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PubMed2006

Prevalence of undiagnosed diabetes and postchallenge hyperglycaemia in Chinese patients with non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease is prevalent in affluent countries and is strongly associated with metabolic syndrome. AIM: To study the prevalence of undiagnosed diabetes and postchallenge hyperglycaemia in Chinese patients with non-alcoholic fatty liver disease. METHODS: 73 consecutive patients with biopsy-proven non-alcoholic fatty liver disease and no history of diabetes underwent comprehensive metabolic screening. Diagnosis of diabetes and impaired glucose regulation was based on the 2006 American Diabetes Association criteria. RESULTS: The prevalence of undiagnosed diabetes and impaired glucose tolerance in non-alcoholic fatty liver disease patients was 33% and 29%, respectively. Among patients with 2-h plasma glucose above 7.8 mm, 47% had normal fasting glucose (below 5.6 mm). Impaired glucose tolerance was more common in patients with non-alcoholic steatohepatitis than those with simple hepatic steatosis (P = 0.036), and 2-h plasma glucose correlated with fibrosis stage (Spearman coefficient: 0.25, P = 0.046). In a binary logistic regression analysis, high fasting glucose and low high-density lipoprotein cholesterol were independent factors associated with diabetes. Nevertheless, if oral glucose tolerance test was only performed in non-alcoholic fatty liver disease patients with impaired fasting glucose, 20.8% of diabetes cases would be missed. CONCLUSIONS: Isolated postchallenge hyperglycaemia is common among Chinese non-alcoholic fatty liver disease patients without history of diabetes. It is associated with histological severe disease, and cannot be accurately predicted by any fasting glucose cut-off.

Blood Glucose↗
PubMed2004

Quality of life assessment in Pakistani patients with chronic liver disease.

OBJECTIVE: To find out if advanced liver disease causes decrement in health related quality of life in Pakistani patients. METHODS: An observational study was conducted at the Shifa International Hospital Islamabad. Chronic Liver Disease Questionnaire (CLDQ) was administered to patients with liver disease who were either admitted or seen as outpatients. Patients were divided into two groups. Those with no cirrhosis or Child's Class A were placed into group A. Those with advanced liver disease i.e. Child's Class B and C into group B. RESULTS: A total of 56 patients (mean age 50.6 years) were included in this study. Hepatitis C was the cause of chronic liver disease (CLD) in 52 (92.9%) patients. Twenty-one (37.5%) patients were in group A and 35 (62.5%) in group B. Patients with advanced liver disease had significantly lower CLDQ scores as well as decrement in five out of the six categories for assessing quality of life. CONCLUSION: Chronic liver disease causes significant impairment in the Quality of Life Index (QLI) in Pakistani patients.

Chronic Disease↗
PubMed2001

Autoimmune liver disease in children.

BACKGROUND AND AIM: Autoimmune liver disease (AILD) in children progresses to cirrhosis and liver failure if not diagnosed and managed in time. We prospectively analyzed our patients with liver disease for autoimmune etiology and their outcome with treatment. METHODS: All patients with liver disease were evaluated with liver function tests, abdominal ultrasonography, endoscopy, liver biopsy, viral markers and investigations for Wilson's disease. Immunoglobin (Ig)M hepatitis A virus, hepatitis E virus (HEV) and IgM hepatitis B core antibody were tested if acute viral hepatitis was suspected. Antinuclear antibody (ANA), antismooth muscle antibody (SMA), and liver kidney microsomal antibody (anti-LKM-1) were done in all cases. Autoimmune liver disease was diagnosed when one or more autoantibodies tested positive (> 1:40), and no other etiology of liver disease was identified. We also applied criteria proposed by the International Autoimmune Hepatitis Group. Cases diagnosed to have AILD were treated with immunosuppressive drugs. RESULTS: Autoimmune liver disease constituted 3.9% (6/153; median age and duration of illness 8.5 years and 3 months, respectively) of chronic liver disease cases. Four patients had acute hepatitis-like presentation. Of the six cases, two each were ANA and SMA +; one was anti-LKM-1 +, and the other was positive for both SMA and anti-LKM-1. Three of the patients achieved remission with combination therapy of oral prednisolone (OP) and azathioprine (AZT), and one with only OP. The other two patients were not treated. Two of the patients in remission have been weaned off from immunosuppressive therapy, and one is in a withdrawal phase. Another patient, while in biochemical remission developed superimposed anicteric acute HEV infection. CONCLUSION: Although AILD is uncommon in children, its search is rewarding, as remission is achieved with immunosuppressive therapy. Superimposed acute viral hepatitis can occur in endemic areas.

Adolescent↗
PubMed1975

Casual blood-ethanol estimations in patients with chronic liver disease.

Patients attending a clinic for diseases of the liver were tested for blood-ethanol by a gas chromatographic technique sensitive to about 5 mg/dl (1 mmol/1). Of 172 patients (51 men, 121 women) 36% gave a history of heavy drinking (greater than 80 g ethanol/day; equivalent to 8 fl oz of whisky or 1 litre of wine) and 13% had ethanol in the bloodstream at values of 8-400 mg/dl. 42 patients (24%) had the liver-biopsy changes of alcoholic liver disease, and 17 of these had ethanol in the blood at one time or another. Nearly half (22/49) of all patients admitting heavy drinking also had detectable blood-ethanol. In all cases but 1 where blood-ethanol was found, a drinking history was admitted on first attendance, and alcoholic liver disease was nearly always found on subsequent biopsy. Blood-ethanol and admission of drinking were most constantly found in association with alcoholic steatosis and hepatitis. Both features were less commonly present in cases of alcoholic cirrhosis. Only 1 patient of 22 with "cryptogenic" cirrhosis on biopsy was found to have both ethanol in the blood and an alcoholic history, although 5 had an alcoholic history alone. The value of serial blood-ethanol estimations in the treatment of alcoholics and the detection of relapses is demonstrated. The findings confirm the relatively low frequency of alcoholism as a contributor to cirrhosis in the United Kingdom. Alcohol does not seem a major cause of cryptogenic cirrhosis. Casual blood-ethanol estimation is a useful and objective adjunct to techniques of investigating diseases of the liver.

Alcohol Drinking↗
PubMed1995

[Immunopathology of chronic liver diseases].

Chronic inflammatory liver diseases can be induced by virus infections, toxic-metabolic factors and/or autoimmune mechanisms. This overview deals with the immunopathogenesis of chronic hepatitis B and C and autoimmune hepatitis (AIH). 1. Chronic hepatitis B: The immune response to HBV-antigens is responsible both for viral clearance and disease pathogenesis during HBV-infection. The humoral immune response to HBsAg contributes to the clearance of circulating virus particles, the cell mediated immune response to HBsAg, HBcAg and polymerase antigen eliminates infected cells. The class I- and class II restricted T-cell-responses to HBV is strong, polyclonal and multispecific in acute HB with successful clearance of the virus, but weak or incomplete in chronic HB with viral persistence. In addition to ineffective immune response host and viral factors as well as abnormalities in virus-host interactions may be the main reasons for the maintenance of HBV-carrier status. 2. Chronic hepatitis C develop in more than 60% of infected patients. There is increasing evidence that the immune response to HCV-epitopes plays an important role in the course and the pathogenesis of the disease. It has been shown that CD4+ and CD8+ T-cells recognize viral peptides in the presence of class I and II molecules. The fine specificity and functional significance of liver infiltrating and peripheral blood T-cells demonstrate HCV specific immunodominant epitopes targeted by class Ii restricted CD4+ cells in patients with chronic HCV infection. The T-cell response correlates with disease activity. The cytokine release of T-cells resemble a TH1-like profile. Studies of the humoral immune response to HCV show a correlation between IgM-anti-HCV and disease activity. In vitro and in vivo anti-HCV secretion by PBMC is due to persistent antigenic stimulation of B-cells by ongoing production of viral antigens and reflects HCV replication in PBMC. Of special interest are several immune mediated disease and immune abnormalities in chronic hepatitis C. 3. Autoimmune hepatitis (AIH) is a distinct group of acute and chronic necro-inflammatory disorders of unknown etiology characterized by immunological and autoimmunological features including the presence of autoantibodies but without an antecedent of viral infections. Marker autoantibodies define 3 subtypes: Type I (ANA/SMA), Type II (LKM1-AB), Type II (SLA-AB). AIH is associated with a distinct genetic background (HLA A1, B8, DR3 or DR4). Several studies clearly demonstrate that liver cell damage in AIH is mediated by autoimmune reactions against normal constituents of hepatocytes. Although the precise mechanisms are not yet fully understood, there is now considerable evidence that autoantigens of the hepatocellular membrane in particular the ASGPR are important targets of liver damaging autoreactions in AIH. Cellular and humoral immune reactions against the human ASGPR correlate with disease activity and usually disappear under immunosuppressive therapy.

Antibody Formation↗
PubMed2002

Xanthine oxidoreductase activity in human liver disease.

OBJECTIVES: The aim of this study was to investigate the level and the form of xanthine oxidoreductase (XOR) in severely diseased human livers, to ascertain whether the modifications of the enzyme activity reported in experimental pathology also occur in human liver disease. METHODS: Total, dehydrogenase, and oxidase activities of XOR were measured in samples of human liver removed for transplantation or partial hepatectomy. Samples included four groups: 1) histologically normal liver tissue, adjacent to metastases from extrahepatic tumors (controls), 2) liver with virus-related cirrhosis; 3) liver with virus-negative cirrhosis, and 4) hepatocellular carcinoma tissue (HCC). RESULTS: The level of total XOR was significantly higher in liver with virus-related cirrhosis, but not in virus-negative cirrhosis, than in controls. In virus-positive cirrhosis, the total XOR activity correlated positively with the level of ALT. The percentage of XOR oxidase activity in cirrhotic liver, regardless of virus infection, correlated positively with aspartate amino-transferase, bilirubin concentration, and partial thromboplastin time, and negatively with prothrombin time. The activity of XOR was significantly lower in HCC than in control tissue or in a nonneoplastic area of the same liver. CONCLUSIONS: Consistent with previous reports in experimental pathology, the level of XOR was increased in cirrhotic liver, in association with viral infection. This increment correlated with ALT, suggesting a relationship between XOR activity and the extent of liver injury caused by viral replication. The percentage of oxidase activity seems to be correlated with tissue damage and consequent liver impairment. The low XOR activity observed in HCC is consistent with reported experimental pathology.

Adult↗
PubMedDate not supplied

The significance of chronic hepatitis B and C virus infections in some connective tissue diseases: the association with chronic liver disease.

BACKGROUND/AIM: We investigated the pathogenic role of chronic hepatitis B virus (HBV) and C virus (HCV) in some connective tissue diseases including systemic lupus erythematosus (SLE), overlap syndrome, rheumatoid arthritis (RA), seronegative spondylarthritis (SS) and the association with chronic liver disease. METHODOLOGY: There were studied 155 patients, aged among 18 to 64 years old: 57 with SLE, 22 with overlap, 26 with RA, 30 with SS. The diagnoses were established using modified ARA criteria. There were performed complex immunology tests, percutaneous liver biopsy, HLA, Elisa tests with Riba confirmation for detecting HCV and HBV. RESULTS: 17% of SLE patients were infected with hepatitis viruses, predominantly B (70%). Half of them had a hepatic involvement due to the hepatitis viruses. 23% of RA patients were equally B\C infected with only one case of hepatic involvement secondary to hepatitis viruses. All the HCV infected patients had rheumatoid factor (RF) IgG-IgM type, with low serum levels of haemolytic complement (CH50), increases serum levels of circulating immune complexes (CIC) and evidence of HLA DR4 In the group of SS 40% of patients were infected mostly with HBV. In HLA B27 (+) anchylosing spondylitis (AS) the incidence of HBV was 100%. CONCLUSIONS: There is no high prevalence of HCV infection in SLE, overlap syndrome or RA, compared to the control group. In SS the prevalence is increased (40%), especially HLA B27 (+) AS group (33%), in which HBV is noticed at a rate of 100%. The association SLE-HCV favours the visceral involvement especially renal ones, while the presence of HBV is associated with decrease of lupus activity. In RA, HCV induces IgG-IgM RF with complement activation, being considered as a trigger of the disease in HLA DR4 patients. In HLA B27 (+) AS. HBV may trigger the development of disease in genetically susceptible individuals.

Adolescent↗
PubMed1995

Prevention and treatment of drug-induced liver disease.

Many drugs may cause liver damage; some damage is predictable, but most is not. The most important preventive measure is judicious drug use by the prescribing physician. Early recognition of hepatotoxicity and cessation of the offending agent is essential for treatment. The best example of a specific treatment for drug-induced liver disease is N-acetylcysteine treatment for acetaminophen hepatotoxicity. Many examples are cited of other attempts at treatment in animal models of drug-induced liver disease. If drug-induced liver disease leads to fulminant hepatic failure, intensive management of the resulting complications is required. Liver transplantation may be the only treatment option.

Animals↗
PubMed2002

Familial association in autoimmune liver disease.

The occurrence of autoimmune liver disease in members of the same family is hardly a frequent observation in clinical practice. In a group of 204 cases of primary biliary cirrhosis (PBC) (196 women) and 219 of type 1 autoimmune hepatitis (AIH) (183 women), seen from 1985 to 2000, family occurrence of autoimmune liver disease was investigated. Diagnosis of both entities was based on clinical criteria, immunological studies and liver biopsy. Six families were identified with 2 members each presenting with autoimmune liver disease. In 4 of them the index case had an AIH. This association was observed between mother and daughter in 3 instances. In the remaining AIH index case the association found was with a PBC in her sister. In the other two families the index cases were PBC. In one of them, PBC and AIH association were observed in sisters. Lastly, in another case, an antimitochondrial (AMA) negative variant of PBC was detected in mother and her daughter. The low frequency of family association observed in this cohort could be due to the fact that only symptomatic cases were included. Concurrent autoimmune manifestations were confirmed in 5 members of 6 families (42%). Our results, given the concurrence of both liver diseases in the same family, suggest a link among diverse entities of the autoimmune lineage. The frequency of AIH family association seems to be more prominent in this series than that of PBC. It is also shown that family association in the case of an AMA-negative variant of PBC is feasible, thus confirming that no substantial differences exist between the latter and AMA-positive PBC.

Adult↗
PubMed1995

Autoantibody against a 78 kDa membrane protein of HepG2 cell in the sera of patients with alcoholic liver diseases.

Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver, n = 8; hepatitis, n = 13; liver cirrhosis, n = 9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing 125I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of 125I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78,000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.

Autoantibodies↗
PubMedDate not supplied

Nonalcoholic fatty liver disease.

The definition of nonalcoholic fatty liver disease has evolved in recent years. Today, it is considered a nonspecific term encompassing several clinicopathologic entities (steatosis alone, steatonecrosis, steatohepatitis and histologic alcoholic-like hepatitis) that are similar to alcoholic liver disease. Studies of nonalcoholic fatty liver disease have come to conflicting conclusions about the course of the disease. It can be argued that the disparate results are largely the result of nonuniform definitions. When histologic features such as hepatocyte ballooning, necrosis, and Mallory hyaline are seen, nonalcoholic fatty liver disease has been shown to be associated with an aggressive outcome. Steatosis alone, in contrast, appears to be benign. The current understanding of nonalcoholic fatty liver disease, the limited treatments available, and two theories of the pathogenesis of the disease are also reviewed here.

Diagnosis, Differential↗
PubMed1980

Autoantibodies to collagen in patients with chronic liver diseases.

Sera of patients with various liver diseases were investigated for the presence of autoantibodies to type I collagen with a sensitive radioimmunoassay employing 3H-labelled collagen type I. A high percentage (69%) of patients with chronic liver diseases, equally distributed between chronic active hepatitis and alcoholic liver disease, was found to possess antibodies to denatured type I collagen, while no antibodies against native collagen were found. These antibodies belonged predominantly to the IgA immunoglobulin class. None of the patients with acute hepatitis or cholestatic liver disease, nor the healthy individual investigated had IgA-anticollagen antibodies. These findings may be useful as a parameter for the detection of chronic liver disease.

Acute Disease↗
PubMed1990

Serum-ascites albumin gradients in nonalcoholic liver disease.

Several studies performed in alcoholics with advanced liver disease have demonstrated a positive correlation between the serum-ascites albumin gradient (SAAG) and measured portal venous pressure. A single study performed in 15 patients with exudative malignant ascites and 29 patients with alcoholic liver disease demonstrated that a SAAG of less than 1.1 was essentially diagnostic of a malignant origin of the ascites. In an effort to confirm and extend these observations to individuals with nonalcoholic liver disease, 24 patients with nonalcoholic liver disease and 11 with alcoholic liver disease undergoing orthotopic liver transplantation (OTLx) were studied. At the time of liver transplantation, each had their serum and ascitic fluid albumin levels determined, the gradient calculated, and their portal venous pressure (PVP) as well as the corrected portal venous pressure (PPc) measured directly. A significant correlation (r = 0.624) between the PPc and the SAAG was found in the 11 alcoholics (P less than 0.05). No such correlation existed for those with nonalcoholic liver disease (r = 0.398). Moreover, a SAAG less than 1.1 was found in three of nonalcoholics with cirrhosis in the absence of an abdominal malignancy. We conclude that (1) the SAAG and PPc are statistically related to each other in individuals with alcoholic liver disease but not in those with a nonalcoholic cause for cirrhosis, and (2) SAAG less than 1.1 is not diagnostic of abdominal malignancy but can occur in those with advanced nonmalignant hepatic disease.

Adult↗
PubMed2005

Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

The liver plays a central role in haemostasis, being the site of synthesis of most of the clotting factors, coagulation inhibitors and fibrinolytic parameters, in addition to its clearance of activated clotting and fibrinolytic factors. Nonetheless, no haemostatic test(s) is included among the routine liver function tests and this study aims to probe this possibility. The liver disease group (n=258) included acute hepatitis (n=25), chronic viral hepatitis (n=128), hepatitis B (HB) carriers (n=25), liver cirrhosis (n=67), and hepatocellular carcinoma (HCC) (n=13). The prothrombin time was significantly prolonged in acute hepatitis, liver cirrhosis and HCC. However, the reptilase time was prolonged in all the groups except in HB carriers, while the thrombin time was prolonged only in the HCC group. Antithrombin III and protein C levels exhibited significant reduction in acute hepatitis, liver cirrhosis and HCC. On the other hand, protein S levels (total and free) were reduced significantly in all the patients groups, including HB carriers when compared with healthy controls. Derangement of haemostatic tests is a common feature in liver disease, being most significant in acute hepatitis, liver cirrhosis and hepatocellular carcinoma. The most sensitive markers of hepatocyte malfunction are protein S (total and free) and the reptilase time as they were abnormal, in the mildest liver affections, when other biochemical tests as well as other haemostatic tests were normal. Further studies are needed to see whether these two tests qualify for inclusion among the routine liver function tests.

Adolescent↗
PubMed2005

Recent events in alcoholic liver disease V. effects of ethanol on liver regeneration.

Liver regeneration is necessary to recover from alcoholic liver injury. Herein, we review evidence that ethanol interferes with liver regeneration. Briefly, alcoholic fatty livers demonstrate increased rates of hepatocyte death. The latter provides a regenerative stimulus. However, unlike mature hepatocytes in healthy adult livers, most surviving mature hepatocytes in alcoholic fatty livers cannot replicate. Therefore, less mature cells (progenitors) must differentiate to replace dead hepatocytes. Little is known about the general mechanisms that modulate the differentiation of liver progenitors in adults. Delineation of these mechanisms and clarification of how ethanol influences them might suggest new therapies for alcoholic liver disease.

Alcohol Drinking↗