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F P Lopasso

Publications and source records attributed to F P Lopasso.

At least 19 recordsLinked to original sources

An evaluation of gastric scintigraphy pre- and postpyloroduodenal peptic stenosis dilation.

BACKGROUND: The usual treatment of pyloroduodenal peptic stenosis has been mainly surgical, through pyloroplasty or gastric resection, with or without vagotomy. Since the first description of treatment for this peptic complication by endoscopic balloon dilation perfomed by Benjamin in 1982 [2], this procedure has become a therapeutic option in association with the medical treatment of peptic disease. The aim of this study is to evaluate the results involving clinical, endoscopic, and gastric emptying scintigraphy parameters. METHODS: Between August 1998 and February 2000, 20 patients with pyloroduodenal stenosis refractory to conservative treatment were treated at the Gastrointestinal Endoscopy Unit of the University of São Paulo Medical School. All patients who presented clinical manifestations of pyloroduodenal stenosis underwent upper gastrointestinal endoscopy to confirm peptic stenosis. Biopsy of the narrowing for the confirmation of a benign disease and gastric biopsy for Helicobacter pylori detection were performed. The treatment consisted of dilation of the stenosis with type TTS (Through The Scope) hydrostatic balloon under endoscopic control, treatment of Helicobacter pylori infection, and gastric acid suppression with oral administration of proton pump inhibitor. All patients, except one who was excluded from this study, were submitted to a clinical endoscopic assessment and gastric emptying evaluation by ingestion of (99m)Tc before and after the treatment. Endoscopic evaluation considered the diameter of the stenotic area before and after treatment. A scintigraphic study compared the time of gastric emptying before and after balloon dilation. RESULTS: Nineteen patients completed treatment by hydrostatic balloon dilation. Clinical symptoms such as bloating (p < 0.0001), epigastric pain (p = 0.0159), gastric stasis (p < 0.0001), and weight gain (p = 0.036) showed significant improvement. The diameter of the stenotic area increased significantly (p < 0.01) after the dilation treatment as well as a better gastric emptying of (99m)Tc (p < 0.0001). CONCLUSION: The dilation of the peptic pyloroduodenal stenosis using a hydrostatic balloon is a safe and effective procedure. The evaluation with gastric scintigraphy by ingestion of (99m)Tc is an effective method of assessment for the improvement of gastric function, because its results corresponded to the clinical improvement after endoscopic treatment.

Catheterization↗

Effect of a selective nonsteroidal anti-inflammatory inhibitor of cyclooxygenase-2 on the small bowel of rats.

The pathogenesis of nonsteroidal anti-inflammatory drug (NSAID) enteropathy is a complex process involving the uncoupling of mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase (COX). Rofecoxib, a selective inhibitor of COX-2, has shown less gastric damage, but the same beneficial effect is not clear in the case of the small bowel. Fifty-seven male Wistar rats (250-350 g) were divided into three groups (N=19 each) to evaluate the effect of this NSAID on the rat intestine. The groups received 2.5 mg/kg rofecoxib, 7.5 mg/kg indomethacin or water with 5% DMSO (control) given as a single dose by gavage 24 h before the beginning of the experiment. A macroscopic score was used to quantify intestinal lesions and intestinal permeability was measured using [51Cr]-ethylenediaminetetraacetic acid ([51Cr]-EDTA). The extent of intestinal lesion, indicated by a macroscopic score, was significantly lower when rofecoxib was administered compared to indomethacin (rofecoxib=0.0 vs indomethacin=63.6 +/- 25.9; P<0.05) and did not differ from control. The intestinal permeability to [51Cr]-EDTA was significantly increased after indomethacin (control=1.82 +/- 0.4 vs indomethacin=9.12 +/- 0.8%; P<0.0001), but not after rofecoxib, whose effect did not differ significantly from control (control=1.82 +/- 0.4 vs rofecoxib=2.17 +/- 0.4%; ns), but was significantly different from indomethacin (indomethacin=9.12 +/- 0.8 vs rofecoxib=2.17 +/- 0.4%; P<0.001). In conclusion, the present data show that rofecoxib is safer than indomethacin in rats because it does not induce macroscopic intestinal damage or increased intestinal permeability.

Animals↗

Protective effect of metronidazole on uncoupling mitochondrial oxidative phosphorylation induced by NSAID: a new mechanism.

BACKGROUND: The pathogenesis of non-steroidal anti-inflammatory drug (NSAID) enteropathy is complex. It involves uncoupling of mitochondrial oxidative phosphorylation which alters the intercellular junction and increases intestinal permeability with consequent intestinal damage. Metronidazole diminishes the inflammation induced by indomethacin but the mechanisms remain speculative. A direct effect on luminal bacteria has traditionally been thought to account for the protective effect of metronidazole. However, a protective effect of metronidazole on mitochondrial oxidative phosphorylation has never been tested. AIMS: To assess the protective effect of metronidazole on mitochondrial uncoupling induced by indomethacin and also on the increased intestinal permeability and macroscopic damage. MATERIAL AND METHODS: The protective effect of metronidazole was evaluated in rats given indomethacin; a macroscopic score was devised to quantify intestinal lesions, and intestinal permeability was measured by means of (51)Cr-ethylenediaminetetraacetic acid. The protective effect of metronidazole against mitochondrial uncoupling induced by indomethacin was assessed using isolated coupled rat liver mitochondria obtained from rats pretreated with metronidazole or saline. RESULTS: Metronidazole significantly reduced the macroscopic intestinal damage and increase in intestinal permeability induced by indomethacin; furthermore, at the mitochondrial level, it significantly reduced the increase in oxygen consumption in state 4 induced by indomethacin and caused less reduction of the respiratory control rate. CONCLUSION: Our study confirmed the beneficial effects of metronidazole on intestinal damage and intestinal permeability, and demonstrated, for the first time, a direct protective effect of metronidazole on uncoupling of mitochondrial oxidative phosphorylation caused by NSAIDs.

Animals↗

Endosonographic diagnosis of intraluminal diverticulum.

After a long symptom period of 19 years a submucosal tumor was suspected on endoscopy to account for the patient's intermittent nausea and abdominal pain. Duodenal waterfilling during endoscopic ultrasound led to the endosonographic diagnosis of an intraluminal duodenal diverticulum which was removed surgically. The patient became completely asymptomatic.

Adult↗

Oxidative stress in the pathogenesis of nonalcoholic fatty liver disease, in rats fed with a choline-deficient diet.

BACKGROUND/AIM: The pathogenesis of Nonalcoholic Fatty Liver Disease remains largely unknown, but oxidative stress seems to be involved. The aim of this study was to evaluate the role of oxidative stress in experimental hepatic steatosis induced by a choline-deficient diet. METHODS: Fatty liver disease was induced in Wistar rats by a choline-deficient diet. The animals were randomized into three groups: I (G1) and II (G2), n=6 each--fed with a choline-deficient diet for four and twelve weeks respectively; Group III (control-G3; n=6)--fed with a standard diet for twelve weeks. Samples of plasma and liver were submitted to biochemical, histological and oxidative stress analysis. Variables measured included serum levels of aminotransferases (AST, ALT), cholesterol and triglycerides. Oxidative stress was measured by lucigenin-enhanced luminescence and the concentration of hydroperoxides (CE-OOH-cholesteryl ester) in the liver tissue. RESULTS: We observed moderate macro- and microvesicular fatty change in periportal zones G1 and G2 as compared to controls (G3). In G2, fatty change was more severe. The inflammatory infiltrate was scanty and no fibrosis was seen in any group. There was a significant increase of AST and triglycerides in G1 and G2 as compared to control group G3. The lucigenin-amplified luminescence (cpm/mg/min x 10(3)) was significantly increased in G1 (1393-/+790) and G2 (7191-/+500) as compared to controls (513-/+170), p<0.05. The concentrations of CE-OOH were higher in G1 (5.7-/+0.9 nmol/mg protein) as compared to control (2.6-/+0.7 nmol/mg protein), p<0.05. CONCLUSION: 1) Oxidative stress was found to be increased in experimental liver steatosis; 2) The production of reactive oxygen species was accentuated when liver steatosis was more severe; 3) The alterations produced by oxidative stress could be an important step in the pathogenesis of nonalcoholic fatty liver disease.

Alanine Transaminase↗

Acid secretory response in the late follow-up of proximal gastric vagotomy for duodenal ulcer without Helicobacter pylori eradication.

BACKGROUND/AIMS: The profile of acid secretory responses was studied in 20 patients who had had proximal gastric vagotomy (PGV) surgery performed 11-22 years previously in order to treat duodenal ulcers (DU). The presence of Helicobacter pylori was detected in all of the patients. METHODOLOGY: The recurrence of DU was diagnosed in 10 patients and the other 10 remained without recurrence during the follow-up period. The control groups included 10 DU patients with refractory responses to H2 receptor antagonists and 10 "normal" subjects. Both control groups had untreated Helicobacter pylori infection. Measures of 1) basal acid output, 2) acid output for 30 min under continuous i.v. infusion of 0.2 ug/kg/h of pentagastrin acid, and 3) the response for 30 and 60 min after starting a sham feeding, modified by the "chew and spit" technique under simultaneous i.v. infusion of 0.2 ug/kg/h of pentagastrin were performed. Serum gastrin was measured during fasting and at sham feeding. The densities of the gastrin cells of antrum and duodenum were estimated by morphometric counting. RESULTS: Both basal output and acid response to sham feeding plus pentagastrin infusion were higher in the DU controls and DU recurrence patients. The response to pentagastrin infusion did not show any discriminant value. Fasting serum gastrin values increased after PGV, either with or without DU recurrence. Gastrin cell hyperplasia was not demonstrated in any of these groups. CONCLUSIONS: The secretory profile of patients with both late DU recurrence after PGV and Helicobacter pylori infection lies between DU patients refractory to the H2 receptor antagonist approach and those free of DU recurrence after PGV--both of them with current Helicobacter pylori infection. The characteristic pattern of late DU recurrence after PGV and untreated Helicobacter infection is that of increased basal acid output and higher acid secretion responsiveness to sham feeding plus pentagastrin in the presence of higher serum levels of gastrin.

Adult↗