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PubMed1994

Acute fatty liver of pregnancy. Case report and review of the literature.

A case of acute fatty liver of pregnancy is presented. This case is characterized by many of the reported diagnostic features of AFLP, including the abrupt onset of symptoms with progressive liver failure, coagulopathy and encephalopathy, during the third trimester of pregnancy. Autopsy findings confirmed the diagnosis. The literature is reviewed, emphasizing the clinical and laboratory features helpful in the diagnosis of this entity.

Acute Disease↗
PubMed1990

Magnetic resonance imaging and computed tomography scan for the diagnosis of acute fatty liver of pregnancy.

Magnetic resonance imaging (MRI) and computed tomography were used to diagnose fatty liver of pregnancy in a patient with preeclampsia and thrombotic thrombocytopenia purpura. The clinical course included multiple system failure that necessitated mechanical ventilation, dialysis, and plasmapheresis. The MRI picture is described in this entity for the first time. Both imaging techniques are discussed and compared.

Adult↗
PubMed1993

Effect of dietary protein and selected antioxidants on fatty liver hemorrhagic syndrome induced in Japanese quail.

The effects of CP and antioxidants on fatty liver hemorrhagic syndrome (FLHS) in Japanese quail hens were studied. In Experiment 1, four treatments were arranged as a 2 x 2 factorial; dietary CP (18 or 24%) and reduced glutathione (GSH, 0 or 120 mg/kg diet) were the major variables, but cysteine and other amino acids were higher in the 24% CP diets. Negative control (NC1) and positive control (PC1) diets were also evaluated. In Experiment 2, the effects of vitamin E (VE) and GSH were evaluated in the presence and absence of adequate dietary sulfur amino acids. Negative control (NC2) and positive control (PC2) diets were used. In both experiments, liver hemorrhage was most severe in quail fed the diets that were formulated to induce hepatic steatosis and limit oxidant defense capability. Liver hemorrhage was least severe in quail fed the diets that were formulated to minimize liver lipid accumulation and support oxidant defenses. Histological evaluation of affected quail livers showed changes consistent with FLHS in chicken hens. In Experiment 1, neither CP concentration nor GSH supplementation influenced liver hemorrhage. In Experiment 2, liver hemorrhagic score was reduced from 3.8 to 2.7 (P < or = .05) by adding VE to the basal diet. The PC2 diet further depressed liver score to only 2.0 (P < or = .05). The data clearly show that Japanese quail are susceptible to FLHS and indicate that a combination of lipotropic and antioxidant nutrients is protective against hemorrhage, even when lipogenic demands are maximized by feeding diets devoid of added fat.

Animals↗
PubMed2006

Fatty liver and hepatic function for residents with markedly high serum PCDD/Fs levels in Taiwan.

This study was designed to examine the associations between serum polychtorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) levels and adverse hepatic-related health outcomes. Residents living in the vicinity of a closed pentachlorophenol (PCP) manufacturing factory (exposure area) and other areas nearby (control area) were identified from prior investigation of serum PCDD/Fs measurements. A total of 85 subjects were recruited for the study, 52 from exposure area and 33 from control, respectively. Average level of serum PCDD/Fs was 80.1 6 50.9 pg WHO-TEQ/g lipid for those residing in exposure area, and 25.5 6 18.2 in control area. Statistically higher odds ratio (ORs) for fatty liver and gamma-glutamyltransferase (GGT) activity was found in subjects with higher serum PCDD/Fs levels and high body mass index (BMI) as compared to those with lower PCDD/Fs levels and less BMI. Data suggest that dioxin exposure and high lipid content affect the prevalence of fatty liver in exposed subjects. Future study should be directed to prevent continuous exposure to environmental PCDD/Fs from the defunct PCP factory, and to characterize prospectively, with a larger study sample size, the potential long-term consequences on hepatic function associated with contaminant exposure.

Adult↗
PubMed2004

Non-alcoholic fatty liver disease--a common and benign finding in octogenarian patients.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD), a common entity in the general population, has been shown to be linked with insulin resistance and metabolic syndrome. Several of the components of the metabolic syndrome are more common in the aged population. The aims of the current study were to determine in the aged, the prevalence and the clinical presentation of NAFLD, as well as the relation to the underlying metabolic abnormalities. METHOD: In this prospective study, we evaluated 91 octogenarians with a mean age of 85.56+/-3.76 years, who were admitted to the rehabilitation departments of a geriatric hospital. Clinical evaluation included: abdominal ultrasound (US), fasting glucose and lipid levels, serum liver enzymes, ferritin, iron and transferrin saturation. Elderly patients with NAFLD were compared with 46 young patients with NAFLD. RESULTS: NAFLD diagnosed by US was a common finding in this aged population, is present in 42/91 patients (46.2%). No significant differences were observed between the patients with or without NAFLD in the following: age, gender, chronic illnesses, anthropometric parameters, lipid profile, fasting glucose levels, metabolic syndrome prevalence, serum levels of transaminases, ferritin and iron. Young patients with NAFLD had significantly higher serum levels of triglycerides and a significantly higher prevalence of glucose intolerance, obesity and the metabolic syndrome compared with the elderly patients with NAFLD. CONCLUSIONS: NAFLD was a common finding in our group of elderly patients and the prevalence was higher than reported in the general population. In contrast to the well-described association between the metabolic syndrome and NAFLD in the general population, we did not find this association in the aged group. In addition, none of the patients had stigmata of advanced liver disease. These data suggest that NAFLD is a common and benign finding in the elderly population, but is not associated with the metabolic syndrome.

Age Factors↗
PubMed1983

Acute fatty liver of pregnancy with complicating disseminated intravascular coagulation.

A description is given of acute fatty liver of pregnancy in a 26-year-old primigravida who survived. Complicating disseminated intravascular coagulation was diagnosed at parturition, and the importance of early diagnosis of this is emphasized. A suggestion for treatment is given as a possible means of improving the prognosis in this mostly fatal disease.

Adult↗
PubMed1994

Genetic parameters from factorial cross breeding in two duck strains (anas platyrhynchos) Brown Tsaiya and Pekin, for growth and fatty liver traits.

1. A total of 655 mule ducklings were produced in three hatches by artificial insemination of common duck females Brown Tsaiya and Pekin "Alienor" and of their 2 reciprocal crossbreds with Muscovy semen. 2. They were fed ad libitum until 6 weeks, then restricted to one meal per day until day 75 and afterwards preforce fed until day 84 and subsequently forced fed by 2 crammers, twice a day, from the age of 85 d and for a maximum of 13 d. 3. Body weight at hatching, 28 d, 56 d, 75 d, 84 d and at slaughter, the number of force-fed meals, the "paletot" weight, the fatty liver weight, the fat release rate after sterilisation of a 60 g portion of liver and the serous melting rate were measured individually. 4. Significant dam genotype and hatch effects were present for all traits. The crammer effect on force feeding traits was also significant. For mule ducks from Brown Tsaiya, Tsaiya x Pekin, Pekin x Tsaiya and Pekin dams respectively, mean body weight was 2356, 3219, 3137 and 3801 g at 12 weeks, "paletot" weight was 1585, 2111, 2110 and 2470 g, fatty liver weight was 441, 585, 563 and 641 g, fat release rate was 35.1, 40.5, 38.2 and 46.0%. 5. The estimated differences between Pekin and Tsaiya genetic effects in their mule progeny were significant and in favour of the Pekin, except for the number of force fed meals and for the serous melting rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

The effect of postpartum rumen undegradable protein supplementation on hepatic gluconeogenic enzyme activities in dairy cows with fatty liver.

The effect of postpartum supplementation with rumen undegradable protein on the activities of gluconeogenic enzymes was studied in cows with induced fatty liver. Prepartum liver and blood samples were collected at about one week before the expected date of calving and postpartum samples were collected at 10 and 20 days (d) postpartum. At 10 d postpartum, concentrations of serum nonesterified fatty acids and hepatic triacylglycerol levels were higher than at one wk before parturition. The postpartum increases in nonesterified fatty acids and hepatic triacylglycerols were significantly higher in the cows that were fed extra protein than in the control cows. There were no differences between the groups with regard to postpartum changes in the concentrations of plasma glucose, liver glycogen, and serum insulin. The postpartum increase in the activity of fructose 1-6-bisphosphatase was higher in the test group than in the control group, but the increase in the activity of glucose-6-phosphatase was lower. There were no group differences in the postpartum activities of phosphoenolpyruvate carboxykinase, pyruvate carboxylase, and propionyl-CoA carboxylase. Our results suggest that intense lipolysis released more glycerol in the protein-supplemented cows, which stimulated the activity of fructose 1-6-bisphosphatase. However, postpartum rumen undegradable protein supplementation did not affect the activities of the other enzymes of gluconeogenesis, and fatty liver was even exacerbated.

Animal Feed↗
PubMed2005

Hepatic gene expression changes in mouse models with liver-specific deletion or global suppression of the NADPH-cytochrome P450 reductase gene. Mechanistic implications for the regulation of microsomal cytochrome P450 and the fatty liver phenotype.

NADPH-cytochrome P450 reductase (CPR) is an essential component for the function of many enzymes, including microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. In liver-Cpr-null (with liver-specific Cpr deletion) and Cpr-low (with reduced CPR expression in all organs examined) mouse models, a reduced serum cholesterol level and an induction of hepatic P450s were observed, whereas hepatomegaly and fatty liver were only observed in the liver-Cpr-null model. Our goal was to identify hepatic gene expression changes related to these phenotypes. Cpr-lox mice (with a floxed Cpr gene and normal CPR expression) were used as the control. Through microarray analysis, we identified many genes that were differentially expressed among the three groups of mice. We also recognized the 12 gene ontology terms that contained the most significantly changed gene expression in at least one of the two mouse models. We further uncovered potential mechanisms, such as an increased activation of constitutive androstane receptor and a decreased activation of peroxisomal proliferator-activated receptor-alpha by precursors of cholesterol biosynthesis, that underlie common changes (e.g. induction of multiple P450s and suppression of genes for fatty acid metabolism) in response to CPR loss in the two mouse models. Additionally, we observed model-specific gene expression changes, such as the induction of a fatty-acid translocase (Cd36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (Cpt1a) and acyl-CoA synthetase long chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis and an altered fatty acid profile observed in liver-Cpr-null mice.

Animals↗
PubMed2006

Non-alcoholic fatty liver disease (NAFLD)--a novel common aspect of the metabolic syndrome.

Non-alcoholic fatty liver disease (NAFLD) is emerging as one of the most common liver disorders claiming the urgent attention of both medical professionals and the public sphere because of the imminent epidemic of advanced liver injury that appendages epidemic of obesity. Recent research reveals simple triglyceride accumulation in hepatocytes (i.e., liver steatosis) frequently becoming complicated by inflammation (i.e., non-alcoholic steatohepatitis, or NASH) that may progress into more advanced stages of the disease including cirrhosis or, eventually, hepatocellular carcinoma. The exact mechanisms of the progression of NAFLD into overt NASH and advanced disease stages are largely unknown. There is urgent need in terms of both intensive research pursuits and effective practical measures to deal with this common threat.

Fatty Liver↗
PubMed1983

Fatty liver and kidney syndrome in chickens as an animal model for Reye's syndrome.

Fatty liver and kidney syndrome (FLKS), a naturally occurring but experimentally reproducible disease in chickens, has several clinical, pathological, and biochemical features in common with Reye's syndrome. Because of this, it has been suggested that FLKS may serve as an animal model of Reye's syndrome. We have examined, therefore, various parameters characteristic of Reye's syndrome in chickens affected with FLKS to further delineate the similarities and differences between the two disorders. Plasma glucose concentrations were significantly lower in chickens affected with FLKS which may be caused by the significantly reduced activity of pyruvate carboxylase in all FLKS-affected animals. The activity of propionyl CoA carboxylase was low in only the most severely affected chickens, and beta-methylcrotonyl CoA carboxylase showed no difference when compared with controls. This may be due to variable sensitivities of the three carboxylases to marginal biotin deficiency which occurs with FLKS. Plasma ammonia concentrations and activities of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, however, were not elevated in the affected birds. Histological changes in the liver and kidney were noted in affected chickens, but these changes were not identical with those observed in Reye's syndrome. Although the mechanisms of nitrogen elimination in fowl differ from those in humans, failure to demonstrate hyperammonemia, elevated serum transaminase activities, or similar histological changes in tissues of affected birds indicates that FLKS is not an appropriate model for the study of Reye's syndrome.

Ammonia↗
PubMed2005

Nonalcoholic fatty liver disease and risk of future cardiovascular events among type 2 diabetic patients.

Nonalcoholic fatty liver disease (NAFLD) is closely correlated to several metabolic syndrome features. We assessed prospectively whether NAFLD predicts future cardiovascular disease (CVD) events among type 2 diabetic individuals, independent of metabolic syndrome features and other classical risk factors. We carried out a prospective nested case-control study in 2,103 type 2 diabetic patients who were free of diagnosed CVD at baseline. During 5 years of follow-up, 248 participants (case subjects) subsequently developed nonfatal coronary heart disease (myocardial infarction and coronary revascularization procedures), ischemic stroke, or cardiovascular death. Using risk-set sampling, 496 patients (control subjects) among those who remained free of diagnosed CVD during follow-up were randomly selected in a 2:1 ratio, matched for age and sex to the case subjects. After adjustment for age, sex, smoking history, diabetes duration, HbA1c, LDL cholesterol, liver enzymes, and use of medications, the presence of NAFLD was significantly associated with an increased CVD risk (odds ratio 1.84, 95% CI 1.4-2.1, P < 0.001). Additional adjustment for the metabolic syndrome (as defined by National Cholesterol Education Program Adult Treatment Panel III criteria) appreciably attenuated, but did not abolish, this association (1.53, 1.1-1.7, P = 0.02). In conclusion, NAFLD is significantly associated with a moderately increased CVD risk among type 2 diabetic individuals. This relationship is independent of classical risk factors and is only partly explained by occurrence of metabolic syndrome.

Aged↗
PubMed2001

Influence of TT virus on the histopathological features of nonalcoholic fatty liver disease.

The sera of 38 patients with nonalcoholic fatty liver disease (NAFLD) including nonalcoholic steatohepatitis (NASH), were tested for TT virus (TTV) DNA by polymerase chain reaction (PCR) using three different primer pairs (UTR PCR, N22 PCR and genotype-1 PCR), and various histological features of the liver biopsy specimens were compared among those who were positive or negative for TTV infection. By UTR PCR which detects all TTV genotypes, TTV DNA was detected in 37 (97%) of the 38 patients. In contrast, N22 PCR which detects primarily TTV genotypes 1-4, detected TTV DNA in 18 patients (47%). In the liver biopsy specimens, moderate to many acidophilic bodies, moderate to marked focal/spotty necrosis of hepatocytes and marked stellate, pericellular or perivenular fibrosis were observed significantly more frequently among those who were positive for TTV DNA by N22 PCR, than among those who were negative by N22 PCR. Twelve patients (32%) were positive for TTV genotype 1. Moderate to marked vacuolation of nuclei, moderate to many acidophilic bodies, and moderate to marked focal/spotty necrosis as well as marked stellate, pericellular or perivenular fibrosis were found significantly more frequently in the TTV genotype 1-positive group than in the TTV genotype 1-negative group. These results suggest that certain TTV genotypes including genotype 1 influence the necrosis and inflammation of hepatocytes and liver fibrosis in NAFLD patients.

Journal Article↗
PubMed2001

Cryptogenic cirrhosis and posttransplantation nonalcoholic fatty liver disease.

Some patients diagnosed with cryptogenic cirrhosis may have "burned-out" nonalcoholic fatty liver disease (NAFL). To test this hypothesis, we used our liver transplant database (November 1984 to November 1998) to assess the incidence of NAFL in patients with cryptogenic cirrhosis after orthotopic liver transplantation (OLT). We also examined the clinicodemographic features associated with post-OLT NAFL, obtained by chart review and telephone interviews. When available, post-OLT liver biopsy specimens were reviewed blindly by a hepatopathologist according to the NAFL pathology protocol. We identified 51 patients with cryptogenic cirrhosis (mean age, 51 +/- 12 years); 60% were women, 94% were white, and 34% had type 2 diabetes mellitus (DM). Mean pre-OLT body mass index (BMI) was 27.33 +/- 5.54 kg/m(2). Twenty-five patients underwent at least 1 post-OLT liver biopsy. Post-OLT NAFL was identified in 13 patients (25.4%), whereas post-OLT nonalcoholic steatohepatitis (NASH) was seen in 8 patients (15.7%). Features associated with post-OLT NASH were pre- and post-OLT type 2 DM (P < or =.05) and an elevated fasting triglyceride level (P <.05). BMI tended to be greater in patients with post-OLT NAFL or NASH. Those who did not develop post-OLT NAFL showed a decrease in BMI. Patients with cryptogenic cirrhosis undergoing OLT resemble patients with NAFL. Post-OLT NAFL and NASH can be seen in a number of patients with cryptogenic cirrhosis. This supports the notion that some cases of cryptogenic cirrhosis represent burned-out NAFL.

Adult↗
PubMed2005

Acute fatty liver of pregnancy complicated with disseminated intravascular coagulation and haemorrhage: a case report.

Acute fatty liver of pregnancy (AFLP) is a rare disorder of unknown aetiology that is diagnosed typically in the third trimester or early postpartum period. The incidence is estimated to be 1/6692-1/13,328. The obstetric team must have a high index of suspicion of this pathology, particularly in the presence of clinical and laboratory findings, such as nausea, vomiting, jaundice, increased serum transaminase levels, increased prothrombin time and hypoglycaemia. Early diagnosis followed by prompt delivery and supportive care provides significantly improved maternal and perinatal outcome. Delay in diagnosis of this obstetric emergency may lead to rapid progression to hepatic failure, disseminated intravascular coagulation (DIC), haemorrhage, encephalopathy, multiple organ failure and finally death. The case of a 34-year-old woman, gravida 3, para 2, with AFLP complicated with DIC is presented herein with a review of literature and discussion of its origin.

Acute Disease↗
PubMed2006

Histologic spectrum of nonalcoholic fatty liver disease in morbidly obese adolescents.

BACKGROUND & AIMS: To characterize the spectrum of nonalcoholic fatty liver disease (NAFLD) in morbidly obese adolescents, we correlated liver histology with clinical features and compared findings with reported adult data. We hypothesized that NAFLD would be less severe as a result of younger age and shorter duration of obesity, but portal inflammation and fibrosis would be more prevalent. METHODS: Cross-sectional study was made of 41 adolescent subjects, 13-19 years old (mean, 16 years), 61% female, 83% non-Hispanic white, mean body mass index 59 kg/m(2), undergoing gastric bypass with liver biopsy. Liver biopsies were graded and staged as proposed by the NASH Clinical Research Network. Data were analyzed by using descriptive statistics, analysis of variance, and Fisher exact tests. RESULTS: Eighty-three percent had NAFLD: 24% steatosis alone, 7% isolated fibrosis with steatosis, 32% nonspecific inflammation and steatosis, and 20% nonalcoholic steatohepatitis (NASH). Twenty-nine percent had fibrosis; none had cirrhosis. Abnormal ALT (P = .05) and AST (P = .01) were more prevalent in NASH. Mean fasting glucose was significantly higher in NASH (P = .05), but prevalence of the metabolic syndrome was not significantly different. CONCLUSIONS: NAFLD was very prevalent in morbidly obese adolescents, but severe NASH was uncommon. In contrast to morbidly obese adults, lobular inflammation, significant ballooning, and perisinusoidal fibrosis were rare, whereas portal inflammation and portal fibrosis were more prevalent, even in those who did not meet criteria for NASH. These findings might support use of a modified scoring system for pediatric NASH. Presence of the metabolic syndrome in morbidly obese adolescents did not distinguish NASH from steatosis alone.

Adolescent↗