[Nursing of patients with liver cirrhosis. Liver cirrhosis and control of alcohol drinking--implementation of health instructions].
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Alcohol Drinking↗
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[Liver cirrhosis, liver neoplasms, and alcohol].
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Adult↗
Decision-making model for a non-invasive diagnosis of compensated liver cirrhosis.
Liver biopsy is used as a gold standard in the diagnosis of chronic liver disease. However, this procedure is not without risk to the patients. This study was aimed to evaluate whether clinical, ultrasonographic, and biochemical variables may discriminate between well-compensated liver cirrhosis and non-cirrhotic chronic liver disease. Logistic regression analysis was used to assess the independent predictive value of each variable. Moreover, the post-test probability of the diagnostic variables was converted into "weights" which positively correlated with the likelihood of diagnosis of liver cirrhosis. We applied a decisional rule based on the diagnostic "weight" of each variable to 412 patients, 278 with well-compensated liver cirrhosis and 134 with non-cirrhotic chronic liver disease, diagnosed by liver biopsy with/without laparoscopy. By adding the diagnostic "weights" of each variable, liver cirrhosis and non-cirrhotic chronic liver disease were correctly diagnosed in 67% and 75% of cases, respectively. This result was validated in a split sample of 100 patients (50 with compensated liver cirrhosis and 50 with non-cirrhotic chronic liver disease) randomly selected from the acquisition sample. Based on this data, diagnosis of well-compensated liver cirrhosis can be reached in over 67% of cases without using invasive procedures. However, a prospective study is needed to confirm the clinical reliability of this method.
Adult↗
[Differentiation alcoholic liver cirrhosis from viral liver cirrhosis].
Liver cirrhosis (LC) in habitual drinkers is divided into three categories: (1) alcoholic LC, (2) LC due to hepatitis C virus and alcohol, and (3) LC due to hepatitis C virus. In Japan, the frequency of LC related to hepatitis B virus in habitual drinkers is comparatively low. Although making a distinct differentiation is very difficult, it is possible to point out some characteristics which ars due to either alcohol or hepatitis C virus: (1) multiple spider angioma, acne rosacea, and palmar erythema are more frequently found in categories 1 and 2 than in 3, (2) levels of AST/ALT, gamma-GTP, TG, ALP, lactate, and UA are higher in category 1 than in 3, (3) enlargement of both lobes is observed in category 1, and (4) abnormality due to alcohol improves relatively soon after abstinence of alcohol.
Alanine Transaminase↗
Gene therapy for liver cirrhosis.
Liver cirrhosis is the irreversible end result of chronic liver disease and is characterized by fibrous scarring and hepatocellular regeneration. It is a major cause of morbidity and mortality worldwide and is induced by factors such as chronic hepatitis virus infection, drug abuse and alcohol abuse. The ideal strategy for the treatment of liver cirrhosis should include prevention of fibrogenesis, stimulation of hepatocyte mitosis and reorganization of the liver architecture. Hepatocyte growth factor (HGF) gene therapy has been investigated in a rat model of liver cirrhosis. In rats with lethal liver cirrhosis produced by dimethylnitrosamine, repeated transfection of the HGF gene into skeletal muscle induced a high plasma level of HGF and tyrosine phosphorylation of the c-Met/HGF receptor. Hepatocyte growth factor gene transduction inhibited fibrogenesis and hepatocyte apoptosis and also produced resolution of fibrosis in the cirrhotic liver. Hepatocyte growth factor gene therapy may have the potential to be useful for the treatment of patients with liver cirrhosis.
Animals↗
[Progress in gene therapy of liver cirrhosis].
Liver cirrhosis is a common progressive pathological lesion in the late stage of chronic liver disease, which is characterized by disorganization of normal hepatic structure of regenerative nodules and hyperplasia of fibrotic tissues. In recent years, with the development of molecular biology, the molecular mechanisms underlying liver cirrhosis has been revealed more and more, which makes the therapy at the gene level possible. The ideal strategy for the treatment of liver cirrhosis should include prevention of fibrogenesis, stimulation of hepatocyte proliferation and reorganization of the liver architecture. Several gene therapy approaches for treatment of liver cirrhosis have been developed by transfer of some genes of cytokines and enzymes (e.g. HGF, TGF beta 1R, MMPs). These gene therapies can inhibit fibrogenesis and hepatocyte apoptosis and also produce resolution of fibrosis in the cirrhotic liver. Thus, gene therapy may be potentially useful for the treatment of liver cirrhosis, which is otherwise fatal and untreatable by conventional therapy.
Animals↗
[Persectives on postgenome medicine: Gene therapy for liver cirrhosis].
Liver cirrhosis is the irreversible end result of chronic liver disease, characterized by diffuse disorganization of the normal hepatic structure of regenerative nodules and fibrotic tissue. It is associated with prominent morbidity and mortality, and is induced by many factors. The ideal strategy for the treatment of liver cirrhosis should include prevention of fibrogenesis, stimulation of hepatocyte mitosis, and reorganization of the liver architecture. We have developed a novel gene therapy approach for rat liver cirrhosis by muscle-directed gene transfer of hepatocyte growth factor(HGF). HGF gene transduction inhibited fibrogenesis and hepatocyte apoptosis, and also produced resolution of fibrosis in the cirrhotic liver. Thus, HGF gene therapy may be potentially useful for the treatment of patients with liver cirrhosis, which is otherwise fatal and untreatable by conventional therapy.
Animals↗
Growth inhibition and apoptosis in liver myofibroblasts promoted by hepatocyte growth factor leads to resolution from liver cirrhosis.
Liver cirrhosis is characterized by hepatic dysfunction with extensive accumulation of fibrous tissue in the liver. In response to chronic hepatic injury, hepatic portal myofibroblasts and activated hepatic stellate cells (HSCs) play a role in liver fibrosis. Although administration or gene expression of hepatocyte growth factor (HGF) leads to improvement in hepatic fibrosis/cirrhosis, the related mechanisms are not fully understood. We investigated mechanisms involved in resolution from liver cirrhosis by HGF, focusing on growth regulation and apoptosis in portal myofibroblasts. Cultured rat HSCs could not proliferate, were withdrawn after passage, and were replaced by proliferating portal myofibroblasts during the passages. In quiescent HSCs, c-Met receptor expression was undetected whereas c-Met receptor expression was detected in activated HSCs and liver myofibroblasts expressing alpha-smooth muscle actin (alpha-SMA), suggesting that activated HSCs and portal myofibroblasts are targets of HGF. For cultured rat portal myofibroblasts, HGF counteracted phosphorylation of extracellular signal-regulated kinase (Erk) 1/2 and mitogenic stimulus induced by platelet-derived growth factor, induced c-jun N-terminal kinase (JNK) 1 phosphorylation, and promoted apoptotic cell death. In the dimethylnitrosamine rat model of liver cirrhosis, administration of HGF suppressed proliferation while promoting apoptosis of alpha-SMA-positive cells in the liver, events that were associated with reduced hepatic expressions of alpha-SMA and histological resolution from liver cirrhosis. Growth inhibition and enhanced apoptosis in portal myofibroblasts by HGF are newly identified mechanisms aiding resolution from liver fibrosis/cirrhosis by HGF.
Adipocytes↗
A comparison of an open and laparoscopic appendectomy for patients with liver cirrhosis.
Liver cirrhosis is a critical factor contributing to morbidity and mortality in abdominal surgery, because patients with cirrhosis have a particularly high risk of developing bleeding, infection, and ascites. Laparoscopic appendectomy (LA) recently has gained a lot of attention around the world; however, comparisons between the benefits of LA and those of conventional open appendectomy (OA) for patients with liver cirrhosis have yet to be sufficiently compiled. In the present retrospective study, 40 patients with liver cirrhosis who were diagnosed with acute appendicitis before surgery underwent an appendectomy (OA in 25 patients and LA in 15 patients). This study focused on the operative time, amount of postoperative pain, use of analgesics, the restart of a normal diet, number of complications, length of hospital stay, and cost-effectiveness of the procedure in such patients. The amount of postoperative pain and the length of hospital stay were significantly smaller in the LA group. The mean values of the serum C-reactive protein on postoperative days 1, 3, and 7 were significantly less in the LA group. The number of wound infections and wound bleeding was also less in the LA group. The difference in the total cost of hospitalization was not significant. The cost of the operation was greater in the LA group than in the OA group, whereas the hospitalization cost in the LA group was less than that in the OA group. The results of this study suggest that LA may be superior to OA for the treatment of postoperative pain and postoperative complications for patients with liver cirrhosis. Long-term follow-up studies are still necessary, however, to determine any possible decrease in the number of late complications.
Aged↗
[Relation of laboratory parameters to complications of liver cirrhosis].
Liver cirrhosis is characterized with alterations in hepatocytic perfusion, decreasing in number of hepatocytes and with seriously impared synthetic function of liver (hypoalbuminemy, inversion of albumino-globulinic ratio, hypoprothrombinemia). In a group of patients, suffered of liver cirrhosis with complication, we attempted to establish relationships between some of the typical clinical values: body weight in function of ascites evacuation, protein, albumin and value of prothrombin time in function of different groups of activity of aminotransferase in sera (AspAT, AlaAT) of improved and dead patients. We found a positive correlation for different groups of aminotransferase activities and laboratory values typical for liver cirrhosis with complications.
Alanine Transaminase↗
Liver transduction with a simian virus 40 vector encoding insulin-like growth factor I reduces hepatic damage and the development of liver cirrhosis.
Liver transplantation is the only treatment for advanced liver cirrhosis. Therapies halting the progression of the disease are urgently needed. Administration of recombinant insulin-like growth factor-I (rIGF-I) induces hepatoprotective effects in experimental cirrhosis. Therefore, we analyzed the efficacy of a recombinant simian virus 40 vector (rSV40) encoding IGF-I (rSVIGF-I) to prevent cirrhosis progression. First, transgene expression was evaluated in mice injected with rSV40 encoding luciferase, which showed long-term hepatic expression of the transgene. Interestingly, luciferase expression increased significantly in CCl(4)-damaged livers and upon IGF-I administration, thus liver injury and IGF-I expression from rSVIGF-I should favor transgene expression. rSVIGF-I therapeutic efficacy was studied in rats where liver cirrhosis was induced by CCl(4) inhalation during 36 weeks. At the end of the study, the hepatic levels of IGF-I and IGF-binding protein 3 were higher in rSVIGF-I-treated rats than in control cirrhotic animals. Cirrhotic rats treated with rSVIGF-I had reduced serum bilirubin, transaminases and liver fibrosis scores and increased hepatic expression of hepatocyte growth factor and STAT3alpha as compared to cirrhotic animals. Furthermore, cirrhotic animals showed testis atrophy and altered spermatogenesis, whereas testicular size and histology were normal in cirrhotic rats that received rSVIGF-I. Therefore, rSV40-mediated sustained expression of IGF-I in the liver slowed cirrhosis progression.
Animals↗
Renal dysfunction in liver cirrhosis.
Liver cirrhosis is an escalating health problem attributed to numerous causes, including an increase in alcohol consumption, morbid obesity and chronic viral hepatitis. The circulatory disturbances seen in advanced cirrhosis lead to the development of ascites, which often lead to progressive renal impairment or the development of hepatorenal syndrome. Furthermore, cirrhotic patients commonly experience clinical situations that predispose them to the development of pre-renal failure, such as dehydration, hypovolaemia, septic shock, or exposure to nephrotoxic drugs. This article provides an overview of the main causes of acute renal failure in liver cirrhosis and describes the current medical and nursing management.
Acute Kidney Injury↗
[Induction of experimental splenomegaly with portal hypertension in rats with liver cirrhosis].
Liver cirrhosis was induced in rats by administering thioacetamide (TAA), and portal hypertension was maintained for at most 35 weeks to study the influence of portal hypertension on the weight of spleen and splenic tissues. TAA was intraperitoneally injected at dose of 200 mg/kg three times a week. The portal pressure was elevated and the weight of the spleen increased with the progression of hepatic fibrosis due to TAA. Liver cirrhosis was obviously observed after TAA was administered 60 times. The maximum ratio of the weight of the spleen to body weight in the group administered TAA was higher by 4.08 times than that in the control group. In all 49 rats used in the experiment there was a high correlation (r = 0.930, p less than 0.01) between the portal pressure and the ratio of spleen to body weight. Histological observation revealed that the red pulp tended to be enlarged, while the white pulp tended to be reduced, with increases in portal pressure and weight of the spleen. It also histologically revealed an increase in the splenic sinus-like structure, narrowing of the splenic cords, fibrosis due to reticular cell proliferation in the red pulp and fibrosis around the central artery in the white pulp. These histological changes in rats were similar to the histological findings of splenomegaly accompanying portal hypertension in humans. This suggests that the animal model prepared in the present experiment is useful as a model of splenomegaly due to portal hypertension.
Animals↗
[Study on improvement of liver cirrhosis and liver function in hepatolenticular degeneration patients treated with integrated Traditional and Western medicine].
OBJECTIVE: To observe the effects of sodium dimercaptosulphonate (DMPS) plus Gandou tablet, DMPS and calcium disodium ethylene diaminotetraacetate (EDTA) on improving liver cirrhosis and liver function of hepatolenticular degeneration (HLD) patients. METHODS: One hundred and forty-six HLD patients were divided into A, B, C three groups, and treated with DMPS plus Gandou tablet, DMPS and EDTA respectively, the therapeutic course was 8 weeks for three groups. The ultrasonography of liver, electrophoresis of serum protein and excretion of urinary copper were observed. RESULTS: The ultrasonography of liver was improved in all groups, the rate of improvement of group A was 54.0%, B was 44.0% and C was 39.1%. The amounts of serum albumin in A and B groups increased (P < 0.01, P < 0.05), and gamma-globulin decreased in all groups (P < 0.05). The excretion of urinary copper increased obviously in all groups (P < 0.01), and A, B groups increased more than that of C group (P < 0.05). CONCLUSIONS: The de-copper therapy could improve liver cirrhosis and liver function. The effect of DMPS plus Gandou tablet was better than that of DMPS and EDTA.
Adolescent↗
[Liver cirrhosis and liver cancer associated with viral hepatitis B and C in republic of Tatarstan].
Clinical and epidemiological data on 93 patients with liver cirrhosis, treated in the Gastroenterological Department of the Republican Clinical Hospital of the of the Republic of Tatarstan MoH in 1998-2000 were analyzed. The retrospective analysis of 856 cases of the liver cancer, diagnosed in the Republic of Tatarstan in 1996-2000, was made. In 20.4% of patients with liver cirrhosis and 16.2% of patients with liver cancer, registered in the Republic of Tatarstan, the serological markers of hepatitis B (HB) and hepatitis C (HC) were detected. The domination of HC markers was observed in the liver cirrhosis and that of HB markers in the cancer of the liver. The liver cirrhosis with HC markers was more often registered in the age group of 45-60 years and with HB markers at the age over 60 years, while the cancer of the liver was more often registered in persons aged 75 years and older. The necessity of introducing the official registration of the liver cirrhosis and cancer associated with chronic infection caused by hepatoviruses B and C is confirmed.
Adolescent↗
Evaluation of 13C-phenylalanine and 13C-tyrosine breath tests for the measurement of hepatocyte functional capacity in patients with liver cirrhosis.
Liver disease is associated with an abnormal elevation of the plasma concentrations of the aromatic amino acids phenylalanine and tyrosine. The liver is the main site of aromatic amino acid metabolism, particularly the hydroxylation of phenylalanine to tyrosine and further tyrosine degradation. In the present study, we have examined the usefulness of the L-[1-13C]phenylalanine breath test (13C-PheBT) and L-[13C]tyrosine breath test (13C-TyrBT) for the detection of hepatic damage in patients with liver cirrhosis. First, the time courses of 13CO2 excretion after the administration of L-[1-13C]phenylalanine and L-[1-13C]tyrosine were compared. The peak times (the time expressed in minutes at which 13CO2 excretion was maximal) were 20 min in both breath tests, but 13C-TyrBT gave a higher peak than 13C-PheBT. Next, the parameters of 13C-PheBT and 13C-TyrBT were compared with biochemical liver function test values. These parameters were well correlated with several liver blood test values conventionally regarded as measures of hepatocyte functional reserve. Therefore, 13C-PheBT and 13C-TyrBT may be useful to assess the degree and progression of hepatic dysfunction.
Adult↗
Liver cirrhosis and "liver" diabetes mellitus are linked by zinc deficiency.
The association between liver cirrhosis and variations of glucose tolerance has been extensively documented and discussed. Zinc is an essential trace element necessary for normal protein metabolism, for the function of more than 200 zinc metalloenzymes, and for a host of physiologic functions. A poor zinc status is common in both liver cirrhosis and diabetes mellitus. Many of the clinical features of liver cirrhosis and diabetes mellitus have been linked to zinc deficiency. Zinc supplementation improved in patients with liver cirrhosis and hepatic encephalopathy with and without diabetes mellitus neurological symptoms and signs of malnutrition. Furthermore, zinc supplementation increased glucose disposal. Summarising these facts, we hypothesise that zinc deficiency is a link between liver cirrhosis and the "liver" diabetes mellitus.
Glucose Intolerance↗
Ascites and spontaneous bacterial peritonitis in patients with liver cirrhosis.
Liver cirrhosis is a frequent phenomenon in chronic liver diseases such as hepatitis B, hepatitis C, alcohol-related liver damage, autoimmune hepatitis and hemochromatosis. Ascites is the most frequent complication of cirrhosis. We discuss pathogenesis, diagnosis and state-of-the-art clinical management of ascites with emphasis on recent promising developments, such as covered transjugular intrahepatic portosystemic shunt (TIPS). Spontaneous bacterial peritonitis occurs in up to 10% of patients with ascites because of bacterial overgrowth with translocation through the increased permeable small intestinal wall and impaired defence mechanisms. The addition of albumin to standard antibiotic therapy may decrease mortality of spontaneous bacterial peritonitis by decreasing the incidence of renal insufficiency. Patients with coexistent marked hyperbilirubinaemia or pre-existent renal impairment could benefit from adjuvant albumin. Probiotics (bacterial food supplements) have been claimed to improve the state of underlying liver disease and may be useful in the primary and secondary prevention of spontaneous bacterial peritonitis.
Anti-Bacterial Agents↗