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PubMed2005

Specific gene expression patterns in liver cirrhosis.

Liver cirrhosis (LC) is a complex disease that can develop into hepatocellular carcinoma (HCC). In an effort to investigate genetic differences between LC and HCC, we used cDNA microarray analysis to characterize the gene expression profiles in LC and HCC tissues. Consistent differences were observed among the expression patterns in LC, HCC, and normal liver tissues. Interestingly, the expression patterns of LC without tumor association (LCT) were also readily distinguished from those of LC tissues near hepatic tumor tissues (near-tumor tissue, NTT). Moreover, 25 cirrhosis-specific genes could be used to divide the NTT samples into two groups: inflammatory active cirrhosis (NTTa) and inflammatory inactive cirrhosis (NTTi). We found that NTTa samples showed gene expression patterns similar to those of the LCT and HCC groups, whereas the expression patterns of the NTTi group were significantly different from those of the LCT, NTTa, and HCC groups. Finally, we selected two of the 25 LC-specific genes and showed that these markers could be used to successfully discriminate among the different LC subtypes. Collectively, these novel results allow the identification of new genetic subgroups of LC and provide new candidate genes for use as early markers for active cirrhosis and HCC.

Biomarkers, Tumor↗
PubMedDate not supplied

Cimetidine prevents and partially reverses CCl4-induced liver cirrhosis.

Liver injury produced by CCl4 depends on its metabolism by the liver cytochrome P450 enzyme system to a highly reactive intermediate (CCl3.). Cimetidine impairs cytochrome P450 and stimulates regenerative processes acting on DNA synthesis. This work was performed to investigate whether cimetidine may prevent CCl4-induced liver cirrhosis. Male Wistar rats were used: animals in group 1 received CCl4 (0.04 g per 100 g, i.p.) three times a week for 8 weeks; group 2 was treated with CCl4 plus cimetidine (120 mg kg-1, p.o.) three times a week for 8 weeks; group 3 received CCl4 for 8 weeks and then cimetidine for 4 weeks. Alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminotransferase (ALT) activities, as well as protein and bilirubin, were measured in serum; collagen and lipoperoxidation were quantified in liver. Intoxication with CCl4 increased (P < 0.05) serum activities of alkaline phosphatase, gamma-GTP and ALT, and bilirubin concentration; liver collagen and lipoperoxidation were also increased. Cimetidine treatment prevented or reverted the increases in the three enzyme activities and in bilirubin content and the fall in proteins. It is worth noting that cimetidine co-treatment completely prevented both the increase in collagen content and the lipid peroxidation. The protective effect of cimetidine can be attributed to a reduction in cytochrome P450. However, it could also stimulate regenerative processes.

Alanine Transaminase↗
PubMed1990

Physico-chemical factors predisposing to pigment gallstone formation in liver cirrhosis.

Liver cirrhosis is associated with a high prevalence of pigmentary cholelithiasis. The major compound of pigment gallstones is unconjugated bilirubin (UCB) in the form of calcium bilirubinate salts or a black pigment polymer. Most of UCB in bile derives from enzymic or non-enzymic hydrolysis of mono- or diconjugated bilirubin. Changes in the relative ratios between these two bilirubin species have been associated with pigment gallstones. It has also been shown that UCB solubilization in bile depends on its interaction with bile salts. In order to clarify the factors predisposing cirrhotic patients to pigment stone formation, we measured UCB, monoconjugated bilirubin (MCB) and diconjugated bilirubin (DCB) in duodenal bile of 15 patients with cirrhosis, ten patients with chronic active hepatitis (CAH) and ten normal subjects, we also analyzed their relationships with lipids. In cirrhotic patients, the MCB concentration in bile was significantly (p less than 0.05) higher than in normal subjects and was correlated with the severity of the disease. Bile salts and lecithin concentrations were significantly lower in cirrhosis (p less than 0.005 vs. CAH or normals). Cirrhotic patients have a bile salts/UCB molar ratio which is one third that of CAH patients or normal subjects (p less than 0.01). No differences were found between CAH patients and controls in each of the parameters tested. In conclusion, we propose that the very low BS/UCB molar ratio and the very high biliary content in MCB represent two independent physico-chemical factors predisposing cirrhotic patients to pigmentary cholelithiasis.

Aged↗
PubMed1985

[The disorder of vitamin D metabolism in patients with liver cirrhosis].

Liver cirrhosis (LC) is often associated with osteomalacia and osteoporosis. Since it has been shown that serum levels of 25 hydroxy vitamin D (25-OH-D) are reduced in LC, defective hepatic hydroxylation of vitamin D has been postulated to be responsible for the low serum 25-OH-D levels and skeletal demineralization. This study was designed, therefore, to determine serum 25-OH-D and 1 alpha, 25-(OH)2-D levels in patients with LC. Further, the response of serum 1 alpha, 25-(OH)2-D to a single oral dose of 1 alpha-OH-D3 (2 micrograms) was investigated. In 5 patients with severe decompensated LC and 3 patients with compensated LC, serum 25-OH-D and 1 alpha, 25-(OH)2-D levels were respectively measured by the modified method of Belsey and by that of Eisman. Serum 25-OH-D in patients with compensated and decompensated LC was significantly higher than that in normals. Serum levels of 1 alpha, 25-(OH)2-D in patients with decompensated LC were significantly lower than those in patients with compensated LC and normals. After a single oral administration of 1 alpha-OH-D3 at a dose of 2 micrograms, the 1 alpha, 25-(OH)2-D rose in each patient within 6h, reaching the maximum levels at 12h. The percent increase over the basal value in decompensated LC was similar to that in compensated LC.(ABSTRACT TRUNCATED AT 250 WORDS)

Dihydroxycholecalciferols↗
PubMed1982

[Liver cirrhosis and liver cancer--types, clinical courses, and progress in their treatment].

There have been several controversies about classification of liver cirrhosis between Western countries and Japan. By the follow-up studies for 5 years on 478 cirrhotic patients diagnosed in Osaka area, relatively higher survival rates were found in cases without HBs-antigen and in heavy drinkers, whereas cases of cryptogenic type showed poor prognosis. The most marked progress in diagnostic procedures in this field seems to be several imaging techniques such as scintiphotography, U.S. echography and computed tomography. Analysis obtained by serial observations on imaging films would be valuable in differentiation between hepatoma and liver cirrhosis. Remarkable improvement has been shown in examinations on etiologic factors, degree of impairment of liver cell functions and precise evaluation of pathophysiological status of patients. Although it is our great regret that radical procedure to cure patients suffering from liver cirrhosis or hepatoma has not yet been known, several palliative treatments have become practical in recent years. For example, percutaneous transhepatic portal occlusion or injection of sclerosing agents for bleeding esophageal varices, parenteral feeding using adjusted amino acids pattern solution for impending coma and selective arterial embolization by sponges or coils infused with anticarcinogenic drugs for inoperable hepatoma have been used and effective to prolong survival period of these patients.

Ascites↗
PubMed1990

[The effect of smoking and drinking habit on the process from liver cirrhosis to liver cancer].

A retrospective cohort study of liver cirrhosis cases was carried out. 270 cases of liver cirrhosis which were confirmed histologically from 1972 to 1981 at Juntendo University Hospital, were followed up until the end of 1988. The average observation period for these cases was 74 months or 6.2 years, and we found 141 death cases including 46 of primary liver cancer (PLC). The analysis of survival rate revealed that the smoking group had a slightly higher death rate of PLC than non-smokers, and the ex-smoker group had a much higher survival rate than the continuous smoking group. On the other hand, it was found that the alcohol-drinking group had a much lower death rate of PLC than the non-drinkers group, and that there was no difference of the survival rate among drinkers, non-drinkers and ex-drinkers.

Adult↗
PubMed1975

[Comparison of laparoscopic and scintigraphic findings in chronic hep-titis, liver cirrhosis and liver tumours (author's transl)].

Results of laparoscopy and scintigraphy were compared and contrasted with ultimate clinical diagnosis in 94 patients with chronic hepatitis or liver cirrhosis and 38 with liver tumours. The findings agreed in 77 cases of chronic hepatitis and cirrhosis and 33 of liver tumour. In the remainder either laparoscopy or scintigraphy gave the wrong results. In one case each of cirrhosis and liver metluded that (1) laparoscopy and scintigraphy are methods complementing but not replacing other clinical tests; (2) if diffuse liver disease is suspected clinically the diagnosis can essentially be done only by laparoscopy and selective biopsy or blind liver biopsy but not scintigraphy; (o) if a circumscribed condition is suspected, scintigraphy is among the most important screening tests, but cannot replace laparoscopy, biopsy or angiography for confirming the diagnosis; (4) liver scan is an important method, of little stress to the patient, in following the progress of chronic hepatitis and liver cirrhosis, additional to clinical examination, enzyme tests, laparoscopy and histology.

Angiography↗
PubMed2006

The antifibrotic effect of TGF-beta1 siRNAs in murine model of liver cirrhosis.

Liver fibrosis results from chronic damage to the liver by chronic hepatitis, alcohol, and toxic agents. A characteristic of liver fibrosis is an accumulation of extracellular matrix (ECM) protein, which distorts the hepatic architecture by forming a fibrous scar, and the subsequent development of regenerating nodules defines cirrhosis. Transforming growth factor (TGF)-beta1, one of the most powerful profibrogenic mediators, plays a major role in the development of liver cirrhosis and regulates ECM gene expression and matrix degradation. This study elucidates the changes of TGF-beta1-mediated signals during liver fibrogenesis by using RNA interference. In this experiment, the TGF-beta1 siRNAs reduced the expression of TGF-beta1 in the livers of CCl(4) injection compared with those of control group, and the expression of type I collagen and alpha-smooth muscle actin was decreased. In conclusion, this study demonstrates that TGF-beta1 siRNAs inhibit TGF-beta1 expression in the murine model of liver cirrhosis and might be a good therapeutic strategy to prevent liver cirrhosis in human.

Actins↗
PubMed1993

Liver cirrhosis and liver cancer. A study of their relationship in 2563 autopsies.

A sample of 2,563 cases of liver cirrhosis diagnosed among 26,879 autopsies performed consecutively in the years 1976/85 was considered in order to study the morphologic feature of the liver cirrhosis and their relationship with primary liver cancer (PLC) outbreak. The study showed that age of patients affected by cirrhosis is a significant risk factor for PLC. In fact, in the 10 years considered, the observed mean annual increase of age at death of the cirrhotic patients was associated with an increase in PLC cases. This may be explained as a well known consequence of the conversion of micronodular type of cirrhosis to mixed and macronodular ones (for which cancer complication is more frequent) but also as a statistically significant higher risk of PLC in the older group of patients affected by micronodular cirrhosis. The older age of cirrhotic patients at death observed in the last few years in the Trieste area is probably correlated to a general European trend: our results, although relative to a restricted geographic area, seem to be of interest in order to identify better the patients at risk of PLC among those affected by cirrhosis.

Aged↗
PubMed1989

Unusually rapid development of a HBsAG-positive liver cirrhosis after liver transplantation.

We report the case of a 44-year-old man who was transplanted in 1986 for hepatocellular carcinoma in a HBsAG-positive liver cirrhosis. The patient had no severe complications postoperatively. He received passive immunization for the prevention of hepatitis B reinfection during the first 6 months after liver grafting. Twelve months after the transplantation the new liver was reinfected with hepatitis B virus. Without any clinical or laboratory signs of severe hepatitis, the patient developed a histologically proven complete liver cirrhosis within 8 months after reinfection of the graft. The reasons for this might have been, first, a deleterious course of the infection under immunosuppressive therapy, and, second, the additional influence of a postoperatively acquired CMV infection or the combined toxic influence of cyclosporin A and its metabolites on the acute inflammation in the liver.

Adult↗
PubMed1992

[Effect of ursodeoxycholic acid (UDCA) therapy for compensatory liver cirrhosis on liver function tests and serum bile acid metabolism].

Effect of ursodeoxycholic acid (600 mg/day 12 weeks) on liver function tests and bile acid metabolism were investigated in 6 patients with compensatory liver cirrhosis (CLC) and 6 with chronic active hepatitis (CAH). Serial determination of serum GOT, GPT and gamma-GTP after the initiation of UDCA revealed significant reduction in mean levels of these enzymes after 4 weeks, and further improvement was observed at the end of the 12-weeks treatment regimen (CLC: 79.3%, 81.1%, 51.5% of initial values, respectively, CAH: 61.2%, 59.3%, 42.8%). On the other hand, after UDCA administration, serum total bile acid increased and UDCA became the predominant bile acid in CLC and CAH patients. Other endogenous bile acids decreased in both groups, but reduction rate of serum chenodeoxycholic acid level in CLC was smaller than that in CAH group (CLC: 86.1% of initial values, respectively, CAH: 54.2%). During UDCA treatment, apparent side effect was not observed. We suggest that UDCA administration might constitute effective treatment for compensatory liver cirrhosis as well as chronic hepatitis.

Adult↗
PubMed1991

Functional liver imaging with 99Tcm-galactosyl-neoglycoalbumin (NGA) in alcoholic liver cirrhosis and liver fibrosis.

Synthesis of 99Tcm-galactosyl-neoglycoalbumin (99Tcm-NGA), a recently described new radioligand with high specificity for hepatic binding protein (HBP), a galactose-residue specific receptor on hepatocytes, was carried out by covalent coupling of 2-imino-2-methoxyethyl-1-thio-beta-D-galactopyranoside to the primary amino groups of human serum albumin. NGA was purified by ultrafiltration and size exclusion high-pressure liquid chromatography (HPLC). Using a computer-based simulation program, time-activity data for the liver and precordium, blood radioactivity 2 min after i.v. injection of the radioligand, the association constant of 99Tcm-NGA-binding to HBP measured on human liver biopsies in vitro, and other patient-related parameters were put into a five-state non-linear model describing the pharmacokinetics of 99Tcm-NGA. By fitting the parameters of the model iteratively to the experimental data, an estimate of HBP concentration in the liver and of total liver blood flow was obtained. Using this model we studied 32 patients (53 +/- 11 years) with different clinical stages of alcoholic liver cirrhosis. Child B and Child C stage cirrhotic patients had a lower HBP concentration in the liver compared to control individuals (0.96 +/- 0.21 mumol l-1). The group with the most advanced cirrhosis (Child C stage) had a significantly lower HBP concentration (0.27 +/- 0.15 mumol l-1) than Child A patients (0.66 +/- 0.21 mumol l-1; P less than 0.01) and Child B patients (0.53 +/- 0.18 mumol l-1; P less than 0.05). In four patients with biopsy-proven liver fibrosis (0.84 +/- 0.20 mumol l-1) no difference in receptor concentration from normal individuals was estimated. Changes in liver blood flow were not significant between the groups. A direct comparison of HBP concentration estimated in vivo by 99Tcm-NGA functional imaging and HBP concentration measured in vitro on a surgically removed liver biopsy specimen from the same patient with a normal liver and liver cirrhosis showed good matching of these two values. The results suggest that in vivo estimation of HBP concentration in the liver by 99Tcm-NGA functional imaging might be a suitable method for determining liver cell mass.

Adult↗
PubMed1997

Does the concentration of alpha 1-proteinase inhibitor reflect the transformation of liver cirrhosis to liver carcinoma?

Serum concentration of alpha1-proteinase inhibitor (alpha1-PI) was determined by nephelometric method in forty seven patients with liver cirrhosis (LC) and fifteen patients with hepatocellular carcinoma (HCC). Our data show an increase in the concentration of alpha1-PI in the group with decompensated LC by 17% and in HCC by 29%. The level of alpha1-PI higher than (220 mg%) may be indicative of the disease progression towards decompensated LC or HCC. In the conclusion, an increase in alpha1-PI concentration in patients with LC may be considered as an alarming factor, but is not sufficiently specific to become a diagnostic tool for the detection of HCC development.

Adult↗
PubMed1984

Diagnosis of hepatocellular carcinoma in patients with liver cirrhosis using liver function assays.

Sex, age and 21 routine liver function assays were analyzed by stepwise selection and the best-of-all-possible-combinations method to identify a small group of assays valuable in establishing which liver cirrhosis (LC) patients have a high risk of hepatocellular carcinoma (HCC), when alpha-fetoprotein (AFP) is not elevated. Data was obtained from 115 HCC and 122 LC patients on admission. Tumor size correlated with AFP (0.73), alkaline phosphatase (ALP, 0.47), leucine aminopeptidase (LAP, 0.42), lactic dehydrogenase (LDH, 0.42), and the glutamic oxaloacetic transaminase (GOT)/glutamic pyruvic transaminase (GPT) ratio (GOT/GPT, 0.41). The mean of the correct diagnosis rates (CDR) of HCC and LC utilizing AFP as the sole parameter (89%) was markedly higher than those of the other parameters. The best-of-all-possible-combinations method presented a more powerful combination than stepwise selection. The best combination of 7 parameters (LAP, GOT/GPT, choline esterase, one-hour erythrocyte sedimentation rate, age, albumin/globulin ratio, and total bilirubin) presented a mean CDR of 80%, HCC CDR of 77%, and false positive rate of 18%. LC patients statistically diagnosed as having HCC by these 7 parameters are proposed as high risk patients. Fourteen (78%) of 18 HCC patients who were AFP-negative were statistically diagnosed. This analysis can be applied to LC patients to distinguish those that should be followed closely by imaging diagnostic techniques.

Adult↗