PubMed Health⌕ Search

Biomedical subjects

H Cortez-Pinto

Publications and source records attributed to H Cortez-Pinto.

12 recordsLinked to original sources
PubMed2006

How different is the dietary pattern in non-alcoholic steatohepatitis patients?

BACKGROUND/AIMS: This study aimed at evaluating whether patients with non-alcoholic steatohepatitis (NASH) had a specific dietary pattern and how it compared with data representative from the same geographical region individuals. SUBJECTS AND METHODS: Clinical, biochemical and anthropometrics: weight, height, body mass index (BMI) and waist circumference were collected in 45 NASH patients. Diet history was assessed using a validated semi-quantitative food frequency questionnaire, analysed with the Food Processor Plus, and was compared, after adjustment for BMI, with data from a sample of 856 free-living individuals, frequency matched for sex and age. RESULTS: Patients' mean age was 49.6+/-10.6 years, 26 F: 19 M, BMI: 31.2+/-5.0 kg/m2. Comparison of their diet history with control data (C) revealed that carbohydrate consumption was lower in patients (P): P-243.6+/-5.7 g vs. C-261.5+/-1.6 g, P<0.05, and most patients had very low fibre intake. Conversely, total fat consumption was higher in patients: P-79.7+/-1.7 g vs. 73.0+/-0.4, P<0.01. A significantly higher intake of n-6 fatty acids (P=0.003) and n-6/n-3 ratio was found in patients, P<0.001. CONCLUSIONS: Our results suggest that the quality and combination of carbohydrates and fat intake may be more relevant than their isolated amount; an increased fat intake with an excessive amount of n-6 fatty acids can be implicated in promoting necro-inflammation, and provides further grounds for individualized dietary therapy.

Adult↗
PubMed2006

Treatment and prognostic factors in patients with hepatocellular carcinoma.

INTRODUCTION: Hepatocellular carcinoma is a leading cause of death from cancer worldwide. Survival of patients depends on tumor extension and liver function, but yet there is no consensual prognostic model. AIMS: To evaluate the influence on survival of pretreatment parameters (clinico-laboratorial, liver function, tumor extension, Okuda and Cancer of the Liver Italian program (CLIP) staging) and treatment modalities. METHODS: We retrospectively analyzed 207 patients, diagnosed between 1993 and 2003. The initial treatment was: surgery--six patients; radiofrequency ablation--21; percutaneous ethanol injection--29; transarterial chemoembolization--49; tamoxifen--49; supportive care alone--53. Factors determining survival were assessed by Kaplan-Meier method and Cox regression models. RESULTS: Median survival was 24 months. In univariate analysis, Child-Pugh classification and Model for end-stage liver disease (MELD) score, portal vein thrombosis (PVT), tumor size, number of lesions, Okuda and CLIP scores were all associated with prognosis (P < 0.001). Alpha-fetoprotein levels were not predictive of survival. Independent predictors of survival were ascites, bilirubin, PVT and therapeutic modalities (P < 0.001). In early stage hepatocellular carcinoma (HCC), survival was similar for both percutaneous ablation modalities, either radiofrequency or ethanol injection (P = NS). In advanced HCC, survival was better in patients receiving tamoxifen than supportive care alone (P < 0.001). CONCLUSION: This study reinforces the importance of baseline liver function (Child-Pugh classification and MELD score) in the survival of patients with HCC, although staging systems allowed the stratification of patients in different prognostic groups. Ascites, bilirubin and PVT were independent pretreatment predictors of survival. All treatments influenced the patient's outcome, whether in early or advanced stages.

Adult↗
PubMed2002

Long-term management of percutaneous endoscopic gastrostomy by a nutritional support team.

BACKGROUND/AIMS: Percutaneous Endoscopic Gastrostomy (PEG) has become a commonly-performed procedure, to provide enteral nutrition for patients who are unable to eat. The aims of this study were to evaluate the long term efficacy, morbidity and mortality of percutaneous endoscopic gastrostomy (PEG). MATERIAL AND METHODS: We analysed 144 patients who underwent a PEG procedure. Survival curves were done with the Kaplan-Meier method. The indication was long-term enteral nutrition in patients unable to maintain adequate nutrition by mouth. RESULTS: The procedure was successful in all but one case. Mean age was 62 (18-85) years, 89 (62%) males. Seven patients recovered from their primary disease and gastrostomy tube was removed. Mean follow-up was 7.3+/-10.8 (1--66) months. Survival rates at 30 days, 1 year and 3 years following gastrostomy were 82%, 36% and 14%, respectively. Survival curves were better in females (P<0.0001). In almost all cases, patients were fed with current home-prepared food, and were ambulatory. There were no differences in survival curves according to the nutritional status. CONCLUSIONS: There were few procedure-related complications, but a high short-term mortality, probably related with the underlying disease. The use of home-prepared food through the gastrostomy was very well tolerated, and should be encouraged.

Adolescent↗
PubMed2002

Plasma total and free fatty acids composition in human non-alcoholic steatohepatitis.

BACKGROUND AND AIM: Non-alcoholic steatohepatitis (NASH), the association of steatosis with an inflammatory response, is a novel liver disease of unknown pathogenesis and prognosis. Triacylglycerols and their precursors, the fatty acids, are the likely candidates to accumulate in the hepatocyte. Disturbed fatty acid metabolism can be involved in the pathogenesis of NASH but there is no information concerning its plasma fatty acid profile. The aim of this study was to evaluate plasma total (esterified plus free) and free fatty acids concentrations to assess the association of NASH with plasma fatty acid accumulation. MATERIALS AND METHODS: Overnight fasting blood samples from 22 biopsy-proven NASH patients and of 6 matched age healthy controls were studied. RESULTS: NASH patients had significantly higher concentration of total and free fatty acids than controls (P<0.05), higher total saturated and monounsaturated levels in both studied lipid fractions (P<0.05), mainly due to the increase of hexadecanoic, hexadecenoic and octadecenoic acids. Absolute polyunsaturated fatty acids (PUFA) concentrations were similar in both groups. The C20:4/C18:2 and the C18:1/C18:0 ratios as well as the peroxidability index were not significantly different. CONCLUSION: In overweight/obese patients NASH is associated with deranged fatty acid metabolism which may be involved in its pathogenesis and/or progression.

Adult↗
PubMed2002

Spontaneous bacterial peritonitis in patients with hepatic cirrhosis: evaluation of a treatment protocol at specialized units.

INTRODUCTION: Spontaneous bacterial peritonitis is a common and severe complication in patients with cirrhosis and ascitis. Its prognosis clearly depends on its precocious clinical recognition and efficacious therapy. AIM: To optimize a treatment protocol, after auditing clinical efficacy and describe microorganisms implicated at our institution. MATERIAL AND METHODS: Retrospective study of clinical files of patients with hepatic cirrhosis with positive culture of ascitic fluid (AF) and/or an AF polymorphonuclear (PMN) count of more than 250/mm3, treated at our units between 1st January, 2000 and 31st December, 2001 (n = 38). Patients showed a median age of 49 years (30-76), 63% of which were male. Forty-eight percent were classified as belonging to Child-Pugh B class, and 52% to C. RESULTS: First, considering cases with PMN > 250/mm3 (n = 29), antibiotics were given to all patients (cefotaxime and ampiciline). Fifty-two percent had hepatic encephalopathy, 42% had fever, 66% abdominal pain. In 42% a microorganism was isolated. Although 24% of fatal cases (only two related to infection), we noted a 73% clinical and laboratorial response. Five patients (72%) that died, showed renal failure by the time of death. Second, in all cases with positive culture of ascitic fluid (n = 21), 42% of which with PMN > 250/mm3 and 9 monobacterial nonneutrocytic bacterascites' cases, one only agent was found: E. coli in 36%, Streptococci (37%), Staphylococci (14%), and other (14%): Klebsiella oxytoca, n = 1; Salmonella enteritidis, n = 1; Enterococcus faecium, n = 1, Acinectobacter anitratus, n = 1. Only one of the agents, E. faecium (3%) showed in vitro sensitivity exclusively to ampiciline; all other were cefotaxime sensitivite. CONCLUSIONS: Our protocol will be modified, to treat patients with spontaneous bacterial peritonitis with cefotaxime, as monotherapy. Albumin infusion will also be added to the protocol, as, we found renal failure to be an important negative prognosis factor.

Adult↗
PubMed2000

Serum gastrin and gastrin-immunoreactive cells in the antral mucosa of patients with alcoholic liver disease.

BACKGROUND/AIMS: Hypergastrinaemia has been reported in liver cirrhosis; meanwhile, it is unclear whether it is associated with an increase in gastrin cell function. The serum gastrin concentration and the number of gastrin cells in antral biopsies were studied in patients with alcoholic liver disease. METHODS: Immunocytochemical and quantification techniques were used to localize and determine the number of gastrin cells. RESULTS: Slight non-significantly higher serum gastrin values were observed in the alcoholic liver disease patients compared with controls, but the individual variation within the groups was considerable. The frequency of gastrin cells did not differ between groups. However, the size of the gastrin cell nuclei was larger in patients with liver disease than in controls, indicating increased cellular activity. CONCLUSIONS: Alcoholic liver disease, with a disturbed liver function, influences the gastrin cells. The observed alterations may reflect the effect of alcohol and/or malnutrition, or may be secondary to the influence of liver disease on other regulatory peptides.

Adult↗
PubMed1999

Alterations in liver ATP homeostasis in human nonalcoholic steatohepatitis: a pilot study.

CONTEXT: The mechanisms that drive progression from fatty liver to steatohepatitis and cirrhosis are unknown. In animal models, obese mice with fatty livers are vulnerable to liver adenosine triphosphate (ATP) depletion and necrosis, suggesting that altered hepatic energy homeostasis may be involved. OBJECTIVE: To determine if patients with fatty liver disease exhibit impaired recovery from hepatic ATP depletion. DESIGN: Laboratory analysis of liver ATP stores monitored by nuclear magnetic resonance spectroscopy before and after transient hepatic ATP depletion was induced by fructose injection. The study was conducted between July 15 and August 30, 1998. SETTING: University hospital. PATIENTS: Eight consecutive adults with biopsy-proven nonalcoholic steatohepatitis and 7 healthy age- and sex-matched controls. MAIN OUTCOME MEASURE: Level of ATP 1 hour after fructose infusion in patients vs controls. RESULTS: In patients, serum aminotransferase levels were increased (P = .02 vs controls); albumin and bilirubin values were normal and clinical evidence of portal hypertension was absent in both groups. However, 2 patients had moderate fibrosis and 1 had cirrhosis on liver biopsy. Mean serum glucose, cholesterol, and triglyceride levels were similar between groups but patients weighed significantly more than controls (P = .02). Liver ATP levels were similar in the 2 groups before fructose infusion and decreased similarly in both after fructose infusion (P = .01 vs initial ATP levels). However, controls replenished their hepatic ATP stores during the 1-hour follow-up period (P<.02 vs minimum ATP) but patients did not. Hence, patients' hepatic ATP levels were lower than those of controls at the end of the study (P = .04). Body mass index (BMI) correlated inversely with ATP recovery, even in controls (R = -0.768; P = .07). Although BMI was greater in patients than controls (P = .02) and correlated strongly with fatty liver and serum aminotransferase elevations, neither of the latter 2 parameters nor the histologic severity of fibrosis strongly predicted hepatic ATP recovery. CONCLUSIONS: These data suggest that recovery from hepatic ATP depletion becomes progressively less efficient as body mass increases in healthy controls and is severely impaired in patients with obesity-related nonalcoholic steatohepatitis.

Adenosine Triphosphate↗
PubMed1999

Lipids up-regulate uncoupling protein 2 expression in rat hepatocytes.

BACKGROUND & AIMS: Hepatic steatosis reflects the accumulation of triglycerides and free fatty acids in hepatocytes. Although lipids and their metabolites are potentially hepatotoxic, the absence of overt injury in fatty livers suggests that adaptive responses to lipid accumulation occur. Fatty acids induce mitochondrial uncoupling proteins (UCP) 2 and 3 in muscle and fat, providing a mechanism to dispose of excessive fatty acids. Although hepatocytes do not normally express uncoupling proteins, UCP-2 is expressed in hepatocytes of genetically obese mice with fatty livers, suggesting that lipids also induce UCP-2 in hepatocytes. METHODS: To test whether lipids up-regulate hepatocyte UCP-2, cultures of rat hepatocytes were treated with lipid emulsions, linoleic or oleic acid, and UCP-2 expression was evaluated by Northern blotting and immunocytochemistry. Because increased reactive oxygen species (ROS) production may contribute to lipid-related UCP-2 induction, the DNA-binding activity of the ROS-activated transcription factor, NF-kappaB, was measured, and the effects of tert-butyl hydroperoxide (TBHP) and glutathione (GSH) on UCP-2 induction were also assessed. RESULTS: Lipid emulsions increased the DNA-binding activity of NF-kappaB and resulted in a dose- and time-dependent induction of UCP-2 transcripts in cultured hepatocytes; after 24 hours, UCP-2 messenger RNA levels were increased 4.5-fold, and increased UCP-2 protein was shown by immunocytochemistry. Consistent with the possibility that ROS generated intracellularly during lipid metabolism participates in UCP-2 induction, addition of the cell-impermeable antioxidant GSH did not alter lipid-related induction of UCP-2. Furthermore, TBHP, which is known to increase hepatocyte mitochondrial ROS production, also increased UCP-2 messenger RNA levels. CONCLUSIONS: Lipids increase ROS and induce UCP-2 in hepatocytes. Thus, the liver may adapt to an excessive supply of lipid substrates by inducing UCP-2 to facilitate substrate disposal while constraining ROS production.

Animals↗
PubMed1999

Non-alcoholic fatty liver: another feature of the metabolic syndrome?

BACKGROUND AND AIMS: Hepatic steatosis and nonalcoholic steatohepatitis (NASH) have been associated with obesity, non insulin-dependent diabetes mellitus and hyperlipidemia. The present study was designed in order to evaluate whether patients with steatosis/NASH presented common features with the metabolic syndrome. METHODS: In 30 patients with nonalcoholic fatty liver the prevalence of hypertension and diabetes; the glucose/insulin profile, lipid profile, and serum leptin were evaluated and correlated with body composition and energy expenditure, assessed by bioimpedance spectroscopy and indirect calorimetry, respectively. Results were compared with a group of eight controls. RESULTS: Obesity was present in 80% of patients, hypertension in 50% and non insulin dependent diabetes in 33%. Glucose metabolism was altered in 69%, with elevated insulin in 14 patients. Serum leptin, higher in women, was increased in patients: 33.9 +/- 38.9 vs 9.6 +/- 6.9 ng/ml, P< 0.05. There was a correlation between insulin and leptin, both of which correlated with body mass index, fat mass and percentage of body fat. Dyslipidaemia was found in 80% of patients: 45% presented low high density lipoproteins cholesterol, 58% high low density lipoproteins and 38% elevated very low density lipoproteins. CONCLUSIONS: There is a strong association between nonalcoholic fatty liver and features of the metabolic syndrome, suggesting a simultaneous insulin resistance and decreased sensitivity to leptin.

Adult↗
PubMed1998

Bacterial lipopolysaccharide induces uncoupling protein-2 expression in hepatocytes by a tumor necrosis factor-alpha-dependent mechanism.

The liver is a target for bacterial lipopolysaccharide (LPS) and participates in the metabolic response to endotoxemia. Recently published evidence indicates that LPS increases the expression of mitochondrial uncoupling protein-2 (UCP-2) mRNAs in several tissues, including the liver. Because hepatocytes in the healthy liver do not express UCP-2, LPS was thought to induce UCP-2 in liver macrophages, which express UCP-2 constitutively. However, the present studies of cultured peritoneal macrophages indicate that LPS reduces steady state levels of UCP-2 mRNAs in these cells. In contrast, UCP-2 mRNAs are induced in hepatocytes isolated from LPS treated rats and transfection of these hepatocytes with UCP-2 promoter-reporter constructs demonstrates substantial increases in UCP-2 promoter activity. LPS induction of hepatocyte UCP-2 expression is virtually abolished by prior treatment of rats with neutralizing antibodies to tumor necrosis factor alpha (TNF). Futhermore, TNFalpha treatment induces UCP-2 mRNA accumulation in primary cultures of hepatocytes from healthy rats. Thus, hepatocytes are likely to be important contributors to endotoxin-related increases in liver UCP-2 via a mechanism that involves the LPS-inducible cytokine, TNFalpha.

Animals↗
PubMedDate not supplied

Hepatic stellate cell activation occurs in nonalcoholic steatohepatitis.

BACKGROUND/AIMS: Hepatic stellate cell activation has a major role in the pathogenesis of hepatic fibrosis, considered to constitute part of the healing response to a necroinflammatory stimulus. However, steatosis per se, has also been shown to induce this activation. This study evaluates if hepatic stellate cell activation is present, and how it correlates with steatosis, in nonalcoholic steatohepatitis, whose hallmark is steatosis. METHODOLOGY: Steatosis, hepatocyte damage, inflammation and fibrosis were graded from 0 to 3+, in liver biopsies from 15 well documented nonalcoholic steatohepatitis and 5 normal controls. Activated hepatic stellate cell activation were identified immunohistochemically using a monoclonal antibody raised against cytoplasmic alpha-smooth muscle actin, and semiquantitatively graded using a scoring method. RESULTS: Nonalcoholic steatohepatitis patients showed significantly greater numbers of alpha-smooth muscle actin-reactive hepatic stellate cell than controls: hepatic stellate cell index of 3.6 +/- 1.9 versus 1.5 +/- 0.5, P < 0.05. The distribution of alpha-smooth muscle actin-reactive hepatic stellate cell was higher in the perivenular areas, than in the intermediate zone and portal area, with no significant association between steatosis and alpha-smooth muscle actin-expressing hepatic stellate cell. However, a significant association was found between portal and lobular inflammation and hepatic stellate cell index, r = 0.72, P = 0.0005 and r = 0.75, P = 0.0002, respectively. CONCLUSIONS: This study demonstrates that hepatic stellate cell activation occurs in nonalcoholic steatohepatitis, clearly correlating with portal and lobular inflammation, but not with steatosis, suggesting that the mechanisms implicated in fibrosis in nonalcoholic steatohepatitis are probably related with inflammation.

Actins↗