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PubMed1977

Nonalcoholic fatty liver with alcoholic hyalin after long-term glucocorticoid therapy.

Alcoholic hyalin was found in liver of a nonalcoholic patient with fatty liver after long-term glucocorticoid therapy for systemic lupus erythematosus. Hepatocytes including hyalin bodies showed fatty change or vesiculated degeneration. Occasionally, basophilic substance which was recognized in the hepatocytes with or without hyalin was noticed showing the feature quite similar to delicate alcoholic hyalin.

Adult↗
PubMed2002

Absence of sterol regulatory element-binding protein-1 (SREBP-1) ameliorates fatty livers but not obesity or insulin resistance in Lep(ob)/Lep(ob) mice.

Obesity is a common nutritional problem often associated with diabetes, insulin resistance, and fatty liver (excess fat deposition in liver). Leptin-deficient Lep(ob)/Lep(ob) mice develop obesity and those obesity-related syndromes. Increased lipogenesis in both liver and adipose tissue of these mice has been suggested. We have previously shown that the transcription factor sterol regulatory element-binding protein-1 (SREBP-1) plays a crucial role in the regulation of lipogenesis in vivo. To explore the possible involvement of SREBP-1 in the pathogenesis of obesity and its related syndromes, we generated mice deficient in both leptin and SREBP-1. In doubly mutant Lep(ob/ob) x Srebp-1(-/-) mice, fatty livers were markedly attenuated, but obesity and insulin resistance remained persistent. The mRNA levels of lipogenic enzymes such as fatty acid synthase were proportional to triglyceride accumulation in liver. In contrast, the mRNA abundance of SREBP-1 and lipogenic enzymes in the adipose tissue of Lep(ob)/Lep(ob) mice was profoundly decreased despite sustained fat, which could explain why the SREBP-1 disruption had little effect on obesity. In conclusion, SREBP-1 regulation of lipogenesis is highly involved in the development of fatty livers but does not seem to be a determinant of obesity in Lep(ob)/Lep(ob) mice.

Adipose Tissue↗
PubMed2004

Non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH): treatment.

Non-alcoholic fatty liver disease is now recognized as a cause of potentially progressive liver damage, posing patients at risk of advanced liver failure. Unfortunately, the natural history of disease is only partly known, the disease is slowly progressive and therapeutic outcomes are difficult to define. These factors have limited therapeutic trials to pilot studies, and very few randomized-controlled studies are available. The concept that insulin-resistance, coupled with oxidative stress, may be the underlying mechanism responsible for fat accumulation and disease progression points to insulin-sensitizing agents (metformin, thiazolidinediones) as the most promising drugs. They proved effective in reducing enzyme levels in the short period, but very limited information is available on liver histology, not to say progression to liver cell failure. Large, long-term, placebo-controlled randomized studies are eagerly awaited. Outside controlled studies, nutritional counselling and physical exercise aimed at moderate weight loss remain the basis of any therapeutic intervention.

Antioxidants↗
PubMed2006

Heritability and genetic loci of fatty liver in familial combined hyperlipidemia.

VLDL overproduction, a process that is driven by an excess amount of hepatic fat, is a well-documented feature of familial combined hyperlipidemia (FCHL). The aims of this study were to investigate whether fatty liver, measured with ultrasound and as plasma alanine aminotransferase (ALT) levels, develops against a genetic background in FCHL and to identify chromosomal loci that are linked to these traits. In total, 157 FCHL family members and 20 spouses participated in this study. Radiological evidence of fatty liver was more prevalent not only in FCHL probands (40%) but also in their relatives (35%) compared with spouses (15%) (P < 0.05). Heritability calculations revealed that 20-36% of the variability in ALT levels could be attributed to genetic factors. Nonparametric quantitative trait locus (QTL) analysis revealed three significant (P < 0.001) loci with either the ultrasound or the ALT trait in the male sample: 1q42.3, 7p12-21, and 22p13-q11; none was found in the female sample or the entire group. Of these QTLs, the 7p region was consistent over time, because reanalysis with ALT levels that were determined during a visit 5 years earlier yielded similar results. This study shows that fatty liver is a heritable aspect of FCHL. Replication of particularly the 7p region is awaited.

Adult↗
PubMed1991

Intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy. An unusual but favorable association?

During the 26th week of a first pregnancy, a 25-year-old woman presented with pruritus suggesting an intrahepatic cholestasis of pregnancy. The pruritus, however, persisted despite the premature delivery of a normal newborn at the 35th week. Moreover, aspartate aminotransferase activity increased, reaching a maximum of 38 times normal level on the 17th day after the delivery. Thus, an acute fatty liver of pregnancy was suspected and confirmed by liver biopsy. This patient appeared to have both intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy, an association not previously reported. It is suggested that intrahepatic cholestasis of pregnancy caused premature delivery, which in turn may have prevented the onset of severe maternal and fetal complications caused by acute fatty liver of pregnancy.

Adult↗
PubMed1992

[Fatal course of peracute fatty liver of pregnancy].

A fatal case of acute fatty liver of pregnancy (AFLP) is reported. After admission, the patient was delivered within 3 hours. Routine laboratory investigation revealed acute liver insufficiency with advanced coagulopathy. Despite substitution therapy, the severe coagulation defect progressed to lethal intracerebral bleeding. Advanced AFLP can only be satisfactorily diagnosed in time, if non-specific symptoms or icterus lead to studies of blood chemistry, especially liver function tests, coagulation parameters (including platelet count, fibrinogen, AT III), blood glucose and renal function (including uric acid). This will enable an adequate management of the patient. The clinical problem of AFLP still remains that of early diagnosis.

Acute Disease↗
PubMed1970

Idiopathic acute fatty liver of pregnancy.

A maternal survivor of idiopathic fatty liver, with the characteristic histological appearance on liver biopsy, is reported. Profound hypoglycaemia was the major complication in this patient and it is suggested that more attention should be given to the blood glucose in this disease. The consideration of future pregnancy in this patient is discussed.

Acute Disease↗
PubMed1990

Carnitine metabolism in rats with 4-pentenoic acid induced fatty liver.

The effects of 4-pentenoic acid, a chemical claimed to induce fatty liver morphologically similar to that seen in Reye's syndrome, on carnitine metabolism and on hepatic histology were studied. Male Wistar rats were injected with 50 mg/kg doses of 4-pentenoic acid intraperitoneally every four hours over a period of 82 hours. Control rats received a similar volume of saline instead. The animals were then sacrificed at 82 hours. Liver, serum and urine were collected and stored in dry ice. The concentrations of free, acyl-, and total (free plus acyl) carnitines determined in serum were found to be significantly decreased in the rats which had received 4-pentenoic acid, while the concentrations of acyl- and total carnitines were significantly elevated in urine. In the liver tissue, the concentrations of short chain- and medium chain-acylcarnitines tended to be elevated, but the differences were not statistically significant. These results suggest that enhanced acylation of free carnitine with metabolites of 4-pentenoic acid, and excretion of the resulting acylcarnitine into urine are likely mechanism of the 4-pentenoic acid-induced hypocarnitinemia. Liver histology revealed marked fatty change with minute fat droplets similar to those observed in Reye's syndrome, and very slight alteration in mitochondrial configuration.

Animals↗
PubMed1987

Obesity-related nonalcoholic fatty liver: CT features and follow-up studies after low-calorie diet.

The features on computed tomographic (CT) scans of nonalcoholic fatty liver were investigated in 24 patients with nonalcoholic fatty liver related to overweight. CT examinations were performed before and after 3 months of a low-calorie diet. The reversibility of fatty infiltration during diet therapy could be monitored by changes in appearance on repeated CT scans. Hepatic steatosis improved, as assessed from increases in attenuation values on CT scans after 3 months of the diet, and the improvement was accompanied by a decrease in the elevated serum glutamic-pyruvic transaminase activity. Hepatic fatty infiltration in these patients was not always uniform, and attenuation values in the right lobe of the liver were significantly lower than those in the left lobe. After the 3-month diet therapy, the mean liver volume was significantly reduced, while the spleen volume was unchanged. Two sequential CT examinations, performed before and after diet therapy, may be useful for evaluating obese patients with elevated serum transaminase activity.

Adult↗
PubMed2004

Nonalcoholic fatty liver disease in individuals with severe obesity.

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disorder occurring in individuals without significant alcohol consumption. It consists of a spectrum of liver disease, ranging from simple steatosis to steatohepatitis, cirrhosis, liver failure, and hepatocellular carcinoma. Although a number of conditions have been identified as risk factors, obesity is by far the most dominant risk factor for developing NAFLD. Over the past decade, it became apparent that NAFLD in some patients is a progressive disorder,leading to cirrhosis and liver failure. Despite lack of direct evidence,due to the ongoing epidemic of obesity in western countries, it is believed that the incidence of NAFLD is increasing, and patients with complicated and uncomplicated NAFLD will present in increasing numbers to primary care physicians as well as specialists. This article discusses the prevalence, histologic spectrum, and natural history of NAFLD in subjects with severe obesity as well as the hepatic effects of drastic weight loss induced by bariatric surgery or severe calorie restriction.

Adult↗
PubMed2003

Vitamin C and vitamin E in prevention of Nonalcoholic Fatty Liver Disease (NAFLD) in choline deficient diet fed rats.

AIM: Oxidative stress has been implicated in the pathogenesis of Nonalcoholic Fatty Liver Disease (NAFLD). Vitamin C and vitamin E are known to react with reactive oxygen species (ROS) blocking the propagation of radical reactions in a wide range of oxidative stress situations. The potential therapeutic efficacy of antioxidants in NAFLD is unknown. The aim of this study was to evaluate the role of antioxidant drugs (vitamin C or vitamin E) in its prevention. METHODS: Fatty liver disease was induced in Wistar rats by choline-deficient diet for four weeks. The rats were randomly assigned to receive vitamin E (n = 6) - (200 mg/day), vitamin C (n = 6) (30 mg/Kg/day) or vehicle orally. RESULTS: In the vehicle and vitamin E-treated rats, there were moderate macro and microvesicular fatty changes in periportal area without inflammatory infiltrate or fibrosis. Scharlach stain that used for a more precise identification of fatty change was strong positive. With vitamin C, there was marked decrease in histological alterations. Essentially, there was no liver steatosis, only hepatocellular ballooning. Scharlach stain was negative. The lucigenin-enhanced luminescence was reduced with vitamin C (1080 +/- 330 cpm/mg/min x 10(3)) as compared to those Vitamin E and control (2247 +/- 790; 2020 +/- 407 cpm/mg/min x 10(3), respectively) (p < 0.05). Serum levels of aminotransferases were unaltered by vitamin C or vitamin E. CONCLUSIONS: 1) Vitamin C reduced oxidative stress and markedly inhibited the development of experimental liver steatosis induced by choline-deficient diet; 2)Vitamin E neither prevented the development of fatty liver nor reduced the oxidative stress in this model.

Journal Article↗
PubMed1989

[Acute fatty liver in pregnancy. Presentation of a case].

Acute fatty liver of pregnancy (AFLP) is not a very frequent disease, of unknown etiology mainly present in the 3rd trimester of the pregnancy. Early diagnosis and treatment including interruption of pregnancy (delivery or caesarean section) had been the key for decreasing fetal-maternal morbidity-mortality in recent years. This paper analyzes a clinical report of a 30 years old woman suffering AFLP histologically confirmed admitted to our hospital two weeks after illness started and who died because of secondary complications which did not respond to management probably because it was too late.

Adult↗
PubMed2006

Non alcoholic fatty liver disease: a clinical approach and review.

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of incidental elevation of liver enzymes in North America and Europe. Risk factors for NAFLD include body mass index of 25 kg/m2 or greater, central obesity and diabetes mellitus. The spectrum of disease is variable, ranging from simple steatosis with benign prognosis, to non-alcoholic steatohepatitis and cirrhosis, conferring increase in morbidity and mortality. The primary abnormality or 'first hit' in patients with NAFLD is insulin resistance leading to hepatic steatosis. The second hit involves multiple proinflammatory cytokines resulting in non-alcoholic steatohepatitis. Treatment is aimed at aggressive risk factor control and weight loss. Currently, there are no pharmacological agents recommended in the treatment of NAFLD, although preliminary studies suggest promising agents in the future.

Antioxidants↗
PubMed1976

Is fatty liver induction a general feature of the administration of foreign sulfhydryl compounds?

The intraperitoneal administration of 2-mercaptoethanol or 2-mercaptoacetate (40 muM/100 g body weight) to the rat induces a fatty liver, a marked and early increase of free fatty acids and a decrease of triacylglycerol and phospholipids in the blood. These changes are accompanied by a decrease of the ketone body level and the beta-hydroxybutyrate/acetoacetate ratio in the liver. Under the same experimental conditions, however, administration of 2-mercaptopropionate fails to induce a fatty liver and does not modify the hepatic ketone body level or the blood triacylglycerol and free fatty acid levels. These results led us to conclude that fatty liver induction is not a general feature of foreign thiols, and suggest that increased peripheral fat mobilization as well as decreased hepatic lipoprotein synthesis and/or release are responsible for the 2-mercaptoethanol- and 2-mercaptoacetate-induced fatty liver.

Animals↗
PubMed2003

A randomized double-blind study of the short-time treatment of obese patients with nonalcoholic fatty liver disease with ursodeoxycholic acid.

In order to determine the effect of ursodeoxycholic acid on nonalcoholic fatty liver disease, 30 patients with body mass indices higher than 25, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) or gamma-glutamyltransferase (gamma-GT) at least more than 1.5 times the upper limit of normality, and hepatic steatosis demonstrated by ultrasonography were randomized into two groups of 15 patients to receive placebo or 10 mg kg-1 day-1 ursodeoxycholic acid for three months. Abdominal computed tomography was performed to quantify hepatic fat content, which was significantly correlated with histological grading of steatosis (r s = -0.83, P < 0.01). Patient body mass index remained stable for both groups throughout the study, but a significant reduction in mean ( +/- SEM) serum levels of ALT, AST and gamma-GT was observed only in the treated group (ALT = 81.2 +/- 9.7, 44.8 +/- 7.7, 48.1 +/- 7.7 and 52.2 +/- 6.3 IU/l at the beginning and after the first, second and third months, respectively, N = 14, P < 0.05). For the placebo group ALT values were 66.4 +/- 9.8, 54.5 +/- 7, 60 +/- 7.6 and 43.7 5 IU/l, respectively. No alterations in hepatic lipid content were observed in these patients by computed tomography examination (50.2 +/- 4.2 Hounsfield units (HU) at the beginning versus 51.1 +/- 4.1 HU at the third month). These results show that ursodeoxycholic acid is able to reduce serum levels of hepatic enzymes in patients with nonalcoholic fatty liver disease, but this effect is not related to modifications in liver fat content.

Adult↗
PubMed2005

Hepatic stellate cells and fibrosis progression in patients with nonalcoholic fatty liver disease.

BACKGROUND & AIMS: Many patients with nonalcoholic fatty liver disease (NAFLD) have a benign clinical course, but a subgroup of patients progress to advanced fibrosis and cirrhosis. However, there are no available clinical tools to predict fibrosis progression in this population. Activated hepatic stellate cells (HSCs) are the source of collagen deposition in the liver. We aimed at determining whether an HSC activation score predicts fibrosis progression in NAFLD patients. METHODS: The cohort consisted of 39 untreated patients with NAFLD with paired liver biopsies performed 5-59 months apart (mean, 22 months). Patients were divided into 2 groups on the basis of whether fibrosis progression was noted on their second liver biopsy. Liver tissue was immunostained for alpha-smooth muscle actin, and the HSC score was determined independently by 2 pathologists in the NAFLD population and in control subjects without liver disease. RESULTS: The HSC activation score was significantly increased in patients with fibrosis progression versus patients in whom no fibrosis progression was observed (4.8 +/- 0.5 vs 1.8 +/- 0.6, respectively; P < .001). The HSC score was accurate in predicting fibrosis progression, with a positive predictive value of 90%, specificity of 94%, and an area under the receiver operating characteristic curve of 0.82. However, the negative predictive value and sensitivity were 56% and 41%, respectively. The inter-pathologist agreement for the HSC score was excellent (kappa coefficient, 0.95). CONCLUSIONS: These findings suggest that the HSC activation score is a suitable clinical tool to determine the risk of fibrosis progression in patients with NAFLD.

Adult↗
PubMed1982

Idiopathic acute fatty liver of pregnancy in 12 patients.

The clinical features, laboratory investigations and histopathology of 12 patients with idiopathic acute fatty liver of pregnancy are presented. Repeated vomiting, starting in the last trimester, was the cardinal symptom. Seven patients had proteinuria, hypertension and peripheral oedema before jaundice appeared. Caesarian section and induction of labour led to a lower than expected maternal mortality (33 X 3 per cent) and foetal mortality (66 X 7 per cent). There was a high incidence of twin and male births. Neutrophilia, thrombocytopenia and normoblasts were a uniform feature and uric acid levels were universally high. These findings may be useful in diagnosis in conjunction with liver function tests. Hepatic histology showed pathognomonic microvesicular fat in swollen hepatocytes with central nuclei and centrilobular distribution. However, a diffuse pattern and the presence of significant inflammation and fibrin deposits led to an initial misdiagnosis in two patients. Histology of fetal livers and five placentae was normal. Seven subsequent normal pregnancies occurred in four patients. Acute fatty liver of pregnancy may be confused with acute hepatitis or toxaemia on both clinical and histological grounds. Accurate diagnosis should lead to improved management and lessen maternal and fetal mortality. This justifies more intensive and urgent investigation of nausea, vomiting and jaundice in the last trimester of pregnancy.

Acute Disease↗
PubMedDate not supplied

Nonalcoholic fatty liver disease: defining a common problem.

Non Alcoholic Fatty Liver Disease (NAFLD), with prevalence of 10-51% in general population involving all ages, is the major cause of elevation of ALT and a common finding by ultrasound screening and may range from simple steatosis, to Non Alcoholic Steatohepatitis (NASH) and its clinical consequences as cirrhosis and hepatocellular carcinoma. In this review will be analyse factors influencing the onset of the disease. NAFLD, primarly associated with insulin resistance, is in fact considered the hepatic manifestation of the metabolic syndrome: a cluster of disorder that includes obesity, diabetes mellitus, dyslipidaemia, arteriosclerosis and hypertension. The increased incidence and prevalence of obesity and diabetes may explain growing interest in NAFLD. Racial, ethnic, enviromental and behaviour models are also reviewed.

Alanine Transaminase↗