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PubMed2006

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

BACKGROUND: Alcohol is a major cause of liver disease and disrupts methionine and oxidative balances. S-adenosyl-L-methionine (SAMe) acts as a methyl donor for methylation reactions and participates in the synthesis of glutathione, the main cellular antioxidant. Randomised clinical trials have addressed the question whether SAMe may benefit patients with alcoholic liver diseases. OBJECTIVES: To evaluate the beneficial and harmful effects of SAMe for patients with alcoholic liver diseases. SEARCH STRATEGY: We searched The Cochrane Hepato-Biliary Group Controlled Trials Register (May 2005), The Cochrane Central Register of Controlled Trials in The Cochrane Library (Issue 2, 2005), MEDLINE (1950 to May 2005), EMBASE (1980 to May 2005), and Science Citation Index Expanded (searched May 2005). SELECTION CRITERIA: We included randomised clinical trials studying patients with alcoholic liver diseases. Interventions encompassed per oral or parenteral administration of SAMe at any dose versus placebo or no intervention. DATA COLLECTION AND ANALYSIS: We performed all analyses according to the intention-to-treat method using RevMan Analyses provided by the Cochrane Collaboration. We evaluated the methodological quality of the randomised clinical trials by quality components. MAIN RESULTS: We identified nine randomised clinical trials including a heterogeneous sample of 434 patients with alcoholic liver diseases. The methodological quality regarding randomisation was generally low, but 8 out of 9 trials were placebo controlled. Only one trial including 123 patients with alcoholic cirrhosis used adequate methodology and reported clearly on all-cause mortality and liver transplantation. We found no significant effects of SAMe on all-cause mortality (relative risks (RR) 0.62, 95% confidence interval (CI) 0.30 to 1.26), liver-related mortality (RR 0.68, 95% CI 0.31 to 1.48), all-cause mortality or liver transplantation (RR 0.55; 95% CI 0.27 to 1.09), or complications (RR 1.35, 95% CI 0.84 to 2.16), but the analysis is based mostly on one trial only. SAMe was not significantly associated with non-serious adverse events (RR 4.92; 95% CI 0.59 to 40.89) and no serious adverse events were reported. AUTHORS' CONCLUSIONS: We could not find evidence supporting or refuting the use of SAMe for patients with alcoholic liver diseases. We need more long-term, high-quality randomised trials on SAMe for these patients before SAMe may be recommended for clinical practice.

Humans↗
PubMed1993

Urinary level of L-fucose as a marker of alcoholic liver disease.

The urinary levels of L-fucose were measured in 93 alcoholics; 20 of these were without liver disease, 57 with noncirrhotic alcoholic liver disease, and 16 with alcoholic liver cirrhosis. In addition, patients with cirrhosis due to viral infection, and healthy subjects were evaluated. The mean urinary L-fucose concentration showed significantly higher values in patients with alcoholic liver disease and alcoholic liver cirrhosis when compared with the healthy subjects or the chronic alcoholics without liver disease (p < 0.001). The urinary L-fucose level was also significantly higher (p < 0.001) in cases of alcoholic liver cirrhosis than in noncirrhotic alcoholic liver disease (384 +/- 97 vs. 240 +/- 95 mumol/g of creatinine). No difference was observed between the healthy subjects and chronic alcoholics without liver disease (143 +/- 29 vs. 155 +/- 60 mumol/g of creatinine). The urinary level of L-fucose was significantly higher with alcoholic cirrhosis (384 +/- 97 mumol/g of creatinine) than with viral cirrhosis (265 +/- 42 mumol/g of creatinine) (p < 0.001). The measurement of urinary L-fucose may be a useful marker of alcoholic liver disease.

Adult↗
PubMed1980

Histological demonstration and frequency of intrahepatocytic copper in patients suffering from alcoholic liver disease.

This study was carried out to determine whether stainable copper accumulates in the hepatocytes of patients with alcoholic liver disease. Liver sections from 44 cases of alcoholic cirrhosis and 32 cases of non-cirrhotic alcoholic liver disease were stained by the rubeanic acid, rhodanine and orcein methods. Intrahepatocytic copper granules were found in 13 cases of cirrhosis (30%), but in none of the non-cirrhotic livers. The abundance of granules did not appear to be related either to the activity of the cirrhotic process or to the presence of cholestasis. It may well be that alcoholic cirrhosis is the most common disease associated with excess of intrahepatocytic copper.

Adult↗
PubMed2001

Hepatic perfusion parameters in chronic liver disease: dynamic CT measurements correlated with disease severity.

OBJECTIVE: The aim of our study was to determine if hepatic perfusion parameters measured with CT change in relation to disease severity in patients with chronic liver disease. SUBJECTS AND METHODS: Dynamic contrast-enhanced single-section CT scans of the liver were obtained in 40 individuals who included six control subjects, 16 patients with noncirrhotic chronic liver disease, and 18 patients with cirrhosis. Hepatic, aortic, and portal venous time-density curves were fitted to a dual-input one-compartment model to calculate the liver perfusion, arterial fraction, distribution volume, and mean transit time. RESULTS: Liver perfusion decreased in patients with cirrhosis (67 +/- 23 mL. min(-1). 100 mL(-1) versus 108 +/- 34 mL. min(-1). 100 mL(-1) in control subjects [p = 0.009] and 98 +/- 36 mL. min(-1). 100 mL(-1) in patients with noncirrhotic chronic liver disease [p = 0.003]), and the arterial fraction and the mean transit time increased (41 +/- 27% and 51 +/- 79 sec versus 17 +/- 16% and 16 +/- 5 sec in control subjects, and 19 +/- 6% and 17 +/- 8 sec in patients with noncirrhotic chronic liver disease [p < 0.05]). A significant correlation was seen between these three perfusion parameters and the severity of chronic liver disease based on clinical and biologic data (p < 0.001). No significant change in distribution volume was observed. CONCLUSION: Hepatic perfusion parameters measured with CT were significantly altered in cirrhosis and correlated with the severity of chronic liver disease.

Case-Control Studies↗
PubMed1992

Modern approach to alcoholic liver disease.

The pathogenesis of alcoholic liver disease is unclear. The recent literature on pathogenic factors, including direct effects of ethanol and its proximate metabolite acetaldehyde, associated nutritional factors, the formation of acetaldehyde-protein adducts, associated immune alterations, and the potential for liver injury due to coexisting hepatitis virus infection, is highlighted. The therapy of patients with advanced alcoholic liver injury, especially alcoholic hepatitis, is also controversial. It seems reasonable that all patients should receive adequate nutrition even if parenteral or enteral supplementation is required. Corticosteroid administration may benefit those patients with alcoholic hepatitis who have coexisting spontaneous hepatic encephalopathy and no gastrointestinal bleeding. For patients with complications from end-stage alcoholic cirrhosis, liver transplantation should be considered, as the patient with alcoholic cirrhosis does as well after liver transplantation as those patients with other forms of end-stage liver disease.

Ethanol↗
PubMed2006

Present status and perspectives of cell-based therapies for liver diseases.

In recent years the interest in liver cell therapy has been increasing continuously, since the demand for whole liver transplantations in human beings far outweighs the supply. From the clinical point of view, transplantation of hepatocytes or hepatocyte-like cells may represent an alternative to orthotopic liver transplants in acute liver failure, for the correction of genetic disorders resulting in metabolically deficient states, and for late stage liver disease such as cirrhosis. Although the concept of cell therapy for various diseases of the liver is widely accepted, the practical approach in humans often remains difficult. An international expert panel critically discussed the recent published data on clinical and experimental hepatocyte transplantation and the possible role of stem cells in liver tissue repair. This paper aims to summarise the present status of cell based therapies for liver diseases and to identify areas of future preclinical and clinical research.

Cell Transplantation↗
PubMed2003

Surgery in the patient with liver disease.

Management of the surgical patient with liver disease begins with a careful preoperative assessment (Fig. 1). Any clues to liver disease on history and physical examination should be investigated to ascertain the cause of the clinical finding. More data on surgical patients with unexpected liver disease are now available. Patients undergoing emergent surgery are at significant risk of developing liver dysfunction. Child's class still correlates strongly to postoperative complications. Cornerstones of perioperative management in these patients are medical treatment of complications of chronic liver disease, such as ascites; coagulopathy; prevention of encephalopathy; and rapid treatment of dangerous postoperative complications, such as acute acalculous cholecystitis. Evolving knowledge of the effects of anesthesia, improving surgical techniques, and use of better diagnostic tests will help in the reduction of perioperative complications in these patients.

Biliary Tract Surgical Procedures↗
PubMed1988

Nonhepatitis B-associated liver disease in a renal transplant population.

The spectrum of liver disease in a population of 293 patients receiving 353 renal transplants (1971-1984) was reviewed. This study looked retrospectively at the histological features of liver disease in this population, and prospectively at the clinical and biochemical features of liver disease associated with renal transplantation. In all patients, infection with hepatitis B was excluded. Six deaths, primarily attributable to hepatic failure have occurred: one, acute herpes simplex infection; one, subacute massive hepatic necrosis of uncertain etiology; two, pretransplant liver disease; and two, posttransplantation cirrhosis of uncertain etiology. Review of the hepatic histology of 26 patients with known liver disease following transplantation revealed a wide range of pathologies with few specific correlations with their clinical status or biochemical tests of liver function. The prevalence of hepatic dysfunction following transplantation in our patient population was assessed by prospective biochemical screening of 111 transplant recipients over a 6-month interval. During this time period, 27 patients (24%) displayed biochemical evidence of hepatic dysfunction. Liver disease was known to have predated transplantation in only three of 27. Episodes of abnormal liver function occasionally occurred during an identifiable acute illness (six of 27), although the majority (21 of 27) had chronic hepatic dysfunction. Transplant recipients with abnormal liver function could not be differentiated from a cohort with normal liver function on the basis of age, sex, duration of graft function, or alcohol/drug intake. The possible etiologies of nonhepatitis B liver dysfunction following renal transplantation are discussed, and the high prevalence of biochemical evidence of hepatic dysfunction in this population free of hepatitis B infection is emphasized.

Adult↗
PubMed2004

[Primary liver disease in the horse].

The clinical signs of liver disease are highly variable and non-specific. Irrespective of the cause or the duration of liver disease, more specific clinical signs, e.g. hepatic encephalopathy, become apparent in the advanced stages of the disease. Due to the non-specific clinical signs, the possible diagnosis of liver disease is frequently not taken into consideration. However, measurement of the plasma or serum concentrations of total bile acids and gamma glutamyl transferase (gamma GT) may provide valuable diagnostic information. The specific diagnosis can be confirmed by ultrasound examination of the liver and histological examination of a liver biopsy specimen. The most frequently documented liver diseases are acute hepatic necrosis, chronic hepatitis caused by pyrrolizidine alkaloids, cholelithiasis, and haemochromatosis. Immediate treatment with antibiotics and polyionic fluids, in association with supportive nutritional care, is usually necessary to maintain the horse until sufficient liver regeneration occurs to provide adequate function. The use of corticosteroids is contraindicated, except for patients with chronic active hepatitis. In some cases, e.g. portosystemic shunts or cholelithiasis, surgical intervention is indicated. Liver disease may be more common than is currently appreciated since little accurate information on the prevalence or incidence is available.

Animal Nutritional Physiological Phenomena↗
PubMed2006

Fetal fatty acid oxidation defects and maternal liver disease in pregnancy.

OBJECTIVE: The objective was to evaluate the relationships between all types of fetal fatty acid oxidation defects and maternal liver disease, including acute fatty liver of pregnancy and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. METHODS: This was a case-control study comparing fetal fatty acid oxidation defects to the outcome of maternal liver disease. Fifty case infants with fatty acid oxidation defects were identified, with 25 matched controls collected per case. This generated a total of 50 case infants and 1,250 control infants. Pregnancies were evaluated for the presence of maternal liver disease (comprised of acute fatty liver of pregnancy, HELLP syndrome, and preeclampsia evolving into HELLP syndrome) using a conditional logistic regression model. Subgroup analysis compared long chain to short and medium chain fatty acid defects. RESULTS: Maternal liver disease was noted in 16.00% of all fatty acid oxidation defect pregnancies compared with 0.88% in the general population (odds ratio 20.4, 95% confidence interval 7.82-53.2). These pregnancies demonstrated an 18.1-fold increase in maternal liver disease when compared with our matched population controls with unaffected fetuses. All classifications of fatty acid oxidation defects were at high risk of developing maternal liver disease. Long chain defects were 50 times more likely than controls to develop maternal liver disease and short and medium chain defects were 12 times more likely to develop maternal liver disease. CONCLUSION: Maternal liver disease is significantly higher across the entire spectrum of fatty acid oxidation defects pregnancies compared with the matched control population. Notably, there is significant risk to the pregnancies with fetuses affected with short and medium chain defects, not just those with fetal long chain fatty acid oxidation defects as previously reported. Future studies should examine the pathophysiology of all infant fatty acid oxidation defects and its implications for maternal liver disease for improved future health outcomes. LEVEL OF EVIDENCE: II-2.

Case-Control Studies↗
PubMedDate not supplied

Serum immunoglobulins (IgG, IgA, IgM) in chronic hepatitis C. A comparison with non-cirrhotic alcoholic liver disease.

BACKGROUND/AIMS: Serum immunoglobulin concentrations are commonly elevated in patients with liver cirrhosis. Immunoglobulin class increase may vary depending on the cause of liver disease. Hepatitis C virus is, together with alcohol, a leading cause of chronic liver disease. The present study aimed to evaluate serum IgG, IgA and IgM levels in chronic hepatitis C. Results were compared with those of patients with non-cirrhotic alcoholic liver disease and healthy controls. Special attention was given to cases with minimal liver disease, as an approach to evaluate if the causing agent, independently of liver damage, influences serum immunoglobulin levels. METHODOLOGY: A total of 274 patients with histologically-proven chronic hepatitis C, 121 alcoholics with non-cirrhotic liver disease (steatosis or alcoholic hepatitis), and 75 healthy controls were studied. Serum IgG, IgA, and IgM were assayed by nephelometry. RESULTS: Serum IgG was increased in patients with chronic hepatitis C with respect to both alcoholics (p < 0.001) and healthy controls (p < 0.001). IgG levels were similar in alcoholics and in controls. IgA was increased in patients with non-cirrhotic alcoholic liver disease with respect to both chronic hepatitis C patients (p < 0.001) and controls (p < 0.001). IgA values were similar in subjects with chronic hepatitis C and controls. Selective IgG or IgA alteration was present in cases with minimal liver disease (chronic hepatitis C with a Knodell index equal or lower than 3, and alcoholics with liver steatosis, respectively). CONCLUSIONS: Hepatitis C virus and alcohol are linked to a selective increase of serum IgG and IgA, respectively, even in cases with mild or minimal liver disease.

Adolescent↗
PubMed1995

Chronic liver disease mortality in the United States, 1979 through 1989.

OBJECTIVES: Rates and trends for chronic liver disease mortality in the United States were examined. METHODS: National Center for Health Statistics data on underlying cause of death for chronic liver disease for the United States from 1979 through 1989 were analyzed. Four groups of diseases and conditions included under the International Classification of Diseases, 9th Revision, code for chronic liver disease were assessed separately. RESULTS: From 1979 through 1989, there were 303,875 deaths from chronic liver disease; 48% were in the cirrhosis without alcohol group, 42% in the alcohol-related liver disease group, 8% in the liver disease without alcohol group, and 1.5% in the biliary cirrhosis group. Chronic liver disease death rates for Blacks were more than 1.5 times greater than those for Whites and for other races. Chronic liver disease mortality declined 22% overall among both sexes. The largest decreases were for liver disease without alcohol (42%) and cirrhosis without alcohol (25%), followed by alcohol-related liver disease (14%) and biliary cirrhosis (12%). CONCLUSION: Although declines in US chronic liver disease deaths have been attributed to declining alcohol consumption, these analyses suggest that greater declines have occurred in deaths not coded as alcohol related.

Adolescent↗
PubMed1978

Associated liver disease in alcoholic pancreatitis.

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.

Acute Disease↗
PubMed1991

Halothane in children with chronic liver disease.

Exacerbation of pre-existing liver disease after halothane anaesthesia has been reported in adult patients. A prospective study was performed in 38 children with biopsy-proven liver disease to assess the effect of surgery and halothane anaesthesia on liver function. Plasma liver enzyme levels were measured immediately preoperatively and again four to eight days after surgery and halothane anaesthesia. Minor elevations of both AST and ALT occurred in four patients but this was not associated with a clinical deterioration in the patients' postoperative recovery. In the children studied pre-existing liver disease did not predispose to a deterioration of liver function following surgery and halothane anaesthesia.

Adolescent↗
PubMed2005

Factors associated with advanced liver disease in adults with alpha1-antitrypsin deficiency.

BACKGROUND & AIMS: Alpha 1 -antitrypsin deficiency (AAT) is an autosomal recessive disease that affects 1 in 2500 persons and might lead to cirrhosis. Our study aim was to characterize the liver disease in AAT and identify factors associated with advanced liver disease. METHODS: A cohort of the Alpha-1 Foundation Registry who reported liver disease was surveyed with a liver disease questionnaire to obtain information related to liver disease, liver transplantation, and AAT phenotype. RESULTS: One hundred sixty-five of the 2175 participants in the registry reported a history of jaundice or liver disease, and 139 (84.2%) completed the questionnaire. Of these, 71.3% were PiZZ, 18.0% were PiMZ, and 5.7% did not know their phenotype. Analysis of 104 participants with a known age of diagnosis included 30 participants diagnosed with liver disease before 18 years, of whom 15 had advanced liver disease defined as liver transplantation or listed for liver transplantation. No differences in age, age at diagnosis, gender, race, phenotype, or infant jaundice were identified. Seventy-four participants were diagnosed after age 18 years, of whom 25 had advanced liver disease. In this group, advanced liver disease was associated with male gender ( P = .006) and a greater mean body mass index ( P = .01), but not with race, Pi phenotype, infant jaundice, diabetes, or hypercholesterolemia. Viral hepatitis was more frequently reported in the nontransplant group (34.7% vs 8.0%, P = .01), and the mean daily alcohol use was significantly greater in this group ( P = .04). CONCLUSIONS: Our results suggest that male gender and obesity but not alcohol or viral hepatitis predispose to advanced liver disease in adults with AAT.

Adult↗
PubMed1995

Hepatic venous outflow obstruction in patients with polycystic liver disease: pathogenesis and treatment.

Polycystic liver disease is commonly asymptomatic but may present with hepatomegaly, abdominal distension, and dull abdominal pain. Transudative ascites is a rare manifestation in these patients but may occur when portal hypertension is present resulting from associated hepatic fibrosis or after deroofing procedure of a cyst. Exudative ascites might suggest hepatic venous outflow obstruction. Four cases are described where hepatic venous outflow obstruction occurred in patients with polycystic liver disease. Three patients had orthotopic liver transplantation and one had a mesocaval shunt. Of the two patients that survived orthotopic liver transplantation both have shown considerable improvement in their symptoms. None of the patients had any confirmed procoagulant disorder. The mechanism of hepatic venous outflow obstruction in these patients seems to be mechanical compression of hepatic veins by the cysts and associated formation of thrombi in small hepatic vein tributaries. Patients with severe polycystic kidney/liver disease are at risk of hepatic venous outflow obstruction and the onset of this complication is heralded by tender hepatomegaly and presence of exudative ascites.

Adult↗
PubMed1994

Diet and liver disease--a glimpse into the future.

The complex interaction between liver disease and food intake is not well defined. There are two aspects to consider: how liver disease affects food intake and whether or not diet can affect liver disease. Acute and chronic liver disease have been shown to influence taste, smell, food preference, and appetite. The liver may also play a role in food selection through reflex pathways. Intake of various macronutrients can alter serum liver enzymes and bilirubin without necessarily being associated with changes in pre-existing liver disease. Nonetheless, there is evidence that diet can be associated with both adverse and beneficial changes in outcome in animal models and patients with liver disease. These issues are difficult to unravel; however, there is potential for significant clinical advances from examining this area.

Diet↗
PubMed1989

Hepatic osteodystrophy. Static and dynamic bone histomorphometry and serum bone Gla-protein in 80 patients with chronic liver disease.

To study the pathogenesis of osteoporosis in patients with chronic liver disease, we performed dynamic bone histomorphometry and measured serum bone Gla-protein in 80 patients with various types of chronic liver disease. These results were compared with results obtained in 40 healthy controls. Mean trabecular bone volume and mean trabecular thickness were significantly reduced in both men and women with chronic liver disease (p less than 0.001 for both measurements in men and p less than 0.01 for both measurements in women). Osteoporosis as defined by histologic parameters was present in 17 (21%) patients with no significant differences in prevalence rates among the various hepatic disorders. No patient had histologic evidence of osteomalacia, although mineralization lag times were prolonged (p less than 0.01 for men and women). Bone formation rates were significantly reduced in 46 (57%) patients, and unlike the static measurements, were related to the type and severity of the underlying liver disease. Patients with alcoholic liver disease, hemochromatosis, and cholestatic liver disease had lower bone turnover rates and osteoblastic surfaces (p less than 0.001 and p less than 0.05, respectively) than patients with chronic active hepatitis. Furthermore, the presence of hepatic cirrhosis was associated with diminished bone formation and lower osteoblast surfaces. Serum bone Gla-protein levels were significantly correlated with bone formation rates and osteoblast surfaces (r = 0.585 and r = 0.434, respectively). A reduction in osteoblast surfaces has not previously been demonstrated in liver disease. This reduction and the associated impairment of osteoblastic activity may contribute to the pathogenesis of osteoporosis and can be assessed by the measurement of serum bone Gla-protein.

Adult↗