute hepatitis and 13 cases of hepatic cirrhosis were comparatively studied with different biochemical parameters. The decrease in APO A-1 and HDL revealed an alteration of the hepatic function. When the APO A-1 and HDL returned to normal a recovery of the hepatic function was observed.
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PMID:[Importance of apolipoproteins A-1 and B in acute viral hepatitis and hepatic cirrhosis]. 357 19

Considering liver cirrhosis a limit model, and therefore a condition suitable for the analysis of changes of lipid metabolism in liver disorders generally, the authors examined the L-CAT pattern, total and free cholesterol, HDL-cholesterol and APO-A in sixty-five subjects; fifty-three were suffering from liver cirrhosis, and were subdivided into those who were diabetic in addition, and those who were not, as well as according to the severity and duration of the liver disease; the remaining twelve were healthy controls. Analysis of the findings showed L-CAT to diminish significantly as the metabolic changes due to liver injury worsen. Contrary to the other parameters studied, L-CAT was the only one for which significant changes were found on analysis of variance comparing non-diabetic cirrhotics of varying severity. Further comparison suggested the idea that the reduction of L-CAT activity was correlated to the rate of progression of the disease rather than to the temporary condition of compensation or decompensation, so much so as to suggest itself as a valid parameter for the prognosis of liver cirrhosis.
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PMID:Pattern of lecithin-cholesterol-acyl-transferase (L-CAT) activity in the course of liver cirrhosis. 661 81

An imbalance between cytoproliferation and apoptosis may be relevant in liver carcinogenesis. The aim of this study was to analyse these parameters in patients with chronic liver damage in relation to the aetiology of the disease. Forty-eight patients were studied: 23 had hepatitis C virus (HCV)- and 11 had hepatitis B virus (HBV)-related chronic hepatitis, seven had alcoholic liver disease, and seven had haemochromatosis. The biopsies were used for routine diagnosis, cytoproliferative indexing (MIB1, Ki67 monoclonal antibody), apoptosis (APO, in situ end labelling) and, in part, liver iron and malondialdehyde determination. Apoptosis was similar in all patient subgroups and correlated with hepatitis grading (P=0.002) and ALT levels (P=0.004); cytoproliferation (MIB1) levels were higher in HCV patients, both as a whole and in the periportal area (P=0.02 and P=0.03). MIB1 correlated with ALT levels (P=0.0001), hepatitis grading (P=0.02) and tissue iron (P=0.04). APO and MIB1 were higher in patients with than in those without cirrhosis (P=0.0006 and P=0.03, respectively). APO correlated with MIB1 (P=0.001), overall but not in HCV patients. The MIB1/APO ratio was significantly higher in HCV patients than in the other groups (P=0.02). In summary, cytoproliferation is more pronounced in chronic HCV-related hepatitis, while APO is not significantly higher than in other types of liver damage, suggesting an imbalance between the two. APO and MIB1 are directly related to the extent of liver damage and, from a biochemical point of view, to tissue iron levels.
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PMID:Imbalance between cytoproliferation and apoptosis in hepatitis C virus related chronic liver disease. 1115 50

The aim of the present study was to determine the apolipoprotein A (APO-A) an the high density lipoprotein (HDL) plasma concentrations in 25 patients with alcoholic liver cirrhosis. To evaluate the severity of liver disease serum albumin, bilirubin and total bile acids were measured. The serum level of APO-A and HDL was significantly lower in patients with alcoholic liver cirrhosis than in normal controls (p < 0.01) and markedly lower in patients with advanced liver cirrhosis. Apolipoprotein A concentrations in plasma correlated positively with serum albumin (p < 0.01) and negatively with serum bilirubin (p < 0.01) and bile acids (p < 0.01). Thus, he apoliprotein A level seems to reflect the severity of liver disease.
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PMID:[Apolipoprotein A in patients with alcoholic liver disease]. 1797 96

The human circulation contains cell-free DNA and non-coding microRNA (miRNA). Less is known about the presence of messenger RNA (mRNA). This report profiles the human circulating mRNA transcriptome in people with liver cirrhosis (LC) and hepatocellular carcinoma (HCC) to determine whether mRNA analytes can be used as biomarkers of liver disease. Using RNAseq and RT-qPCR, we investigate circulating mRNA in plasma from HCC and LC patients and demonstrate detection of transcripts representing more than 19,000 different protein coding genes. Remarkably, the circulating mRNA expression levels were similar from person to person over the 21 individuals whose samples were analyzed by RNAseq. Liver derived circulating transcripts such as albumin (ALB), apolipoprotein (APO) A1, A2 & H, serpin A1 & E1, ferritin light chain (FTL) and fibrinogen like 1 (FGL1) were significantly upregulated in HCC patient samples. Higher levels of some of these liver-specific transcripts in the plasma of HCC patients were confirmed by RT-qPCR in another cohort of 20 individuals. Several less abundant circulating transcripts associated with cancer were detected in most HCC samples, but not in healthy subjects. Liver specificity of circulating transcripts was confirmed by investigating their expression in HCC tumor and liver cancer cell lines. Liver specific mRNA sequences in the plasma were predominantly present outside circulating extracellular vesicles. Conclusions: The circulating "mRNA" transcriptome is remarkably consistent in diversity and expression from person to person. Detection of transcripts corresponding to disease selective polypeptides suggests the possibility that circulating mRNA can work as a biomarker analyte for cancer detection.
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PMID:Profiling the circulating mRNA transcriptome in human liver disease. 3257 66