Liver disease and alcohol: fatty liver, alcoholic hepatitis, cirrhosis, and their interrelationships.
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Alcoholism↗
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Fatty liver hepatitis and cirrhosis in obese patients.
Liver function and liver biopsy findings were studied in a selected group of 29 overweight patients. Fatty liver, fatty hepatitis, fatty fibrosis and fatty cirrhosis were seen with equal frequency. Diabetes was also present with an equal incidence in each of these four pathologic groups. Lipoprotein abnormalities, particularly type IV hyperlipoproteinemia, were found mostly in the two groups with the lesions with less fibrosis (fatty liver and fatty hepatitis). The pathologic picture resembled that of alcohol and postjejunoileal bypass-induced liver diseases suggesting a common denominator in these three conditions.
Adolescent↗
Auxiliary liver transplant in acute fatty liver of pregnancy.
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Adult↗
Associations between plasma adiponectin concentrations and liver histology in patients with nonalcoholic fatty liver disease.
OBJECTIVES: To explore associations between plasma adiponectin concentrations and liver histology in patients with nonalcoholic fatty liver disease (NAFLD). DESIGN AND PATIENTS: In a cross-sectional study, we enrolled 60 consecutive NAFLD patients and 60 age-, sex- and body mass index (BMI)-matched healthy controls. MEASUREMENTS: NAFLD (by liver biopsy), plasma adiponectin concentrations, insulin resistance (by homeostasis model assessment, HOMA-IR) and metabolic syndrome (MetS) features. RESULTS: NAFLD patients had a marked decrease in plasma adiponectin concentration (6.1 +/- 2.8 vs. 13.6 +/- 3.8 microg/ml, P < 0.001) compared with matched controls. MetS, as defined by the Adult Treatment Panel III (ATP III) criteria, and its individual components were more frequent among NAFLD patients. The marked differences in adiponectin concentrations that were observed between the groups were little affected by adjustment for age, sex, BMI, HOMA-IR score and MetS components. Notably, decreased adiponectin levels were closely associated with the degree of hepatic steatosis, necroinflammation and fibrosis (P < 0.001 for all) among NAFLD patients. By logistic regression analysis, low adiponectin levels independently predicted hepatic steatosis [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.5-5.8, P < 0.001] and necroinflammation (OR 3.1, 95% CI 1.9-7, P < 0.001), but not fibrosis (P = 0.07), after adjustment for age, sex, BMI, HOMA-IR and MetS components. CONCLUSIONS: NAFLD patients have markedly lower plasma adiponectin concentrations than control subjects. Low adiponectin levels are strongly associated with the severity of liver histology, thus further supporting the hypothesis that adiponectin might be involved in the development of NAFLD.
Adiponectin↗
[Treatment of liver diseases, especially of fatty liver with betaine citrate].
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Adult↗
Altered basal C-peptide/insulin molar ratios in obese patients with fatty liver.
To elucidate if the presence of fatty liver in obesity influences hepatic insulin extraction under basal conditions, serum immunoreactive insulin (IRI) and C-peptide immunoreactivity (CPR) were measured in 20 obese patients with normal glucose tolerance and in 8 normal subjects. The obese patients were subdivided into two groups matched for age and body weight according to the presence or absence of fatty liver: 8 obese patients without fatty liver (OBN) and 14 with fatty liver (OBF). Basal levels of IRI and CPR were significantly greater in the obese patients than in the normals, but were similar in the two obese groups. In the OBF group, the CPR/IRI molar ratios, a relative measure of hepatic insulin uptake, were significantly lower than in the other two groups, while the ratios of the normal and OBN groups were similar. The CPR/IRI molar ratios in all obese patients correlated well with the degree of fatty liver (r = 0.785, p less than 0.001). These results suggest that hepatic insulin extraction in a subgroup of obese patients is either reduced or indistinguishable from that of non-obese subjects, and that basal CPR/IRI molar ratio may serve as a useful indicator of the presence of fatty liver in simple obesity.
Adult↗
Rupture of the liver associated with acute fatty liver of pregnancy.
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Acute Disease↗
[Expression of uncoupling protein 2 and its relationship to the content of adenosine triphosphate in the nonalcoholic fatty livers of rats fed a high-fat diet].
OBJECTIVE: To investigate the expression of uncoupling protein 2 (UCP2) and its relationship to the content of adenosine triphosphate (ATP) in livers of nonalcoholic fatty liver disease (NAFLD) rats fed a fat-rich diet. METHODS: To produce a NAFLD model, a fat-rich diet, consisting of 10% lard oil + 2% cholesterol, was given to Sprague-Dawley rats for a period of 8, 12, 16 and 24 weeks. The normal control rats were fed normal diets. The expressions of UCP2 in the liver were detected by immunohistochemistry and semi-quantitative RT-PCR. The content of ATP of liver was measured by fluorometry. RESULTS: Simple fatty livers were observed in the model group after 8 weeks. From 12 week to 24 week, the livers of the model group rats gradually progressed from simple steatohepatitis to steatohepatitis with pericellular fibrosis. Both immunohistochemistry and semi-quantitive RT-PCR suggested the up-regulated expression of UCP2 in these NAFLD rat livers. The hepatic expression of UCP2 mRNA in the model group was increased with time, and peaked in 24 week by 4.2 times compared to the control group ( t = 16.474, P < 0.01). The ATP content of livers was significantly reduced in the model group compared with the control group at 16 weeks [(2.97+/-0.48) x 10(-8) micromol/g vs. (2.25+/-0.55) x 10(-8) micromol/g, t = 2.419, P < 0.05] and 24 weeks [(2.97+/-0.48) x 10(-8) micromol/g vs. (1.99+/-0.66) x 10(-8) micromol/g, t = 3.248, P < 0.01]. Furthermore, there was a negative correlation between the UCP2 mRNA expression and the content of ATP in the livers of the NAFLD group (r = -0.93, P < 0.01). CONCLUSIONS: The rat model of NAFLD could be replicated sucessfully by feeding a fat-rich diet for 24 weeks, and the mRNA and its protein of UCP2 were expressed un-regulated in livers of NAFLD. The increasing UCP2 might play a role in the reduction of ATP content in livers of the NAFLD rats.
Adenosine Triphosphate↗
Role of liver biopsy in the assessment of non-alcoholic fatty liver disease.
Assessments of liver biopsies are important in the diagnosis and management of non-alcoholic fatty liver disease. Histology remains the 'gold standard' for making the important distinction between simple steatosis, which is generally non-progressive and readily reversible, and steatohepatitis, which has the potential to progress to severe fibrosis or cirrhosis. Liver biopsy may also identify other causes of liver disease in patients thought to have fatty liver disease and vice versa. Histological grading and staging of fatty liver disease require further study but these are potentially important approaches for studying disease severity and progression, particularly in the context of clinical trials to assess novel therapeutic approaches.
Alcoholism↗
Acute fatty liver of pregnancy.
Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that occurs during the third trimester. The obstetric team must be familiar with this disease because early diagnosis and prompt delivery have dramatically improved prognosis, which was often fatal for both mother and child. Clinicians must have a high index of suspicion for this condition when a woman has nausea or vomiting, abdominal pain (particularly epigastric), jaundice, polyuria-polydipsia (without diabetes), increased serum transaminase activity or thrombocytopenia in late pregnancy. The disease rarely recurs during a subsequent pregnancy. The cause is unknown, but some cases of acute fatty liver of pregnancy have been associated with a genetic deficiency of fatty acid beta-oxidation. Because of the possibility of this congenital deficiency, infants of affected mothers should undergo close follow-up from birth.
Acute Disease↗
Effect of pyrazole administration on the isopropanol induced fatty liver.
The isopropanol induced fatty liver is prevented in the rat by prior administration of pyrazole. Acetone administration, on the other hand, determines an increase in the hepatic triglyceride level. These results suggest the implications of acetone in the induction of the fatty liver following acute isopropanol administration in the rat.
1-Propanol↗
Recurrent acute fatty liver of pregnancy associated with a fatty-acid oxidation defect in the offspring.
A case of a 29-year-old woman who has had two episodes both clinically and biochemically consistent with acute fatty liver of pregnancy is described. These episodes occurred in two successive pregnancies, and liver biopsy confirmed the diagnosis in the second pregnancy. Both pregnancies were managed by prompt fetal delivery; on both occasions this led to a complete biochemical resolution of the liver function abnormalities. Two healthy babies were delivered by ceasarian sections. This case is of particular importance because a rapidly progressive and devastating illness developed in both infants, leading to death at 6 1/2 and 6 months, respectively. The illness in both babies was characterized by wide-spread fatty infiltration of several vital organs and a failure of any treatment to influence the outcome of that illness. Studies suggested that the illness in the children was caused by a still ill-defined disorder of fatty acid oxidation. The biochemical disorder evidenced in this family is discussed, in an attempt to shed light on the etiology of acute fatty liver of pregnancy.
Acute Disease↗
Genes or environment to determine alcoholic liver disease and non-alcoholic fatty liver disease.
While the vast majority of heavy drinkers and individuals with obesity, insulin resistance, and the metabolic syndrome will have steatosis, only a minority will ever develop steatohepatitis, fibrosis, and cirrhosis. Genetic and environmental risk factors for advanced alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) seem likely to include factors that influence the severity of steatosis and oxidative stress, the cytokine milieu, the magnitude of the immune response, and/or the severity of fibrosis. For ALD, the dose and pattern of alcohol intake, along with obesity are the most important environmental factors determining disease risk. For NAFLD, dietary saturated fat and antioxidant intake and small bowel bacterial overgrowth may play a role. Family studies and interethnic variations in susceptibility suggest that genetic factors are important in determining disease risk. For ALD, functional polymorphisms in the alcohol dehydrogenases and aldehyde dehydrogenase alcohol metabolising genes play a role in determining susceptibility in Oriental populations. No genetic associations with advanced NAFLD have been replicated in large studies. Preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, TNF-alpha, transforming growth factor-beta, and angiotensinogen may be associated with steatohepatitis and/or fibrosis.
Environment↗
Acute fatty liver of pregnancy.
Acute fatty liver of pregnancy is a serious complication of the 3rd trimester associated with high rates of maternal-fetal morbidity and mortality. Prompt diagnosis and treatment are essential to achieve optimal maternal-fetal outcomes. Collaboration between critical-care and perinatal nursing staffs is a crucial component of managing patient care. A recent case of acute fatty liver of pregnancy is reported. A team approach resulted in the survival of the patient and the delivery of healthy twins.
Acute Disease↗
An ultrastructural study of the liver, kidney and myocardium in the fatty liver and kidney syndrome in the fowl.
In birds with the fatty liver and kidney syndrome large lipid droplets measuring up to 4 mum in diameter were observed in increased numbers in liver, kidney and heart muscle, particularly in the livers and the proximal convoluted tubules (PCT) of the kidneys. In the hepatocytes and the PCT a much smaller type of lipid particle (LP) was also observed, both intracellularly within the cisternae of the Golgi-ER system and outside the plasma membranes in the space between neighbouring parenchymal cells, within the space of Disse and among the basal processes of the PCT. The origin of these LP is discussed.
Animals↗
Safety and effectiveness of rosiglitazone in type 2 diabetes patients with nonalcoholic Fatty liver disease.
BACKGROUND/PURPOSE: Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease ranging in severity from steatosis to cirrhosis. Type 2 diabetes mellitus is a cause of primary NAFLD. Thiazolidinediones have been shown to enhance insulin sensitivity, improve glycemic control in type 2 diabetes patients and to improve the histologic markers of nonalcoholic steatohepatitis. This study aims to determine the safety and effectiveness of rosiglitazone in inadequately controlled type 2 diabetes patients with NAFLD. METHODS: Taiwanese type 2 diabetes patients with inadequate control on insulin secretagogues and metformin, with no history of significant alcohol ingestion, with mildly elevated serum aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) and a diagnosis of fatty liver determined by ultrasonography were enrolled. Patients were treated for 24 weeks with rosiglitazone, 4-8 mg daily. Primary endpoints were change in AST and ALT levels from baseline and reduction in A1C < 6.5%. RESULTS: Out of a total of 68 patients, 60 (88.2%) completed the study treatment without serious adverse events. Treatment in two (2.9%) patients was discontinued due to elevated AST or ALT levels to more than three times the upper limit of normal, and noncompliance or loss of follow-up in six (8.8%) patients. Of the 60 patients who completed the study treatment, mean fasting plasma glucose, A1C, fasting plasma insulin, mean ALT and homeostasis model assessment for insulin resistance were all significantly reduced. Normal AST and ALT levels were achieved and maintained for at least three consecutive measurements and through to the end of the study period in 20 (33.3%) patients. Weight increased by a mean of 2.6 +/- 2.4 kg (p < 0.001). CONCLUSION: Rosiglitazone was reasonably well tolerated in patients with inadequately controlled type 2 diabetes and NAFLD. One-third of patients showed improved liver function after treatment.
Analysis of Variance↗
Ultrastructure of lipogranulomas in human fatty liver.
Lipogranulomas from severe fatty livers due to alcoholism, diabetes or overweight were examined in the electron microscope. When a fat droplet protrudes through the cell membranes of a liver cell histiocytes and lymphyocytes settle around it, and a lipogranuloma is formed. Remnants of the liver cell may be seen between the fat droplet and the histiocytes. It is confirmed that the fat droplets are situated extracellularly in the fully developed lipogranulomas.
Cell Nucleus↗
[The relationship between serum adiponectin level and serum alanine aminotransferase elevation in Korean male with nonalcoholic fatty liver disease].
BACKGROUND/AIMS: Nonalcoholic fatty liver disease (NAFLD) comprises a large part of chronic liver diseases. Recently it was reported that adipokines are closely associated with the common risk factors for NAFLD, such as obesity, diabetes, dyslipidemia, and insulin resistance. We aimed to evaluate the changes in serum adiponectin, resistin and leptin concentrations related to alanine aminotransferase (ALT) elevations in Korean men with NAFLD. METHODS: We studies 38 men who were diagnosed with fatty liver by abdominal ultrasonography. None had a history of excessive alcohol consumption, autoimmune hepatitis, inherited or metabolic liver disease or viral hepatitis. The subjects were divided into two groups. One group had normal levels of ALT (n=28) and the other had increased ALT (n=10). We compared anthropometrical parameters, biochemical items and serum adipokine levels between these two groups. RESULTS: Serum adiponectin levels were lower in the increased ALT group than in the normal ALT group (3.89 +/- 1.77 vs 7.01 +/- 2.54 microgram/dL, P=0.001). But there were no significant differences in serum leptin and resistin levels between two groups (4.02 +/- 2.04 vs 3.26 +/- 1.41 ng/mL, p=0.245, 80.14 +/- 14.8 vs 80.5 +/- 11.34 ng/mL, P=0.937, respectively). Multiple linear regression analyses demonstrated that the serum adiponectin level is inversely correlated with serum ALT level and that the serum aspartate aminotransferase (AST) level is positively correlated with the serum ALT level. CONCLUSIONS: Our study shows that hypoadiponectinemia is associated with an ALT elevation in patients with NAFLD. Adiponectin may play an indirect role in the development of NAFLD.
Adiponectin↗