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.

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.

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 percent 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 percent; 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 percent; ns), but was significantly different from indomethacin (indomethacin = 9.12 ± 0.8 vs rofecoxib = 2.17 ± 0.4 percent; 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.

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.

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.

Effects of small bowel exclusion on intestinal myoelectrical activity pattern: comparison between innervated and denervated (transplanted) Thiry-Vella loops in rats.

Small bowel transplantation (SBT) leads to several changes in normal intestinal physiology with special reference to lymphatic disruption and graft denervation. Intestinal myoelectrical activity (MA) has been studied in different conditions, but little is known about MA in excluded bowel segments without the influence of nutrients. We performed this study to evaluate the effects of bowel exclusion on MA pattern. Fifteen Wistar rats were divided into two groups: five were used as donors and five as recipients for SBT; the remaining five underwent isolation of a jejunal segment as Thiry-Vella loop (TVL). On the 20th postoperative day, four bipolar electrodes were implanted in the small bowel of each rat: proximally and distally on the transplanted and the native intestine (SBT group); proximally and distally on the TVL and across the jejunal anastomosis (TVL group). On the 30th postoperative day, MA was recorded for 30 min after a 12 h fast. MA pattern was not altered by the exclusion of innervated jejunal segments (TVLs) with maintenance of high amplitude and migrating myoelectric complex (MMC) occurrence independent of MA in the continuity bowel. The characteristic regular spiking activity was not observed in transplanted grafts and MA analysis showed slow waves containing superimposed irregular spiking activity.

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.

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.

Site of peptic ulcer. comparison of hydrochloric acid output, pepsinogen and gastrin serum levels.

BACKGROUND/AIMS: Basal (BAO) and maximum (PAO) hydrochloric acid output after Histalog stimulation, basal pepsinogen (SPL-B), at 60 (SPL-60) and at 90 minutes (SPL-90), and basal gastrin (BG) levels were measured and compared in different gastric (GU) and duodenal (DU) ulcer sites. MATERIAL AND METHODS: Fifty nine patients with peptic ulcer were grouped according to Johnson's classification for gastric ulcers: type I (15), type II (16) type III (12) GU and (16) DU. Fifteen normal subjects were studied as controls. RESULTS: The BAO was greater in the DU than in the control or GU groups. No significant difference was noted in the production of hydrochloric acid after stimulation with Histalog. The SPL-B, at 60 and at 90 minutes was higher in type II GU than in the DU group and controls. The SPL-60 was higher in type II GU patients than in type III GU. Basal gastrin was higher in group DU and types II and III GU compared to the type I GU patients and controls. CONCLUSION: The topographic criteria for differentiating peptic ulcers has low discrimination capacity based on comparison of mean values of HCl acid production, pepsinogen and gastrin serum levels both basal and after stimulation with Histalog due to heterogeneity of these variables in group studies. In these studies, peptic ulcers from different sites should not be grouped as distinct entities except for type II gastric ulcers.

Squamous cell carcinoma of the pancreas with gastric metastasis. Case report.

The squamous cell carcinoma of the pancreas is an uncommon form of pancreatic cancer, with a frequency in the range of 0.5-3.5%. A rare case of a primary squamous cell pancreatic carcinoma, with gastric invasion and upper digestive bleeding, requiring surgical control is reported. The surgical technique to treat the bleeding is also detailed.

Identification of heterogenous motility patterns of the stomach in duodenal ulcer disease.

This study aims to compare gastric emptying of solid meals in two different duodenal ulcer populations and their respective control groups. The same authors, utilized the same methods, but on different occasions. Four study groups were composed as follow: DU I--15 patients, CI--12 patients, DU II--16 patients, C II--15 patients. All individuals underwent high gastrointestinal tract evaluation. Endoscopy was normal in all subjects of the control groups. The ulcers were active but without reducing of the duodenal lumen. Gastric emptying was studied with the use of 30 grams of Tc tagged chicken liver. Measurements of Gastric emptying were taken by a gamma camera Ohio-series ON-150) with 15 minutes intervals during 120 minutes. Emptying rates expressed as percent of the test meal remaining in the stomach were submitted to KRUSKAL-WALLIS STATISTICAL analysis at each time and were identical in the groups, DU I, C I and C II. Emptying rates were significantly lower in the DU II group compared to the others. This study permits us to conclude that the gastric emptying in duodenal ulceration can be normal or delayed for reasons not clearly understood.

[Cholelithiasis in young individuals]. / Colelitíase no jovem.

It is presented a retrospective study of 20 patients under 30 years of age that underwent surgery for cholelithiasis in the "Hospital Ipiranga-INAMPS", São Paulo, from 1987 to 1990. The incidence in this group was 6.8% with sex distribution higher in the female. Only one patient had associated hemolytic disease (5%). The clinical findings were not different in this population and the diagnosis prior to surgery was possible in all cases. The high incidence found for acute cholecystitis (45%) and calculi migration (20%) should emphasize the importance of diagnostic and therapeutic approach in the young patient.