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PubMed1999

Low body mass index and use of corticosteroids, but not cholestasis, are risk factors for osteoporosis in patients with chronic liver disease.

BACKGROUND/AIMS: Metabolic bone disease is known to complicate chronic liver disease. In a cross-sectional, controlled study we have studied the prevalence of osteoporosis in patients with various types of chronic liver disease. We also identified risk factors predisposing to osteoporosis in this patient group. METHODS: Seventy-two hospitalised patients, 46 females and 26 males, were included. Age- and sex-matched individuals from the background population served as controls. Bone mineral density was measured by dual energy X-ray absorptiometry at the lumbar spine and femoral neck. RESULTS: Bone mineral density was significantly lower in patients with chronic liver disease than in controls at the lumbar spine (Z-score: -0.35 SD+/-1.36 vs. 0.26 SD+/-1.19, p<0.01) but not at the femoral neck (Z-score: -0.18 SD+/-1.48 vs. 0.17 SD+/-1.08, NS). Patients with cholestatic chronic liver disease did not have lower bone mineral density compared with patients with non-cholestatic chronic liver disease (Z-score: -0.35 SD+/-1.30 vs. -0.34 SD+/-1.45). Osteoporosis was found in 30% of the patients and 15% of the controls, respectively. In a multivariate regression analysis on risk factors in the patient group, the following factors were associated with osteoporosis: use of corticosteroids (odds ratio=18.9; p<0.01), low body mass index (odds ratio=14.1; p=0.001), high age and female sex. CONCLUSION: Patients with chronic liver disease are at risk of developing osteoporosis. Risk factors for osteoporosis in chronic liver disease are low body mass index and corticosteroid therapy, in addition to high age and female sex. Cholestatic liver disease per se is not associated with an increased risk for osteoporosis.

Absorptiometry, Photon↗
PubMed1987

Hepatic alcohol and aldehyde dehydrogenases in liver disease.

To investigate the influence of liver injury on the activities of hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), these enzymes have been measured in tissue from alcoholic and non alcoholic patients with different severity of liver damage. ADH and ALDH activities decreased proportionatelly with the progression of liver disease in alcoholics. By contrast, in non-alcoholics, there was a reduction of Low-Km ALDH related with the severity of liver injury but ADH was similar in patients with chronic hepatitis and non-alcoholic cirrhosis. Furthermore, ADH was significantly lower in alcoholic than in non-alcoholic cirrhotics. These results suggests that the decreased ADH and ALDH in alcoholics are not primary abnormalities predisposing to alcoholism and alcoholic liver disease. The diminution of ADH found only in alcoholics could be due to the loss of the enzyme produced by centrolobulillar cell necrosis, that is often observed in alcoholic liver disease.

Adult↗
PubMed2005

Nitric oxide in patients with chronic liver diseases.

AIM: Chronic liver disease (CLD) may be accompanied by portal hypertension (PHT). Nitric oxide (NO) system disturbances seem to play a key role in the pathogenesis of CLD and PHT. In this study we aim to assess if in chronic active hepatitis (CAH) and cirrhosis (CIR), CLD severity and etiology can be correlated with the serum level of NO metabolites. METHOD: The study was performed on 92 patients divided according to the diagnosis and Child-Pugh class, and a control group of 10 healthy volunteers. Serum nitrite/nitrate and citrulline levels were measured in order to evaluate NO synthesis. RESULTS AND CONCLUSION: In CLD patients there was an increased NO production. In CIR NO synthesis increased more than in CAH. In CIR patients only nitrite/nitrate concentrations were correlated with citrulline levels. NO metabolites from CAH and CIR patients varied according to disease etiology, namely NO synthesis was more important in HCV-CLD than in alcoholic-CLD and HBV-CLD. In CIR patients, NO metabolites level increased with disease severity.

Adult↗
PubMed2004

Non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and orthotopic liver transplantation.

Obesity, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are becoming increasingly common medical problems in the developed world, often in the setting of the metabolic or insulin resistance syndrome (IRS). It is predicted that by the year 2025 > 25 million Americans may have NASH-related liver disease. NASH and NAFLD also affect the donor population. The use of steatotic donor livers for liver transplantation (LT) is associated with an increased risk of primary nonfunction (PNF) in the allograft. There is particular reluctance to use steatotic livers for living donor LT. There is indirect evidence to suggest that patients undergoing LT for cirrhosis resulting from NASH may have poorer outcome, despite careful selection of LT candidates. Indeed it is likely that many potential LT candidates with NASH are excluded from LT due to co-morbid conditions related to IRS. The post-LT patient is at risk of several components of IRS, such as diabetes mellitus, hypertension, hyperlipidaemia and obesity and there is increasing recognition of de novo and recurrent NAFLD and NASH after LT. Thus NAFLD and NASH affect all aspects of LT including donors, patients in evaluation and the LT recipient.

Fatty Liver↗
PubMed1991

Theophylline pharmacokinetics and liver function indexes in chronic liver disease.

Since patients with chronic liver disease present with greatly varying theophylline disposal reductions, in cirrhotics the acute theophylline dose schedule must be guided by an index of liver function that predicts theophylline pharmacokinetics. We therefore studied 26 patients with severe chronic liver disease to ascertain the efficacy of the routinely used clinical and biochemical liver function tests in predicting theophylline pharmacokinetics. The prealbumin plasma level, recently proposed as a valuable index of liver function, was also considered. With respect to 10 controls, theophylline clearance was found to be significantly reduced (30 +/- 2 vs. 75 +/- 11 ml/kg/h, mean +/- SD, p less than 0.01). However, only 7 patients had a reduction great enough to require a reduced intravenous theophylline dose schedule. An analysis of clinical utility, made on the basis of ROC curves, showed that the albumin/globulin ratio was the most effective index for identifying patients requiring lower doses of theophylline. Prealbumin and albumin were also useful, whereas bilirubin, prothrombin time, pseudocholinesterase, the presence of ascites and Pugh-Child's classification of the severity of liver disease were found to be worthless.

Adult↗
PubMed2005

Recent concepts in non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors, including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however, staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as cirrhosis and hepatocellular carcinoma, which occur in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with 'cryptogenic cirrhosis'. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy.

Fatty Liver↗
PubMed1977

[Immunological indices in chronic liver diseases].

The study aimed at the confrontation of the results from the investigation of the immunoglobulines G, M, and A (IgG, IgM and IgA), the test for spontaneous rosette formation and the determination of Australian antigen (HBsAg) in 110 patients with chronic liver disease (liver steatosis, chronic persisting hepatitis, chronic aggressive hepatitis and liver cirrhosis). The diagnosis was morphologically confirmed and some of the patients were repeatedly examined. No significant interrelations among the three main classes of immunoglobulines were established in the majority of the groups of chronic liver diseases, speaking for the individual information, carried by the separate immunoglobuline classes. Correlation was established between IgG and IgM in chronic active hepatitis. The mean values of IgG and IgM are considerably higher in cases with splenomegaly. IgG is more often increased when the patients are carriers of HBsAg, being in agreement with the contemporary concepts about the differences in immune pathological mechanism in chronic liver diseases, with and without HB5-antigenemia.

Chronic Disease↗
PubMed2004

Screening in liver disease: report of an AASLD clinical workshop.

This report summarizes an AASLD Clinical Workshop that was presented at Digestive Diseases Week 2003 on screening in liver diseases. As newer diagnostic tests become available, many liver diseases and complications of liver disease can be detected at an early asymptomatic stage. In many cases, early detection can lead to earlier treatment and an improved outcome. However, screening for liver diseases in asymptomatic persons has the potential for adverse consequences, including discrimination and stigmatization. The cost of screening programs is significant, and access to screening tests varies in different countries. Future screening programs require careful planning and implementation to balance the benefits, risks, and cost-effectiveness. This review outlines the concepts of screening and their application to a broad range of liver diseases.

Cost-Benefit Analysis↗
PubMed2001

S-adenosyl-L-methionine for alcoholic liver diseases.

BACKGROUND: Alcohol is a major cause of liver disease in the Western world today. S-adenosyl-L-methionine (SAMe) acts as a methyl donor for all known biological methylation reactions and participates in the synthesis of glutathione, the main cellular anti-oxidant. Randomised clinical trials have addressed the question whether SAMe has any efficacy in patients with alcoholic liver diseases. OBJECTIVES: The objectives were to assess the efficacy of SAMe on mortality, clinical symptoms, complications, liver biochemistry, and liver histology in patients with alcoholic liver diseases. Adverse events were also analysed. SEARCH STRATEGY: The Cochrane Hepato-Biliary Group Controlled Trials Register, The Cochrane Library, MEDLINE, EMBASE, and full text searches were combined. SELECTION CRITERIA: Randomised clinical trials studying patients with alcoholic liver diseases were included. Interventions encompassed peroral or parenteral administration of SAMe at any dose versus placebo or no intervention. The trials could be double blind, single blind, or unblinded. The trials could be unpublished or published as an article, an abstract, or a letter, and no language limitations were applied. DATA COLLECTION AND ANALYSIS: All analyses were performed according to the intention-to-treat method. The statistical package (RevMan and MetaView) provided by the Cochrane Collaboration was used. The methodological quality of the randomised clinical trials was evaluated by components of quality and the Jadad-score. MAIN RESULTS: Eight placebo-controlled randomised clinical trials including a heterogeneous sample of 330 patients with alcoholic liver disease were identified. Only one trial including 123 patients with alcoholic cirrhosis used adequate methodology and reported clearly on mortality and liver transplantation. It demonstrated no significant effects of SAMe on mortality (Peto odds ratio (OR) 0.53, 95% confidence interval (CI) 0.22 to 1.29), liver related mortality (OR 0.63, 95% CI 0.25 to 1.58), mortality or liver transplantation (OR 0.47; 95% CI 0.20 to 1.09), or patients without complications (OR 0.63, 95% CI 0.30 to 1.31). SAMe was not significantly associated with adverse events (OR 3.95, 95% CI 0.77 to 20.24). REVIEWER'S CONCLUSIONS: This systematic review could not demonstrate any significant effect of SAMe on mortality, liver related mortality, mortality or liver transplantation, and liver complications of patients with alcoholic liver disease. SAMe should not be used for alcoholic liver disease outside randomised clinical trials.

Humans↗
PubMed1997

Absence of LKM-1 antibody reactivity in autoimmune and hepatitis-C-related chronic liver disease in Sweden. Swedish Internal Medicine Liver club.

BACKGROUND: Type-2 autoimmune hepatitis is a subgroup of chronic hepatitis characterized by the presence of liver/kidney microsomal autoantibodies type 1 (LKM-1). A frequent association with chronic hepatitis C suggests that hepatitis virus might trigger autoimmune reactivity. LKM-1-positive chronic hepatitis is not uncommon in southern Europe but is rarely seen in the USA and the UK. The prevalence in Scandinavia is hitherto unknown. METHODS: We used an automated prototype LKM-1 immunometry-based assay (IMx) to detect LKM-1 antibodies in sera from 350 Swedish patients with chronic liver diseases (100 with primary biliary cirrhosis, 80 with primary sclerosing cholangitis, 100 with hepatitis C, and 70 patients with various forms of chronic hepatitis, including 36 autoimmune cases), and from 17 children with autoimmune hepatitis. Sera reactive in the IMx assay were subjected to immunofluorescence testing. RESULTS: No clearly LKM-reactive sera were detected. Serum samples from 29 patients were borderline reactive in the IMx assay but tested negative in the confirmatory immunofluorescence test. Positive tests in the former assay were likely caused by reactivity against microsomal antigens other than LKM-1/cytochrome P450IID6. CONCLUSIONS: LKM-1-positive type-2 autoimmune hepatitis is very rare in Sweden. Furthermore, chronic hepatitis C did not trigger this type of autoimmune reactivity in our patients, probably owing to genetic insusceptibility.

Adolescent↗
PubMed1984

Ultrasound determination of liver size and assessment of patients with malignant liver disease.

The value of ultrasound-measured liver volume in assessing response to therapy in patients with malignant liver disease was determined by the method originally described by Carr, which was modified and validated. Volumes measured in five cadavers by ultrasound and, after removal, by water displacement agreed to within 8% and the wide range of volumes in 20 normal subjects (800-2400 ml) was closely correlated with body weight. In 20 patients with non-malignant diffuse liver disease (cirrhosis or fatty liver) and 33 with malignant liver disease, initial volumes ranged from 1000 to 4900 ml and did not correlate with body weight. Changes in response to therapy in 15 patients with malignant liver disease were monitored by serial measurements with demonstrable changes in volume which, in those with alpha-fetoprotein tumours, were in parallel with changes in serum alpha-fetoprotein levels.

Carcinoma, Hepatocellular↗
PubMed1990

[Gonad function in men with alcoholic liver disease].

The connection between alcoholic liver disease and hypogonadism has long been recognized. In this study of 112 males admitted to a medical department, altogether 87 had alcoholic liver disease. Serum testosterone was depressed (less than 12 nmol/l) in 47 out of 51 (92%) patients with alcoholic liver cirrhosis and in 13 out of 36 (36%) with alcoholic fatty liver (p less than 0.001). Primary hypogonadism was found in 8% of the patients with alcoholic fatty liver and in 16% of the patients with alcoholic cirrhosis and secondary hypogonadism in 28% of the patients with fatty liver and in 76% of those with alcoholic cirrhosis. Serum sex hormone binding globulin (SHBG) was increased (greater than 40 nmol/l) in 65% of the patients with fatty liver and in 67% of the patients with alcoholic cirrhosis. Serum testosterone was significantly correlated to liver function tests Normotest (NT), bilirubin and albumin. In conclusion, hypogonadism is very common in men with alcoholic liver disease.

Adult↗
PubMed2006

Impact of model for end-stage liver disease (MELD) scoring system on pathological findings at and after liver transplantation.

The Model for End-Stage Liver Disease (MELD) scoring system, a validated objective liver disease severity scale, was adopted in February 2002 to allocate cadaveric organs for liver transplantation (LT). To improve transplantability before succumbing to advanced disease, patients with low-stage hepatocellular carcinoma (HCC) are given extra points in this system commensurate with their predicted mortality. Our aims were to determine 1) any change in the pathological findings at LT following the implementation of this system and 2) the impact of scoring advantage given to early-stage HCC. Clinicopathologic findings were compared before (pre-MELD, n = 87) and after (MELD, n = 58) the introduction of the MELD system. The findings in the pre-MELD vs. MELD groups were as follows: HCC, 27.5% vs. 48.3% (P = 0.001); portal vein thrombosis (PVT), 13.7% vs. 25.9% (P = 0.08); cholestasis, 16.1% vs. 32.7% (P = 0.026); inflammation grade of 2 or more, 43.7% vs. 48.3% (P = not significant); hepatitis C (HCV), 45.9% vs. 51.7% (P = not significant); HCV with lymphoid aggregates, 25% vs. 60% (P = 0.003); HCV with hyperplastic hilar nodes, 15.0% vs. 36.6% (P = 0.001); and post-LT HCC recurrence, 4.1% vs. 3.4% (P = not significant). Non-HCC-related findings were further compared in the 2 subgroups of pre-MELD (n = 57) and MELD (n = 31) after exclusion of HCC and fulminant hepatic failure (FHF) cases, and only cholestasis was significantly increased in the subgroup MELD. In conclusion, increased incidence of native liver cholestasis in the MELD era may be the histologic correlate of clinically severe liver disease. The scoring advantage given to low-stage HCC did result in a significantly increased incidence of HCC in the MELD group, but it did not adversely affect the post-LT recurrence rate.

Adult↗
PubMed2004

Pathologic features associated with fibrosis in nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of clinicopatholologic conditions ranging from steatosis alone to nonalcoholic steatohepatitis (NASH), with varying risks for progression to cirrhosis. Although steatosis alone seems to be nonprogressive, some patients with NASH can progress. This study focuses on the clinical and pathological characteristics of patients with NAFLD associated with the development of histological fibrosis. Patients with an established diagnosis of nonalcoholic fatty liver were identified through our NAFLD database containing extensive clinical, demographic, and laboratory data. Liver biopsy specimens were read blindly by one hepatopathologist using a 19-item pathological protocol and by another hepatopathologist using a second pathological protocol. Clinical and pathological data were matched to the presence of different types of histological fibrosis. Univariate and multivariate analyses helped determine all of the variables independently associated with histological fibrosis. Of 132 NAFLD patients, 21.2% had advanced fibrosis (septal/bridging fibrosis or well-established cirrhosis). Sinusoidal fibrosis was present in 20.3% of patients, whereas perivenular fibrosis was seen in 17.2%. Ballooning degeneration and Mallory bodies were independently associated with both sinusoidal fibrosis and perivenular fibrosis. Aspartate aminotransferase/alanine aminotransferase ratio and ballooning degeneration were also independently associated with periportal-portal fibrosis. We conclude that the presence of hepatocyte injury in NAFLD is associated with fibrosis. These pathological features can be used to establish the pathological criteria for diagnosis of the progressive form of NAFLD or NASH.

Adult↗
PubMed2006

The association between increased alanine aminotransferase activity and metabolic factors in nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) has been associated with metabolic disorders, including central obesity, dyslipidema, hypertension, and hyperglycemia. Metabolic syndrome, obesity, and insulin resistance are major risk factors in the pathogenesis of NAFLD. The aim of this study was to identify the relative contribution of the metabolic syndrome, obesity, and insulin resistance to alanine aminotransferase (ALT) activity in NAFLD. A total of 3091 subjects diagnosed with fatty liver by ultrasonography were enrolled. All components of metabolic syndrome criteria, anthropometric parameters, fasting insulin levels, high-sensitivity C-reactive protein (hs-CRP) as an inflammation marker, and ALT were measured in each subject. Homeostasis model assessment--insulin resistance (HOMA-IR) as a measure of insulin resistance and body mass index (BMI) as a measure of obesity were calculated. The prevalence of increased ALT levels (>40 IU/L) was 26.7%. Increased ALT activity was significantly associated with the following characteristics: male sex, young age, increased triglycerides, fasting glucose, fasting insulin, HOMA-IR, hs-CRP, waist circumference, BMI and diastolic blood pressure, and decreased high-density lipoprotein cholesterol (HDL-C). According to the increase in the number of metabolic syndrome components, BMI, HOMA-IR, and hs-CRP, the prevalence and odds ratio for having increased ALT activity were significantly increased. Central obesity, raised triglycerides, reduced HDL-C, and raised fasting glucose were strongly associated with increased ALT activity. In conclusion, a number of metabolic syndrome components, obesity, insulin resistance, and hs-CRP, are strong predictors of increased ALT activity in NAFLD. Central obesity, raised triglycerides, reduced HDL-C, and raised fasting glucose are metabolic syndrome components that contributed to increased ALT activity.

Adult↗
PubMed1977

[Osmolar and mechanic resistance of erythrocytes in chronic liver diseases].

Out of 120 patients with chronic liver diseases (45 liver cirrhosis, 38 chronic hepatitis, 15 fatty degeneration of the liver and 22 stasis liver) the osmotic resistance of the erythrocytes after Hennemann and the mechanic resistance after Schubothe was determined. 24% of the patients had a decreased osmotic resistance of the erythrocytes, even 55% a decreased incubation resistance. 16% of the patients with liver diseases had a decreased mechanic resistance of the erythrocytes. The comparison of the groups of disease and the stages of the diseases resulted in an increased mechanical resistance of the erythrocytes only for the decompensated liver cirrhosis. A positive correlation was the result between the degree of the haemolysis and the spherical index of the erythrocytes.

Chronic Disease↗
PubMed2001

Keratin 8 mutations in patients with cryptogenic liver disease.

BACKGROUND: About 10 percent of patients who undergo liver transplantation have cryptogenic liver disease. In animal models, the absence of heteropolymeric keratins 8 and 18 or the presence of mutant keratins in hepatocytes causes or promotes liver disease. We have previously described a mutation in the keratin 18 gene in a patient with cryptogenic cirrhosis, but the importance of mutations in the keratin 8 and keratin 18 genes in such patients is unclear. METHODS: We tested for mutations in the keratin 8 and keratin 18 genes in purified genomic DNA isolated from 150 explanted livers and 89 peripheral-blood specimens from three groups of patients: 55 patients with cryptogenic liver disease; 98 patients with noncryptogenic liver disease, with causes that included alcohol use, autoimmunity, drug use, and viral infections; and 86 randomly selected inpatients and outpatients who provided blood to the hematology laboratory. RESULTS: Of the 55 patients with cryptogenic liver disease, 3 had glycine-to-cysteine mutations at position 61 (a highly conserved glycine) of keratin 8, and 2 had tyrosine-to-histidine mutations at position 53 of keratin 8. These mutations were not detected in the patients with other liver diseases or in the randomly selected patients. We verified the presence of the mutations in specimens of explanted livers by protein analysis and by the detection of unique restriction-enzyme cleavage sites. In transfected cells, the glycine-to-cysteine mutation limited keratin-filament reorganization when the cells were exposed to oxidative stress. In contrast, the tyrosine-to-histidine mutation destabilized keratin filaments when transfected cells were exposed to heat or okadaic acid stress. CONCLUSIONS: Mutations in the keratin 8 gene may predispose people to liver disease and may account for cryptogenic liver disease in some patients.

Amino Acid Sequence↗
PubMed2004

[The short term prognosis in alcoholic liver disease with metabolic acidosis].

BACKGROUND/AIMS: Alcoholic liver disease with metabolic acidosis may have possible causes such as alcoholic ketoacidosis, diabetic ketoacidosis, lactic acidosis. Salicylate, methanol, and ethylene glycol intoxication should also be considered. The aim of this study was to investigate the short-term prognostic factors in patients with alcoholic liver disease with metabolic acidosis. METHODS: Clinical data related to twenty-nine patients with alcoholic liver disease and metabolic acidosis was analysed retrospectively. Patients were divided into two groups according to the outcome (survival or death). Past medical history, and physical, laboratory and radiologic data at admission were compared. RESULTS: The amount of daily alcohol intake differed significantly between the two groups (P=0.034), but duration and total amount of alcohol intake did not differ significantly between the two groups (P=0.128; P=0.360). The presence of ascites differed significantly between two the groups (P=0.019). On laboratory testing, the following differed significantly: base excess (P=0.038), hemoglobin (P=0.019), platelet (P=0.040), total bilirubin (P=0.007), albumin (P=0.012), creatinine (P=0.014), phosphorus (P=0.021), chloride (P=0.010), ammonia (P=0.003), prothrombin time (P=0.033), fibrinogen (P=0.011) and D-dimer (P=0.024). Review of the medical history of the patients showed diabetes (10/29), cirrhosis (10/29), and hepatocellular carcinoma (1/29). Combined conditions at admission were sepsis (8/29), pneumonia (7/29), acute renal failure (6/29), rhabdomyolysis (5/29), gastrointestinal hemorrhage (4/29), acute pancreatitis (3/29), acute respiratory distress syndrome (2/29), and acute myocardial infarction (1/29). CONCLUSIONS: The amount of daily alcohol intake, base excess, hemoglobin, platelet, total bilirubin, albumin, creatinine, phosphorus, chloride, ammonia, prothrombin time, fibrinogen and D-dimer seemed to be useful parameters in predicting short-term prognosis of patients with alcoholic liver disease with metabolic acidosis. Further study is needed to define the significance of these factors.

Acidosis↗