Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic steatosis is an ongoing problem in total parenteral nutrition (TPN). The etiology of this deranged hepatic morphology is unclear, but lack of enteral stimulation and excess carbohydrate calories have been suggested as altering the intestinal hormone profile. In this study, adult male Sprague-Dawley rats (n = 28) received internal jugular catheters: group 1 (n = 7) received saline (3 cc/hr) and chow ad libitum; groups 2, 3, and 4 (n = 7) received 15, 20, and 25% dextrose-base TPN solutions, respectively, in quantities matching the caloric intake of paired ad libitum animals. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay, and livers were removed for histologic examination and determination of total hepatic lipid content. Portal and peripheral insulin levels rose in a linear fashion with increasing dextrose concentration. Lipid content increased with elevated portal venous insulin/glucagon ratio in groups 3 and 4. Periportal fatty infiltration increased with increasing dextrose concentrations. The results suggest that the liver's response to altered portal insulin/glucagon ratio may play an important role in changes of hepatic morphology associated with TPN.
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PMID:Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats. 313 73

Percutaneous transhepatic portal catheterization was performed in 68 cases of liver diseases in the 2 year period from 1978 to 1980. The Chiba University method was modified. Portal vein catheterization was successful in 61 cases (90%). Selective splenic vein catheterization was successful in 55 of the 61 cases (90%) and selective superior mesenteric vein catheterization in 59 cases (97%). The liver was punctured an average of 4.6 times in order to successfully insert the catheter into the main portal vein, and the number of punctures was less than 10 in 57 of the 61 cases (93%). The portal vein pressure was 310+/-67 mm H2O in idiopathic portal hypertension (8 cases), 290+/-83 in liver cirrhosis (33 cases), 193+/-71 in chronic hepatitis (7 cases) and 166+/-50 in fatty liver (4 cases). Portal vein pressure rose from 205+/-75 to 380+/-55 mm H2O in 11 cases after forced Valsalva maneuver. No major complications were encountered.
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PMID:Percutaneous transhepatic portal catheterization-modification of Chiba method and portal vein pressure in liver diseases. 713 52

Liver granulomas have long been known to pose diagnostic problems for pathologists; however, their prevalence and associated etiologic factors have not been studied in liver transplant patients. We reviewed 3632 liver biopsy specimens from 563 patients at two institutions and identified 42 patients with posttransplant granulomas. A possible or probable etiologic factor was identified in 30 (71%) cases. Most were epithelioid granulomas and microgranulomas located in the parenchyma associated with hepatocyte necrosis (21 cases, 50%). Portal-based granulomas were associated with recurrent primary biliary cirrhosis (5 cases, 12%), acute cellular rejection (2 cases, 4.8%), and a foreign body-type reaction (1 case, 2.4%). One case was associated with tuberculosis (2.4%), 4 cases occurred in a fatty liver (9.5%), and 8 patients had liver granulomas but no other significant abnormality. The granulomas were most frequent in the first 7 months after transplantation when the patients were biopsied more often and underwent episodes of rejection or acute hepatitis. Portal-based granulomas in this period were usually associated with acute cellular rejection. After 7 months, the frequency of granulomas as well as the number of biopsies decreased and portal-based granulomas associated with recurrent primary biliary cirrhosis were most common (5 cases, 12%). Rare, late-appearing parenchymal granulomas were also seen (3 cases) and consisted of 1 lipogranuloma and 2 cases of epithelioid granuloma. The latter were thought, in 1 patient, to be associated with parenchymal hepatocyte necrosis; the others were of unknown etiology.
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PMID:Hepatic granulomas following liver transplantation. Clinicopathologic features in 42 patients. 749 95

This study was designed to test the hypothesis that deprivation of enteral feeding contributes to the development of total parenteral nutrition (TPN)-induced hepatic dysfunction and that alterations of gut hormones are involved in its pathogenesis. Twenty-one adult Sprague-Dawley rats were randomized into three groups: group 1 received chow feeding ad libitum (288 kcal/kg per day); group 2 received dextrose-based TPN (320 +/- 5 kcal/kg per day); and group 3 received TPN (315 +/- 15 kcal/kg per day) plus chow feeding ad libitum (74 +/- 1 kcal/kg per day). After 7 days, portal blood was assayed for insulin, glucagon, gastrin, peptide YY, secretin, and vasoactive intestinal polypeptide; systemic blood for determination of liver function tests and serum lipid analysis. Liver biopsies were taken for histology and staining for fat, and the remainder of the livers were removed for tissue lipid analysis. TPN induced striking hepatic steatosis with prominent histologic changes and accumulation of lipids, mainly triglycerides and cholesterol ester, in the liver. Addition of enteral feeding to TPN-treated animals significantly reduced the histologic changes as well as lipid accumulation in the liver. Portal plasma levels of gastrin and peptide YY were reduced in animals maintained on TPN alone, with no change in secretin or vasoactive intestinal polypeptide levels. Enteral supplementation increased peptide YY levels in group 3, but not to normal, while gastrin secretion remained decreased. The serum triglyceride levels were decreased in both TPN groups; no differences were detected in the serum cholesterol levels or liver function tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of enteral feeding on hepatic steatosis induced by total parenteral nutrition. 816 98

A rabbit model for long-term total parenteral nutrition (TPN), specially provided with cholecystostomy tube, was designed to investigate further aspects of TPN-associated cholestasis (TPN-AC). Modified surgical procedures concerning vascular access, cholecystostomy tube implantation and authors' original modalities for prolonged infusion management in the rabbit were used. Continuous TPN was performed in 30 young rabbits. Five animals died during the experiment (16.6%) and were excluded from final evaluation. Twenty-five rabbits were successfully maintained on continuous TPN for 28 days without restraint, having a cholecystostomy tube implanted 1 week after initiation of TPN. The collection of blood samples and daily parenteral administration of drugs were simply accomplished via a central venous catheter. At the same time the cholecystostomy tube enabled us to perform daily bile sampling. Saline irrigation of the biliary tree could be carried out in conscious animals maintained on TPN. A 4-week duration of TPN in this rabbit model made it possible for the first time to accomplish serial liver biopsies in order to verify the evolution of histologic changes in TPN-related hepatic dysfunction and possible effects of surgical and medical treatment. A preliminary analysis of operative findings and histology was carried out. An enlarged gallbladder containing hyperviscous bile was found in 80% of the animals 1 week after initiation of TPN. At this time it was possible to observe the first histologic changes consistent with TPN-associated hepatic disease, such as moderate to severe hepatocyte degeneration and portal inflammation. Biliary sludge was seen after 3 weeks of TPN in 70% of the rabbits, as well as a subsequent progression of TPN-associated histologic findings. Portal fibrosis and fatty liver degeneration occurred in 50% of the rabbits and bile duct proliferation in all animals. After 4 weeks of TPN (at autopsy) gallstones were found in 20% of TPN animals, as well as further progression of bile duct proliferation and fibrosis. Our first experiences with this model and preliminary results suggest that this concept offers new possibilities for further elucidation of TPN-associated hepatic dysfunction.
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PMID:Long-term total parenteral nutrition and cholecystostomy tube in a rabbit model surgical procedure: management and preliminary results. 890 99

The effect of significant weight loss on nonalcoholic fatty liver disease remains unclear. In this case series of 36 selected obese patients, we examined the effect of weight loss on nonalcoholic fatty liver disease, including nonalcoholic steatohepatitis (NASH) and hepatic fibrosis. These 36 patients (11 males, 25 females) had paired liver biopsies, the first at the time of laparoscopic adjustable gastric band placement and the second after weight loss. Second biopsies were obtained from two groups: those requiring a subsequent laparoscopic procedure (n = 19) and those with index biopsy score of 2 or greater for zone 3-centric hepatic fibrosis (n = 17). All biopsies were scored, blinded to the patient's identity and clinical condition, for individual histological features and for NASH stage and grade. Initial biopsies demonstrated NASH in 23 patients and steatosis in 12 patients. Repeat biopsies were taken at 25.6 +/- 10 months (range, 9-51 months) after band placement. Mean weight loss was 34.0 +/- 17 kg, and percentage of excess weight loss was 52 +/- 17%. There were major improvements in lobular steatosis, necroinflammatory changes, and fibrosis at the second biopsy (P <.001 for all). Portal abnormalities remained unchanged. Only four of the repeat biopsies fulfilled the criteria for NASH. There were 18 patients with an initial fibrosis score of 2 or more compared with 3 patients at follow-up (P <.001). Those with the metabolic syndrome (n = 23) had more extensive changes before surgery and greater improvement with weight loss. In conclusion, weight loss after surgery provides major improvement or resolution of obesity and metabolic syndrome-associated abnormal liver histological features in severely obese subjects.
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PMID:Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss. 1518 6

Portal vein embolization is evolving as an important adjunctive tool in hepatic surgery. In select patients, preoperative hypertrophy of the future remnant liver via contralateral portal vein embolization decreases postoperative liver dysfunction. Hepatic steatosis is the most common liver parenchymal disorder in Western populations. Moderate and severe degrees of hepatic steatosis convey an increased risk of postoperative liver dysfunction following major hepatic resections, but no studies exist examining the role of preoperative portal vein embolization in patients with hepatic steatosis. In this manuscript, we review the indications for portal vein embolization currently supported by the literature and present a patient with moderate to severe steatosis who successfully underwent portal vein embolization and a subsequent major liver resection.
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PMID:Contralateral portal vein embolization for hepatectomy in the setting of hepatic steatosis. 1527 84

Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that can lead to hepatic fibrosis and cirrhosis. Portal fibrosis in the absence of NASH, called isolated portal fibrosis (IPF), has received less attention and has not been classified as a spectrum of NAFLD. The aims of this study were to determine the prevalence of IPF in subjects undergoing gastric bypass surgery, to identify biochemical variables associated with IPF, and to assess the metabolic syndrome as defined by the AdultTreatment Panel III criteria. We analyzed liver biopsies from 195 morbidly obese subjects after excluding all other causes of liver disease. The prevalence of fatty liver (FL) only, IPF, and NASH was 30.3%, 33.3%, and 36.4%, respectively. Several biochemical parameters significantly trended across the 3 groups, with IPF falling between FL and NASH. Hyperglycemia was the only metabolic parameter associated with NASH (OR, 5.4; 95% CI, 2.4-12; P < .0001) and IPF (OR, 2.8; 95% CI, 1.2-6.5; P = .01). Subjects with diabetes had the greatest risk for NASH (OR, 8; 95% CI, 3.3-19.7; P < .0001) and IPF (OR, 4.3; 95% CI, 1.6-11.6; P = .003). The metabolic syndrome was identified in 78.5% of subjects, and a significant trend for the number of metabolic criteria was observed across the spectrum of FL, IPF, and NASH. In conclusion, a significant subset of morbidly obese individuals has portal fibrosis in the absence of NASH that is associated with glycemic dysregulation. Therefore, IPF should be considered a spectrum of NAFLD that may prelude NASH in morbid obesity.
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PMID:Portal fibrosis and hepatic steatosis in morbidly obese subjects: A spectrum of nonalcoholic fatty liver disease. 1536 53

Clinical and pathological features were reviewed in 76 Japanese patients with non-alcoholic steatohepatitis (NASH). Forty-one were male and 35 were female with the mean age of 49.7 years old (range 15-75 years old, males; 46.3, females; 53.7 years old). Fifty-four percent of patients were preobese with a body mass index (BMI) between 25 and 30, while 16% of the patients were non-obese, and only 30% of the cases were morbidly obese, indicating that Japanese have a greater tendency to develop insulin-resistance and fatty liver disease than Western people. Hyperlipidemia was found in 51%, diabetes mellitus in 38%, and hypertension in 33% of the patients. Abnormally elevated liver function tests were found in one-third to two-thirds of the patients and were characteristically mild with 2- to 3-fold elevation from the normal range in the majority of the cases. Histological features of the liver were similar or identical to those reported in English literature and were characterized by fatty change, perivenular and pericellular fibrosis in zone 3, hepatocyte ballooning and necrosis with occasional Mallory's body formation and polymorphonuclear leukocyte infiltration. Mallory's bodies were found in 39% of patients and were characteristically small and poorly formed compared with those in alcoholic hepatitis. Eosinophilic granular or dirty foggy aggregated, not sufficient to be identified as Mallory's bodies, were a rather characteristic cytoplasmic expression in NASH patients. Portal inflammation and fibrosis were not found in the early stage of NASH, but were found as the disease progresses with formation of C-C and/or P-C bridging fibrosis, and eventually resulting in liver cirrhosis.
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PMID:Clinical and pathological features of non-alcoholic steatohepatitis. 1627 57

Hepatotoxicity is a significant complication of therapeutic drug use. As ist can imitate nearly all hepatopathies, the diagnosis of drug-induced liver disease is difficult. Most often, it is a diagnosis of exclusion. The following morphological changes are known, dependent on the target cell type: acute and chronic hepatitis, granuloma formation, and fatty liver disease, cholestatic type acute and chronic liver damage with or without inflammation,or mixed forms of liver injury. Portal or perisinusoidal fibrosis can occur following each type of liver damage. Vascular changes or neoplasms are rare. Drug induced liver injuries are more likely induced by type B damage, which is not expected and cannot be reproduced in animal testing. Type A damage, which is known from toxicity assays, is less likely. A specific therapeutic regime is not available. Therefore, early recognition and cessation of the use of the drug is necessary.
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PMID:[Morphology of drug induced liver damage]. 1658 91


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