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PubMed2003

Gene expression profiling of preneoplastic liver disease and liver cancer: a new era for improved early detection and treatment of these deadly diseases?

Hepatocellular carcinoma (HCC) is a multi-step process associated with changes in gene expression. Currently, several technologies enable global gene expression profiling. The number of studies to probe global gene expression profiles of HCC or preneoplastic chronic liver diseases has increased exponentially in recent years. These studies have quickly provided rich information and some additional clues to the genesis of liver cancer. The application of gene expression profiling to preneoplastic liver diseases and HCC is growing in importance and practicality. In this commentary, we review the recent advances in the utilization of global gene expression profiling to liver cancer, which have provided new insight into the molecular mechanisms underlying the development of HCC. We have also discussed the problems related to these new technologies, as well as their contributions and implications. By recognizing the shortcomings, we can reassess our current approaches, which allow us to better design and analyze global gene expression-based experiments. These new approaches will undoubtedly contribute to a better understanding of hepatocarcinogenesis.

Gene Expression Profiling↗
PubMed1984

[Ultrasound-guided thin-needle biopsy in focal liver diseases. II. Benign focal liver diseases].

Sixty patients with benign focal liver disease underwent sonography-guided percutaneous fine needle biopsy for definitive diagnosis. The benignancy of all lesions was determined accurately by cytohistologic evaluation. All 44 liquid space-occupying lesions (30 hepatic cysts, 9 abscesses, 3 hematomas, 2 serous residual cavities after surgery) could be classified by cytological, biochemical and bacterial examination. The diagnosis of hepatic hemangiomas by fine needle puncture is problematic, because the cytological identification of benign endothelial cells is difficult. The histological examination of tissue cylinders of 4 small echogenic lesions revealed focal fatty change of the liver. Tissue fragments of focal nodular hyperplasias and liver cell adenomas showed histologically typical liver cells arranged in trabecular structure. The additional identification of bile ducts supplies proof of focal nodular hyperplasia and excludes liver cell adenoma. Percutaneous puncture of liver abscesses and cysts afforded effective therapeutic decompression. Eight out of 9 liver abscesses were cured by evacuating fine needle puncture. More than 50% of the liver cysts showed long-term growth shrinkage subsequent to puncture. The histological confirmation of benign and malignant liver tumors by sonographyguided fine needle biopsy is considered a decisive step forward in the diagnostic possibilities of update imaging methods.

Adult↗
PubMed2003

Liver Transplantation for Cholestatic Liver Disease.

Liver transplantation is an effective form of therapy for patients with end-stage cholestatic disease that improves both survival and quality of life. Liver transplantation is very effective for the treatment of intractable pruritus but less effective for the treatment of lethargy. Survival rates are good (more than 70% at 5 years); these patients are at greater risk of developing acute and chronic rejection and are more likely to require long-term immunosuppression. Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) recur in the graft. Recurrent PSC may be difficult to differentiate from secondary sclerosing cholangitis, but it recurs in up to 60% of patients at 5 years and may reduce graft survival. PBC recurrence, noted in up to 40% of patients at 10 years, has little effect on graft survival with respect to cancers. Patients with PSC are at greater risk of both colonic cancer (which may be reduced by ursodeoxycholic acid) and cholangiocarcinoma. Diagnosis of cholangiocarcinoma before transplantation usually contraindicates transplantation. The main challenges facing liver transplantation are the need to expand the donor pool and the need to find immunosuppressive regimens with fewer long-term toxicities.

Journal Article↗
PubMed2004

Hepatopulmonary syndrome: a concern for the anesthetist? Pre-operative evaluation of hypoxemic patients with liver disease.

Liver cirrhosis and other chronic hepatic diseases are followed in a subset of affected patients by gas exchange abnormalities resulting from a syndrome called hepatopulmonary syndrome (HPS). The structural basis of this clinical entity is an alteration of pulmonary vasculature resulting in abnormal vasodilatation and mismatching of ventilation and perfusion of the lung. Dilatation of the capillary bed near the gas exchange area is the most important factor implicated; it precludes O2 molecules diffusing to the centrum of the dilated vessels to oxygenate venous blood. Contrast (microbubbles) echocardiography and lung perfusion scan are, respectively, the screening tests with the highest sensitivity and specificity for HPS diagnosis. Because of the high morbidity and mortality of HPS, clinicians have been trying to understand the pathophysiology of pulmonary vasodilatation in the hope that the process can be reversed pharmacologically or surgically. An imbalance between production and clearance of vasoactive circulating substances has been implicated in the pathogenesis of HPS with glucagon and nitric oxide among the principal responsible factors. To date various molecules have been implicated for therapy but without definitive positive results. Liver transplantation remains the only real therapy for HPS, and resolution of gas exchange defects outlines the possible functional reversible nature of vascular abnormalities of this syndrome. The need to perform surgery under general anesthesia for hepatic and extrahepatic procedures in patients with HPS is followed by an increased peri-operative risk. The authors emphasize the role of pre-operative clinical evaluation for proper patient management during the peri-operative period.

Anesthesia↗
PubMed1994

Monosaccharide composition of haptoglobin in liver diseases and alcohol abuse: large changes in glycosylation associated with alcoholic liver disease.

Liver damage through prolonged intake of high amounts of alcohol is a serious problem that affects many members of the population. The aim of this study was to investigate changes in the glycosylation of haptoglobin (Hp) resulting from alcoholic liver diseases. The monosaccharide composition was measured in Hp isolated from 48 healthy individuals, 15 alcohol abusers (AA); 25 patients with alcoholic liver disease, including those with alcoholic cirrhosis (ALD/AC), and 17 other patients with either chronic active hepatitis (AH) or primary biliary cirrhosis (BC). Fucose was elevated per mol of Hp in 70%, 44%, and 33% of the individuals in the ALD/AC, BC and AA groups, respectively. Fucose was not elevated in the AH group. N-acetylglucosamine was also elevated in the ALD/AC group. Expressing results per 3 mol of mannose suggested the presence of higher branching with increased fucose content in Hp from all the abnormal groups except the AH group. More structural information is required to develop the diagnostic potential of carbohydrate measurements of Hp in alcoholic liver diseases.

Acetylglucosamine↗
PubMed1984

[Serum cholesterol ester level in patients with ischemic heart disease and liver disease].

The blood serum of coronary and liver patients was shown to display a similar increase in the relative levels of cholesterololeate and a some what less marked elevation in the content of cholesterol esters with saturated fatty acids. The cholesterollinoleate concentration was enhanced in patients with viral hepatitis and decreased in coronary heart disease patients. The differences were especially distinct in changes of the relative content of cholesterolarachidonate and esters of cholesterol with eicosopentaen acid. Cholesterolarachidonate levels showed no changes in CHD whereas they lowered markedly in various diseases of the liver and biliary tracts. The role of changes in the relative content of cholesterol ester fractions in the genesis of atherosclerosis in patients with liver diseases is discussed.

Arachidonic Acids↗
PubMed1998

Hepatitis G infection: role in cryptogenic chronic liver disease and primary liver cell cancer in the UK. Trent Hepatitis C virus Study Group.

Hepatitis G virus (HGV) is a flavivirus that can cause acute hepatitis and persistent infection but its role in chronic liver disease or primary liver cancer is unproven. In this study we have examined the prevalence of HGV RNA in the serum of patients with hepatitis C virus (HCV) infection and in patients with cryptogenic chronic liver disease, including non-alcoholic steatohepatitis (NASH), and in patients with HCV-related hepatocellular carcinoma (HCC) and HCC arising in patients with cryptogenic liver disease. One-hundred and thirty patients who were positive for antibody to HCV (anti-HCV), 54 patients with cryptogenic chronic liver disease (including 17 patients with NASH) and 46 patients with hepatitis C-related (n = 27) or cryptogenic liver disease-related HCC (n = 19) were studied. HGV RNA was detected using nested reverse transcriptase-polymerase chain reaction (RT-PCR) and was found in 16.1% of patients with HCV infection. HGV RNA was not detected in any patient with cryptogenic liver disease. In patients with HCC, 7/34 samples were positive for HGV RNA and six out of seven HGV-positive subjects also had HCV infection. Only one patient with HCC in cryptogenic liver disease was positive for HGV RNA. Hence, cryptogenic liver disease in the UK is not caused by HGV/GBVc infection. It seems unlikely that HGV plays a significant role in hepatocarcinogenesis.

Carcinoma, Hepatocellular↗
PubMed1987

[Acemetacin in patients with rheumatic disease with concomitant liver diseases. Pharmacokinetics, effectiveness and tolerance].

10 male patients suffering from rheumatic diseases and from a liver disease (fat liver, cirrhosis) received acemetacin (Rantudil forte capsules) t.i.d. for 10 days. Blood levels were measured on days 2, 4, 7 and 9, 2 and 4 hours after the administration at noon, as well as after the last dose (day 10) during a 48 hours elimination period. The following kinetic parameters were determined: maximal blood level (cmax), elimination half life (during the 48 hours elimination period), area under the blood level time curve (AUC). Values are compared to corresponding data of rheumatic patients and healthy volunteers. Daily doses were 180 mg acemetacin each. Mean maximal blood levels (cmax) were 1.51 +/- 0.19 (rheumatic patients with liver diseases), 1.85 +/- 0.33 (rheumatic patients without liver diseases) and 1.24 +/- 0.05 mumol/l (healthy volunteers). Elimination half lives are 4.63 +/- 2.25, 4.52 +/- 2.81 and 4.03 hours. AUC-values were in the same range for rheumatic patients with liver diseases (11.62 +/- 5.56) and volunteers after Rantudil forte (14.30 +/- 8.79) or Rantudil retard (12.52 +/- 5.90 mumol.l-1.h). Toxic or infective liver damage therefore does not substantially change kinetics of acemetacin. The drug was efficient and well tolerated in all patients. There were no hints as for a special risk for patients with liver damage taking this drug.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Clinical usefulness of serum matrix metalloproteinase-2 concentration in patients with chronic viral liver disease.

BACKGROUND/AIMS: The production of matrix metalloproteinase (MMP)-2 was reported to be increased in chronically diseased livers. Our aims in the present study were to elucidate the clinical usefulness of the serum MMP-2 concentration in chronic viral liver disease. METHODS: We measured serum MMP-2 concentrations with a sandwich enzyme immunoassay in 62 patients with chronic hepatitis, 35 patients with liver cirrhosis, 55 patients with hepatocellular carcinoma and 24 healthy individuals. The assay detects proMMP-2 and proMMP-2 complexed with tissue inhibitor of metalloproteinase-2, but not active forms of MMP-2. The liver MMP-2 content was also measured in autopsied cirrhotic and non-cirrhotic livers. Gelatin zymography and gel filtration chromatography were carried out using the serum. RESULTS: The serum MMP-2 concentration was significantly increased in the liver cirrhosis and hepatocellular carcinoma patients, but not in the patients with chronic hepatitis. There was no significant difference in the serum MMP-2 level between the liver cirrhosis and hepatocellular carcinoma groups. In the patients with chronic viral liver disease, serum MMP-2 concentration showed the best correlation with the degree of liver fibrosis and with serum hyaluronate level. The zymography of serum showed the majority of MMP-2 in serum exists as a proMMP-2. The chromatography of serum revealed a single peak at the position of about 90 kDa corresponding to an MMP-2 complexed with tissue inhibitor of metalloproteinases-2. The liver MMP-2 content was markedly increased in the cirrhotic livers compared with the non-cirrhotic livers, and was positively correlated with the liver collagen content. When investigating the utility of the serum MMP-2 test for differentiating liver cirrhosis from chronic hepatitis, the utility of serum MMP-2 was equal to that of serum hyaluronate, which is known as the best current test for diagnosing liver cirrhosis. CONCLUSIONS: The serum MMP-2 concentration reflects mainly the amount of proMMP-2 complexed with tissue inhibitor of metalloproteinase-2. The serum MMP-2 level was markedly increased in cirrhotic patients, and may be explained by an overproduction in the cirrhotic liver. In the clinical state, the measurement of serum MMP-2 was as useful a test for diagnosing liver cirrhosis as is the serum hyaluronate level.

Biomarkers↗