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PubMed2002

A preliminary evaluation of the differences in the glycosylation of alpha-1-acid glycoprotein between individual liver diseases.

During the acute phase response (APR) to tissue injury or infection, the liver is responsible for the level of mediators such as cytokines required at the site of inflammation and providing the essential components for wound healing and tissue repair. Additionally there are substantial alterations in the expression of plasma proteins of hepatic origin such as alpha-1-acid glycoprotein (AGP). The APR also results in alterations to the branching, sialylation and fucosylation of the oligosaccharide chains of AGP. This study investigated whether liver damage could be correlated with changes in AGP glycosylation in groups of patients with various liver diseases (alcoholic liver disease, hepatitis B, hepatitis C, cirrhosis). Hyperfucosylation occurred in all cases of liver disease, although the hepatitis B and C samples showed a more significant increase in comparison with the others. Additionally N-acetylgalactosamine (GalNAc) was detected in the majority of the hepatitis C samples, which was unexpected since this monosaccharide is not a usual component of the N-linked oligosaccharide chains. It was also determined by concanavalin (con) A chromatography that there is a shift towards the increased branching of the oligosaccharide chains in inflammatory liver diseases compared to normal serum.

Adult↗
PubMed2004

Functional portal flow competition after auxiliary partial orthotopic living donor liver transplantation in noncirrhotic metabolic liver disease.

Auxilliary partial orthotopic liver transplantation (APOLT) was introduced initially as a tentative or permanent support for patients with potentially reversible fulminant hepatic failure and has extended its indication to congenital metabolic disorder of the liver that has otherwise normal functional integrity. Postoperative management of APOLT is complicated because of functional portal flow competition between the native and graft liver. The native portal vein diversion to the graft is sometimes indicated to prevent functional competition; however, it is still an open question whether this technique can be theoretically indicated for APOLT patients. The authors report a on patient with ornithine transcarbamylase deficiency who received APOLT from a living donor without native portal vein diversion. Because of functional portal vein competition between the native and graft liver, the patient had to have portal vein diversion, portal vein embolization, and finally native hepatectomy to induce the graft regeneration after APOLT. After the experience of the current case, primary portal vein diversion for APOLT with noncirrhotic metabolic liver disease patients to prevent functional portal flow competition is recommended.

Anastomosis, Surgical↗
PubMed1983

In vivo evaluation of lipoprotein cholesterol ester metabolism in patients with liver disease.

Fifteen patients with liver disease were found to have marked reductions in both plasma lecithin-cholesterol acyltransferase activity (62%) and cholesterol ester concentration (46%) when compared with 11 normal subjects. The changes in cholesterol ester concentration were confined to high-density lipoprotein and very-low-density lipoprotein; the low-density lipoprotein fraction was not significantly altered. Examination of the plasma lecithin and lipoprotein cholesterol esters revealed that patients with liver disease had significantly greater amounts of saturated and monounsaturated fatty acids and less linoleic acid than normal subjects. Lipoprotein cholesterol ester kinetic studies were carried out in 2 normal subjects and 2 severely cirrhotic patients who simultaneously received [14C]mevalonic acid and high-density lipoprotein labeled with free [3H]cholesterol. A lipoprotein cholesterol ester model was developed that fit both the 3H and 14C data. The precursors of high-density lipoprotein cholesterol esters were free cholesterol and low-density lipoprotein cholesterol esters; the distribution pattern was in favor of low-density lipoprotein cholesterol esters in both groups of subjects (71% for normals and 88% for cirrhotics). The turnover of high-density lipoprotein cholesterol esters was similar in both groups of subjects, but the flux of free cholesterol into high-density lipoprotein cholesterol esters was greatly reduced in the cirrhotic patients. In cirrhotic patients, this represented only 9% and 12% of the total lipoprotein cholesterol ester synthesized; in the normal subjects, the values were 68% and 74%. The turnover of very-low-density lipoprotein cholesterol esters was greatly suppressed in the cirrhotic patients, and their precursor sources were high-density lipoprotein cholesterol esters and tissue free cholesterol. The low-density lipoprotein cholesterol ester precursors were very-low-density lipoprotein, low-density lipoprotein, and tissue free cholesterol. In the cirrhotic patients, much greater proportions (78% and 88%) of low-density lipoprotein cholesterol ester were derived from free cholesterol. Also, the turnover rates of these esters were reduced in the cirrhotic patients. The present report has provided evidence that cirrhotic patients derive most of their plasma lipoprotein cholesterol esters from an acyl-CoA-cholesterol acyltransferase free-cholesterol tissue source--most likely the intestine. By contrast, in normal subjects, the major contribution to plasma esters is via the introduction of newly formed cholesterol esters into the high-density lipoprotein fraction.

Adult↗
PubMedDate not supplied

Antifibrotic properties of botanicals in chronic liver disease.

Cirrhosis of the liver is a major complication of various chronic liver diseases and results from excess production and decreased degradation of extracellular matrix. Proinflammatory cytokines, toxic metabolites and certain drugs can trigger enhanced fibrogenesis in hepatic stellate cells and myofibroblasts, the major matrix-producing cells. Since treatment of established cirrhosis is limited, therapeutic interventions that inhibit or mitigate fibrogenesis are needed. Numerous drugs have been investigated for their antifibrotic potential and botanicals constitute a significant fraction of them. Colchicine has been used to treat various chronic liver diseases with controversial results. To date, there is a lack of studies in appropriate animal models and well-controlled human trials to demonstrate its antifibrotic properties. Silymarin has so far failed to clearly show an antifibrotic effect in human studies, whereas animal experiments suggest that this mixture of flavolignanes may be beneficial in patients which have not yet developed cirrhosis. Animal studies indicate an antifibrotic potential of Shosaiko-to, a herbal combination frequently used in China and Japan for the treatment of chronic viral hepatitis, but mechanisms of action need to be further explored. Other botanicals include trans-resveratrol, a flavonoid extracted from grapevine, and Salvia miltiorrhiza which were shown to interfere with the process of hepatic stellate cell activation. Herbal combinations, such as compound 861 and LIV.52 were advocated as antifibrotics or hepatoprotectives, but studies in humans have either been of questionable design or resulted in cessation of the trial due to adverse outcomes.

Animals↗
PubMed2004

Angiopoietin-1 causes reversible degradation of the portal microcirculation in mice: implications for treatment of liver disease.

In many different liver diseases, such as cirrhosis, degradation of the microcirculation, including obliteration of small portal or hepatic veins contributes to disease-associated portal hypertension. The present study demonstrates the importance of angiogenesis in the establishment of arteriovenous shunts and the accompanying changes to the venous bed. One aspect of angiogenesis involves the branching of new vessels from pre-existing ones, and the molecular mechanisms controlling it are complex and involve a coordinated effort between specific endothelial growth factors and their receptors, including the angiopoietins. We modulated the hepatic vasculature in mice by conditionally expressing angiopoietin-1 in hepatocytes. In mice exposed to angiopoietin-1 during development, arterial sprouting, enlarged arteries, marked loss of portal vein radicles, hepatic vein dilation, and suggestion of arteriovenous shunting were observed. Most importantly, these phenotypic changes were completely reversed within 14 days of turning off transgene expression. Expression of excess angiopoietin-1 beginning in adulthood did not fully recapitulate the phenotype, but did result in enlarged vessels. Our findings suggest that controlling excessive angiogenesis during liver disease may promote the restoration of the portal vein circuit and aid in the resolution of disease-associated portal hypertension.

Angiopoietin-1↗
PubMed1984

Significance of serum aminograms in diagnosis and prognosis of liver diseases.

The diagnosis, prognosis, and treatment of various liver diseases are still frequently equivocal despite the various liver function tests and invasive procedures presently available to the clinician. The introduction of the Beckman Amino Acid Analyzer Model 119 Cl, greatly facilitated the determination of the individual amino acids in serum and cerebrospinal fluid, and the data thus obtained seem to help in the differentiation of some of the commoner types of liver disease. These data indicate that changes in the concentration of some of the aromatic amino acids (AAA) and branched chain amino acids (BCAA) are helpful in the diagnosis, evaluation of the severity of the hepatic morphologic changes, and prognosis of the type of liver disease. Moreover, the ratio between the AAA and the BCAA seems to be indicative of certain liver diseases. We describe the alterations in the amino acid patterns which may help in the diagnosis, prognosis, and treatment of patients with certain types of liver disease.

Amino Acids↗
PubMed2005

Milk thistle for alcoholic and/or hepatitis B or C virus liver diseases.

BACKGROUND: Alcohol and hepatotoxic viruses cause the majority of liver diseases. Randomised clinical trials have assessed whether extracts of milk thistle, Silybum marianum (L) Gaertneri, have any effect in patients with alcoholic and/or hepatitis B or C virus liver diseases. OBJECTIVES: To assess the beneficial and harmful effects of milk thistle or milk thistle constituents versus placebo or no intervention in patients with alcoholic liver disease and/or viral liver diseases (hepatitis B and hepatitis C). SEARCH STRATEGY: The Cochrane Hepato-Biliary Group Controlled Trials Register, The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and full text searches were combined (December 2003). Manufacturers and researchers in the field were contacted. SELECTION CRITERIA: Only randomised clinical trials in patients with alcoholic and/or hepatitis B or C virus liver diseases (acute and chronic) were included. Interventions encompassed milk thistle at any dose or duration versus placebo or no intervention. The trials could be double blind, single blind, or unblinded. The trials could be unpublished or published and no language limitations were applied. DATA COLLECTION AND ANALYSIS: The primary outcome measure was mortality. Binary outcomes are reported as relative risks (RR) with 95% confidence interval (CI). Subgroup analyses were performed with regard to methodological quality. MAIN RESULTS: Thirteen randomised clinical trials assessed milk thistle in 915 patients with alcoholic and/or hepatitis B or C virus liver diseases. The methodological quality was low: only 23% of the trials reported adequate allocation concealment and only 46% were considered adequately double-blinded. Milk thistle versus placebo or no intervention had no significant effect on mortality (RR 0.78, 95% CI 0.53 to 1.15), complications of liver disease (RR 0.95, 95% CI 0.83 to 1.09), or liver histology. Liver-related mortality was significantly reduced by milk thistle in all trials (RR 0.50, 95% CI 0.29 to 0.88), but not in high-quality trials (RR 0.57, 95% CI 0.28 to 1.19). Milk thistle was not associated with a significantly increased risk of adverse events (RR 0.83, 95% CI 0.46 to 1.50). AUTHORS' CONCLUSIONS: Our results question the beneficial effects of milk thistle for patients with alcoholic and/or hepatitis B or C virus liver diseases and highlight the lack of high-quality evidence to support this intervention. Adequately conducted and reported randomised clinical trials on milk thistle versus placebo are needed.

Hepatitis B↗
PubMed1992

[Treatment of cholestatic liver diseases; the role of ursodeoxycholic acid].

Ursodeoxycholic acid (UDCA) allows symptomatic treatment of cholestatic liver diseases such as primary biliary cirrhosis, primary sclerosing cholangitis, intrahepatic biliary atresia, and cholestasis of cystic fibrosis. Patients should be treated at an early stage of the disease in order to prevent progression to cirrhosis. Since UDCA has no toxic effects longterm treatment with this substance is possible without the risk of undesired side effects. In patients with primary biliary cirrhosis and rapid progression of the disease, UDCA may be combined with an immunosuppressive substance (i.e. cyclosporin). In primary sclerosing cholangitis, biliary atresia and cholestasis of cystic fibrosis, UDCA at present seems the only treatment of which a benefit for the patients can be expected. In endstage disease liver transplantation is indicated. The role of UDCA in chronic hepatitis and alcohol induced liver disease needs to be clarified in further studies. Whether the improvement of laboratory tests in such patients indicates amelioration of the course of disease, still is unclear.

Animals↗
PubMed1990

[Estimation of the reticuloendothelial function by positron emission computed tomography (PET) study in chronic liver disease].

We have developed a new liver scanning agent (Ga-68 human serum albumin microspheres) in a convenient kit for use in positron emission computed tomography (PET). In this study, this scanning agent was evaluated for clinical usefulness as a function test for the reticuloendothelial system. A dose of 5 micrograms/kg (1-2 mCi) of Ga-68 microspheres was injected intravenously to 25 patients, 11 with chronic hepatitis and 14 with liver cirrhosis, and 5 normal volunteers for PET imaging of the liver and spleen using HEADTONE-III (SET 120W). The volumes of the liver and the spleen and the uptakes of Ga-68 microspheres were calculated as an index of the reticuloendothelial system function. In liver cirrhosis the liver volume estimated by PET was decreased and the spleen volume was increased. Both the liver uptake rate and differential absorption ratio (DAR) of the radioactivity were decreased corresponding with the degree of chronic liver disease. The spleen uptake rate was increased with progression of chronic liver diseases, but there was no difference in DAR between normal volunteers and patients with chronic liver disease. it was concluded that PET using Ga-68 microspheres is useful in the evaluation of the function of the reticuloendothelial system.

Chronic Disease↗
PubMed1994

Liver disease in the elderly.

While there are no liver diseases specific to advanced age, the presentation, clinical course and management of liver diseases in the elderly may differ in important respects from younger individuals. The management of older patients with specific liver diseases should be informed by these differences. Alcoholic liver disease presents at a more advanced stage, drug induced liver disease and viral hepatitis may also be more severe. It is increasingly recognised that primary hepatocellular cancer arises in elderly cirrhotics regardless of the etiology of the cirrhosis, the risk highest in hemochromatosis and cirrhosis arising from hepatitis B and C.

Aged↗
PubMed1985

Long term prognosis for babies with neonatal liver disease.

A total of 123 patients with neonatal liver disease without extrahepatic bile duct obstruction or arteriohepatic dysplasia have been studied for six to 18 years. Idiopathic neonatal hepatitis, present in 73 babies, carried a high mortality due to liver failure (18%), septicaemia (6%), and associated defects (14%), especially in the first year of life (25%). Progression to chronic liver disease in non-familial idiopathic cases occurred in three of 40 reviewed patients. Only 12 of these children were completely healthy, the remainder having other permanent disabilities (57%). Four of nine familial cases of idiopathic neonatal hepatitis died in the first 12 months of life as did two of the four reviewed survivors. Progression to chronic liver disease or to death was a continuous process without any interval of recovery in all but one of these patients. Among patients with a presumed infective cause, cytomegalovirus infection caused a particularly benign form of neonatal hepatitis but was a frequent cause of brain damage or other disabilities. Babies who survived other infective liver diseases showed complete healing of the liver damage. Neonatal liver disease associated with alpha 1 antitrypsin deficiency progressed to death or chronic liver disease in three of nine patients and was not associated with a paucity of interlobular bile ducts.

Chronic Disease↗
PubMed2002

Liver disease in alcohol abusers: clinical perspective.

Alcoholic liver disease remains one of the most common causes of chronic liver disease in the world. The severity of liver damage related to alcohol varies among different individuals and even within any given individual at different times. Certain symptoms, signs, and abnormal findings on laboratory tests help clinicians distinguish among the various stages of alcohol-induced liver damage and, thus, have some prognostic significance. However, because all stages of this disease can persist for decades without causing overt evidence of serious liver damage, liver biopsy is the only test that can reliably distinguish among the various stages of alcohol-induced liver damage in many patients. The therapy of alcohol-induced liver disease varies according to the severity of histologic liver damage and clinically overt portal hypertension and hepatic dysfunction. Abstinence from alcohol consumption improves the clinical outcome of all stages of alcoholic liver disease. However, only two agents have proved to lessen early mortality in patients who require hospitalization for acutely decompensated alcoholic liver disease. It is not known whether either of these agents or other treatments prevent the development of alcohol-induced cirrhosis or improve the survival of patients who have already developed cirrhosis.

Alcoholism↗
PubMed2001

Nonalcoholic fatty liver disease: predictors of nonalcoholic steatohepatitis and liver fibrosis in the severely obese.

BACKGROUND AND AIMS: Nonalcoholic fatty liver disease (NAFLD) is common in severely obese subjects and can progress to cirrhosis and liver failure. Predicting advanced or progressive disease may help in selecting patients for liver biopsy and assist the development of therapeutic options. METHODS: Liver biopsies were taken at laparoscopic obesity surgery in 105 consecutive patients. The clinical and biochemical variables were analyzed for correlation with specific histologic features. RESULTS: Twenty-six patients (25%) were found to have nonalcoholic steatohepatitis (NASH), and 11 (42%) of these had advanced fibrosis. A raised index of insulin resistance (odds ratio [OR] 9.3, 95% confidence interval [CI] 3.4-26), systemic hypertension (OR 5.2, 95% CI 2.0-13.5), and raised alanine aminotransferase (OR 8.6, 95% CI 3.1-23.5) were independent predictors of NASH. A combination of 2 or 3 of these predictors allows a sensitivity of 0.8 and specificity of 0.89 for NASH. Alcohol consumption was associated with a reduction in NASH (OR 0.35, 95% CI 0.12-1.00) and diabetes (OR 0.18, 95% CI 0.047-0.67). CONCLUSION: Insulin resistance and systemic hypertension, features of the metabolic syndrome, are independently associated with advanced forms of NAFLD. Moderate alcohol consumption seems to reduce the risk of NAFLD in the severely obese, possibly by reducing insulin resistance.

Adult↗
PubMed1978

Liver disease in renal transplant recipients.

Liver disease is a common complication in renal transplant recipients. Several types of liver disease can occur. The most common are acute and chronic hepatitis. The variety of acute hepatitis include hepatitis A, hepatitis B, cytomegalovirus hepatitis, herpes simplex hepatitis and azathioprine hepatitis. The incidence of azathioprine hepatitis may not be as high as initially suggested. Chronic hepatitis is a serious problem because the disease seems to be progressive despite prednisone therapy. The causes of this chronic hepatitis are not fully known, although hepatitis B, cytomegalovirus and herpes simplex virus have been implicated. Discontinuation of azathioprine therapy has no appreciable effect on the course of chronic hepatitis.

Animals↗
PubMed1982

Liver disease and protein needs.

Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

Amino Acids↗
PubMed2007

The effect of a low-carbohydrate, ketogenic diet on nonalcoholic fatty liver disease: a pilot study.

Nonalcoholic fatty liver disease is an increasingly common condition that may progress to hepatic cirrhosis. This pilot study evaluated the effects of a low-carbohydrate, ketogenic diet on obesity-associated fatty liver disease. Five patients with a mean body mass index of 36.4 kg/m(2) and biopsy evidence of fatty liver disease were instructed to follow the diet (<20 g/d of carbohydrate) with nutritional supplementation for 6 months. Patients returned for group meetings biweekly for 3 months, then monthly for the second 3 months. The mean weight change was -12.8 kg (range 0 to -25.9 kg). Four of 5 posttreatment liver biopsies showed histologic improvements in steatosis (P=.02) inflammatory grade (P=.02), and fibrosis (P=.07). Six months of a low-carbohydrate, ketogenic diet led to significant weight loss and histologic improvement of fatty liver disease. Further research is into this approach is warranted.

Adult↗
PubMed2001

Guinea pig transglutaminase immunolinked assay does not predict coeliac disease in patients with chronic liver disease.

BACKGROUND: It has been suggested that serological screening for coeliac disease (CD) should be performed in patients with chronic unexplained hypertransaminasaemia. AIMS: To evaluate the specificity for CD diagnosis of serum IgA antitissue transglutaminase (tTG) determination in consecutive patients with chronic hypertransaminasaemia using the most widely utilised ELISA based on tTG from guinea pig as the antigen. PATIENTS AND METHODS: We studied 98 patients with chronic hypertransaminasaemia, evaluated for the first time in a hepatology clinic. Serum anti-tTG and antiendomysial (EmA) assays were performed. Patients positive for EmA and/or anti-tTG were proposed for intestinal biopsy. Finally, all sera were reassayed for anti-tTG using an ELISA based on human recombinant tTG as the antigen. RESULTS: A total of 94/98 hypertransaminasaemic patients were positive for hepatitis virus markers, with 82/98 (83%) positive for anti-hepatitis C virus. Liver histology showed that most patients had mild or moderate chronic hepatitis while severe fibrosis or overt liver cirrhosis was found in 20/98. CD screening showed that 15/98 (16%) hypertransaminasaemic subjects had anti-tTG values in the same range as CD patients; however, IgA EmA were positive in only 2/98 (2%). Distal duodenal biopsy, performed in nine patients, showed subtotal villous atrophy in the two EmA+/anti-tTG+ patients but was normal in 7/7 EmA-/anti-tTG+ subjects. The presence of anti-tTG+ values in EmA- patients was unrelated to particular gastrointestinal symptoms, other associated diseases, severity of liver histology, or distribution of viral hepatitis markers. There was a significantly higher frequency of positive serum autoantibodies (antinuclear, antimitochondrial, antismooth muscle, and anti-liver-kidney microsomal antibodies) in anti-tTG+/EmA- patients than in the other subjects (9/13 v 10/83; p<0.003). Also, a correlation was found between serum gamma globulin and anti-tTG values (p<0.01). When sera were tested with the ELISA based on human tTG as the antigen, no false positive results were observed: only the two EmA+ patients with atrophy of the intestinal mucosa were positive for anti-tTG while all others were negative, including those false positive in the ELISA based on guinea pig tTG as the antigen. CONCLUSIONS: In patients with elevated transaminases and chronic liver disease there was a high frequency of false positive anti-tTG results using the ELISA based on tTG from guinea pig as the antigen. Indeed, the presence of anti-tTG did not correlate with the presence of EmA or CD. These false positives depend on the presence of hepatic proteins in the commercial tTG obtained from guinea pig liver and disappear when human tTG is used as the antigen in the ELISA system. We suggest that the commonly used tTG ELISA based on guinea pig antigen should not be used as a screening tool for CD in patients with chronic liver disease.

Adolescent↗