Antral Ulcers Research Articles

A Reliable Method for the Production of Antral Gastric Ulcer by a Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats

A Reliable Method for the Production of Antral Gastric Ulcer by a Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats

Effects of 2-(E-2-Decenoylamino)ethyl 2-(Cyclohexylethyl) Sulfide on Various Ulcer Models in Rats.

The effects of 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide (compd. III-1a) on various experimental ulcers were investigated. The oral administration of compd. III-1a at doses ranging from 30 to 300 mg/kg inhibited the acute gastric ulcerations induced by ethanol, HCl.aspirin and indomethacin in rats. Compound III-1a significantly inhibited the water immersion stress-induced gastric ulcer at doses of 3 mg/kg, p.o. The anti-ulcer activity of plaunotol as a reference drug was equivalent on an ethanol-induced ulcer to that of compd. III-1a, but weaker on HCl.aspirin, indomethacin and stress-induced ulcers than that of compd. III-1a. On indomethacin-produced gastric antral ulcer, compd. III-1a showed the same significant inhibitory activity as spizofurone did at a dose of 100 mg/kg, p.o. Compound III-1a also inhibited hemorrhagic shock-, diethyldithiocarbamic acid (DDC)-and platelet activating factor (PAF)-induced ulcers dose-dependently. Plaunotol only showed significant inhibitory activity on PAF-induced ulcer in these three ucler models. The consecutive administration of compd. III-1a (100 mg/kg, p.o.) twice a day significantly accelerated the healing of an acetic acid-induced ulcer and that of plaunotol (200 mg/kg, p.o.) showed the same activity. Moreover, orally administered compd. III-1a at a dose of 100 mg/kg decreased the gastric acid secretion in pylorus-ligated rats. The results in the present study suggest that compd. III-1a has the dual action on ulcer formation.

Gastric mucosal prostaglandin E 2 levels in cirrhosis and portal hypertension

Prostaglandin E 2 (PGE 2) tissue levels were measured, using radioimmunoassay, in specimens from the gastric antral mucosa in (a) healthy subjects, (b) patients without liver diseases in the absence or presence of gastric ulcers, and (c) patients with alcoholic cirrhosis in the absence or presence of gastric ulcers. These groups were divided further into subgroups with or without portal hypertension. PGE 2 tissue levels in subjects without liver diseases were not significantly different from those of cirrhotic patients without portal hypertension. However, in cirrhotic patients with portal hypertension, the PGE 2 content was significantly lower, especially in the presence of congestion in the mucosa (about 70–80%). When a gastric antral ulcer was present, a further statistically significant decrease of the PGE 2 levels was observed. It was concluded that a decrease in the PGE 2 tissue levels in the gastric mucosa of cirrhotic patients is related to the presence of portal hypertension. Congestion in the mucosa, as a pathogenetically relevant factor for mucosal PGE 2 deficiency, may play a role.

Duodenogastric Reflux in Children

The duodenogastric reflux (DGR) is a suspected cause in some esogastric pathologies in adults: esophagitis, peptic gastric ulcers, stress ulcers, ulcers secondary to drugs, gastric cancer, and gastritis. The toxic substances of the reflux are essentially bile acids, lysolecithin, and trypsin. A number of diagnostic methods have been proposed in the adult. This study suggests a diagnosis technique for DGR in the child. Fasting gastric juice was collected by gastric intubation during 1 h and three substances were measured: phospholipids as markers of biliary reflux, trypsin as a marker of pancreatic reflux, and sialic acid as a marker of the degradation of gastric mucus. The sialic acid enabled us to evaluate some of the toxicity of DGR on the stomach. The study of 49 child subjects permitted us to show the existence, in the normal child, of biliopancreatic markers in the stomach under fasting conditions through a physiological DGR; to define the norms in the child, varying according to three age groups: 0-2 months, 2-12 months, and 1-4 years (the maximum values for an age above 4 years seemed to correspond to those in the adult); and to suggest the existence of a pathological DGR in children with antral gastritis or ulcers.

Duodenogastric Reflux in Children

SummaryThe duodenogastric reflux (DGR) is a suspected cause in some esogastric pathologies in adults: esophagitis, peptic gastric ulcers, stress ulcers, ulcers secondary to drugs, gastric cancer, and gastritis. The toxic substances of the reflux are essentially bile acids, lysolecithin, and trypsin. A number of diagnostic methods have been proposed in the adult. This study suggests a diagnosis technique for DGR in the child. Fasting gastric juice was collected by gastric intubation during 1 h and three substances were measured: phospholipids as markers of biliary reflux, trypsin as a marker of pancreatic reflux, and sialic acid as a marker of the degradation of gastric mucus. The sialic acid enabled us to evaluate some of the toxicity of DGR on the stomach. The study of 49 child subjects permitted us to show the existence, in the normal child, of biliopancreatic markers in the stomach under fasting conditions through a physiological DGR; to define the norms in the child, varying according to three age groups: 0–2 months, 2–12 months, and 1–4 years (the maximum values for an age above 4 years seemed to correspond to those in the adult); and to suggest the existence of a pathological DGR in children with antral gastritis or ulcers.

The Role of Motility in Gastric Mucosal Injury and Protection

Several animal studies have helped to investigate the role of motility in gastric mucosal injury. The administration of solid food to rats receiving subcutaneous indomethacin (indometacin) 30 mgj kg reduced the incidence of lesions in the body of the stomach compared with that in rats receiving indomethacin alone; however, lesions in the antrum and intestine became more prominent, and it was proposed that increased antral activity was involved in this mechanism. Similarly, fasted rats who received indomethacin and then were fed developed antral ulcers. However, a low residue diet decreased the incidence and number of lesions, although it is not known whether such a diet affects gastric motility. To determine whether stomach lesions, induced by cold-restraint stress in rats, were a result of increased acid secretion or increased gastric motility, animals were given papaverine, a strong smooth muscle inhibitor. The antral lesions decreased and it was postulated that, at least in this model, antral ulcers were mainly a result . of increased gastric antral motility, with antral contractions in these animals being more prolonged and of higher amplitude. Although it is difficult to extrapolate these results to the human situation, information suggests that gastric emptying is accelerated in duodenal ulcer patients, presumably resulting in increased acid delivery to the duodenal bulb. Studies in animals with induced duodenal ulcers indicated that increased duodenal motility was associated with an increased clearance of bicarbonate, reducing the buffering capacity in the duodenal bulb. However, measurement of duodenal transit and duodenal bulb clearance in patients with active or inactive duodenal ulcer failed to demonstrate any differences from a control group, suggesting this may not be a mechanism in humans. In patients with gastric ulcers, antral contractions are decreased and this may be related to impaired or delayed gastric emptying. Additionally, decreased pyloric pressure has been demonstrated and there is some evidence for increased duodenalgastric reflux in these patients. However, it has not been demonstrated that increased duodenalgastric reflux produces gastritis or gastric ulcer, and, after gastric ulcer healing, abnormal antral motility, decreased pyloric pressure and increased duodenal-gastric reflux persist. Thus, the role of . duodenal-gastric reflux in the pathogenesis of gastric lesions, particularly of gastric ulcer, remains questionable. In animal studies, stress has been associated with a decrease in antral contractions. However, in general, the response depends on the type of stress used, and both humans and animals may adapt to repeated stress by producing a change in response. In conclusion, the role of motility in gastric mucosal injury and protection remains to be defined, and as yet there is no strong evidence that motility per se is an important predisposing factor in gastroduodenal mucosal lesions.

Cumulative 10-Year Risk of Symptomatic Duodenal and Gastric Ulcer in Patients with or without Chronic Gastritis: A Clinical Follow-up Study of 454 Outpatients

The cumulative rate of symptomatic peptic ulcer (PU) was examined in a 10-year clinical follow-up study of 454 consecutive outpatients who had undergone diagnostic gastroscopy, from whom routine biopsy specimens were taken from the antral and corpus mucosa, and who were found to be ulcer-free before and at the time of this initial gastroscopy. During the follow-up period 34 (11%) of 321 patients who showed gastritis in the biopsy specimens at the initial gastroscopy had contracted symptomatic PU (18, 5, 7, and 4 cases of duodenal, pyloric, antral, and angular or corpus ulcer, respectively), which was verified by endoscopy. Only 1 (0.8%) of 133 patients with normal antral and corpus mucosa had contracted PU. It was calculated that the 10-year cumulative probability of PU was 10.6% (95% confidence interval (CI95), 7.2-14.0%) in the patients with gastritis, whereas this probability was only 0.8% (0-2.2%) in the patients who had normal antral and corpus mucosa in the initial specimens. The cumulative probability of PU was found to be highest, 27.3% (1.0-53.6%), in middle-aged men (41-60 years of age) who had chronic antral gastritis or chronic pangastritis (gastritis in both antrum and corpus). It is concluded that chronic gastritis precedes the appearance of PU and that the cumulative 10-year risk of PU is very low when both antral and corpus mucosa are normal but may be high if chronic gastritis is present.

Effects of restraint stress on catecholamine concentrations in the glandular stomach of rats

Restraint stress is known to induce gastric ulcers in rats. Peripheral sympathetic activity and catecholamines are involved in the pathogenesis of these gastric ulcers. The aim of the present study was to evaluate the effects of restraint on mucosal and muscle catecholamine concentrations in the glandular stomach of rats. In unrestrained rats, noradrenaline concentration was higher in the muscle than in the mucosa of the glandular stomach (629 +/- 106 vs 18 +/- 3 pg/mg and 217 +/- 37 vs 18 +/- 8 pg/mg, respectively in the corpus and the antrum, p less than 0.01). This can be explained by the existence of an abundant noradrenergic innervation in the muscle layer. After 20 hours of restraint, adrenaline and noradrenaline concentrations were significantly decreased in adrenals, in comparison with unrestrained animals (255 +/- 53 vs 638 +/- 160 ng/mg and 113 +/- 17 vs 198 +/- 37 ng/mg, respectively for adrenaline and noradrenaline, p less than 0.05). In the glandular stomach, noradrenaline and adrenaline concentrations in restrained rats were not significantly different from those in unrestrained rats. However, adrenaline concentrations in the muscle of restrained rats were higher than in the mucosa. Moreover, restraint induced a significant decrease in dopamine concentration in the antral mucosa (from 100 +/- 12 pg/mg in unrestrained rats to 15 +/- 5 pg/mg in restrained rats), suggesting that a depletion in dopamine in the antral mucosa could be one of the pathogenetic factors involved in antral gastric stress-induced ulcers in rats.

Indomethacin-induced gastric antral ulcers in hamsters

Antral ulcers account for about half of gastric ulcers in humans. An animal model was developed to produce such ulcers. Indomethacin given subcutaneously to normally fed hamsters produced antral ulcers within 1–5 h, dose dependently. These ulcers penetrated the muscularis mucosae. With repeated administration of indomethacin and longer duration of treatment, the lesions became more severe and most animals died with perforated antral ulcers after 2–5 days. Like indomethacin, aspirin given orally also produced antral ulcers in hamsters. Indomethacin reduced the formation of prostaglandin E2, prostaglandin F2α, and 6-keto prostaglandin F1α by the antral mucosa, and increased gastric acid output more than twofold. The ulcers were prevented by various antisecretory agents (cimetidine, methscopolamine bromide, and omeprazole), and the antiulcer dose of each of these agents corresponded to the antisecretory dose. By contrast, several prostaglandins prevented the ulcers at very low, nonantisecretory doses. 16,16-Dimethyl prostaglandin E2 prevented the ulcers at a dose nearly 3000 times lower than the gastric antisecretory ED50. The mechanism by which prostaglandins prevent formation of these ulcers is unknown, but the effect is consistent with cytoprotection, i.e., protection of the gastric mucosa by nonantisecretory doses. Indomethacin-induced antral ulcers appear to depend on two factors: a depletion of prostaglandin content of the antrum and gastric hyperacidity.

Deficiency of endogenous prostanoids in gastric and duodenal ulcer diseases

The levels of prostaglandin E2 (PGE2), 6‐keto‐prostaglandin F1α (PGF1α) and thromboxane B2 (TXB2) in endoscopic biopsy specimens from the gastric and duodenal mucosa of healthy volunteers and ulcer patients were measured by radio‐immunoassay. The PGE2 and PGF1α levels in the mucosa of the corpus of the stomach were lower and the TXB2 level was higher in 10 patients with gastric ulcer in the corpus than in the 16 healthy subjects. The PGE2 level in the antral mucosa of 14 patients with gastric ulcer in the antrum was lower than in the controls. In 18 patients with duodenal ulcer, PGE2 deficiency was more widespread in the entire gastric and duodenal mucosa while the reduced PGF1α level was limited in the gastric corpus. Lower levels of PGE2 in patients with antral or duodenal ulcer and of PGE2 and PGF1α in patients with corpus ulcer in the anatomical mucosal area including the ulcer site may predispose the mucosa to ulceration.

Prognostic Value of Serum Pepsinogen I in Children with Peptic Ulcer

SummarySerum pepsinogen I (PG I) levels were determined by radioimmunoassay in 23 children with peptic ulcer disease (PUD) before and after treatment with ranitidine and in 44 children who were being investigated for recurrent abdominal pain. Upper gastrointestinal endoscopy was performed in all. No lesions were detected in controls, while 18 patients showed a duodenal ulcer, 4 had an antral ulcer, and 1 had both. An 8‐week course of ranitidine healed PUD in 93.5% of them, while long‐term (1–5 years) endoscopic follow‐up showed a 41.9% ulcer relapse rate after stopping treatment. Gastric acid secretion after pentagastrin stimulation [maximal acid output (MAO)] was tested in all controls and in 22 PUD patients: While controls had normal MAO values for their age. 65% of patients had a secretion above the normal range. No significant correlation was detected between serum PG I and MAO either in controls or in patients. Mean serum PG I concentrations were not significantly higher in the whole patient group than in controls, but PUD patients who relapsed after discontinuing ranitidine treatment had shown on admission significantly higher PG I levels when compared both with those who did not relapse and with controls. All patients who relapsed, but only 42.8% of those who did not, had a serum PG I concentration above the normal upper limit for a pediatric population (56.7 ng/ml). None of the PUD patients who had serum PG I levels under this limit relapsed. Our results suggest that pretreatment serum PG I levels in children with PUD may predict fairly accurately which will not relapse after attaining ulcer healing by a short‐term ranitidine course.

Prognostic value of serum pepsinogen I in children with peptic ulcer.

Serum pepsinogen I (PG I) levels were determined by radioimmunoassay in 23 children with peptic ulcer disease (PUD) before and after treatment with ranitidine and in 44 children who were being investigated for recurrent abdominal pain. Upper gastrointestinal endoscopy was performed in all. No lesions were detected in controls, while 18 patients showed a duodenal ulcer, 4 had an antral ulcer, and 1 had both. An 8-week course of ranitidine healed PUD in 93.5% of them, while long-term (1-5 years) endoscopic follow-up showed a 41.9% ulcer relapse rate after stopping treatment. Gastric acid secretion after pentagastrin stimulation [maximal acid output (MAO)] was tested in all controls and in 22 PUD patients: While controls had normal MAO values for their age, 65% of patients had a secretion above the normal range. No significant correlation was detected between serum PG I and MAO either in controls or in patients. Mean serum PG I concentrations were not significantly higher in the whole patient group than in controls, but PUD patients who relapsed after discontinuing ranitidine treatment had shown on admission significantly higher PG I levels when compared both with those who did not relapse and with controls. All patients who relapsed, but only 42.8% of those who did not, had a serum PG I concentration above the normal upper limit for a pediatric population (56.7 ng/ml). None of the PUD patients who had serum PG I levels under this limit relapsed. Our results suggest that pretreatment serum PG I levels in children with PUD may predict fairly accurately which will not relapse after attaining ulcer healing by a short-term ranitidine course.

72 PEPTIC-ULCER IN CHILDREN: 5 YEARS FOLLOW-UP AFTER RANITIDINE THERAPY

H2 receptor antagonists changed the prognosis of peptic ulcer in adults, but long term follow-up studies in children after ulcer has been healed with ranitidine are lacking. We carried a 5 yrs follow-up on 31 children (20 males) 3 to 14 yrs old with endoscopically diagnosed duodenal (23 cases) or antral ulcer (8 cases). After an 8 weeks course of ranitidine (5-10 mg/kg) 93% healed their ulcer and therapy was discontinued. Endoscopy was repeated every 6 months or when symptoms recurred. Campylobacter Pylori (CP) was searched in antral mucosa in 22 and serum Pepsinogen I (PG I) determined in 29 cases. After 1 to 3 yeas 14 children (12 males) showed a recurred ulcer crater at endoscopy, an 8 weeks course of ranitidine was repeated and maintenance never discontinued. Serum PG I was higher in relapsed children (80.5 vs. 54.9 pg/ml P<.001), CP was present in 12 (85%) of relapse and in 5 (29%) of non relapsed children. None relapsed on maintenance treatment. CONCLUSION: Peptic ulcer relapse rate in children is 45%, elevated serum PG I, CP in antral mucosa and male sex have an unfavourable prognostic value

Endoscopic ethanol sclerotherapy in non‐variceal gastrointestinal bleeding

Upper gastrointestinal bleeding still causes significant morbidity and mortality in spite of an aggressive medical and surgical approach. Endoscopic methods of treatment promise early and effective non‐surgical control of bleeding. Endoscopic injection of ethanol has been used to control gastrointestinal bleeding in a prospective study of 28 high risk patients. Twenty‐two had chronic ulcers (12 duodenal, 10 gastric) and six had angiodysplastic lesions (three gastric, three caecal). The 22 patients with chronic peptic ulcers were either elderly (median age 69 years) or had serious associated medical disorders (73%); 64% presented with shock. Primary haemostasis was achieved in all, but two re‐bled from their ulcer. Surgery was required in one patient who re‐bled 48 h after treatment and in one patient with an ulcer which perforated 45 days after injection; three patients with chronic ulcers refractory to medical therapy also underwent surgery. One patient developed a closed perforation of an antral ulcer after treatment which settled with conservative management; two patients died from causes unrelated to their ulcer. It is concluded that ethanol sclerosis is a safe, effective method for controlling bleeding from chronic peptic ulcers and angiomatous malformations.

O-82 - Effect of OPC-12759, a novel antiulcer agent, on DDC-induced gastric antral ulcer in rats

O-82 - Effect of OPC-12759, a novel antiulcer agent, on DDC-induced gastric antral ulcer in rats

Gastric Antral Ulcer Produced by Diethyldithiocarbamate in Rats

Gastric Antral Ulcer Produced by Diethyldithiocarbamate in Rats

Diethyldithiocarbamate-induced gastric antral ulcer in rats

Diethyldithiocarbamate-induced gastric antral ulcer in rats

Antral G-cell hyperplasia (Pseudo-Zollinger-Ellison syndrome) and chronic duodenal ulceration in a child

A 13-year-old boy with hypergastrinaemia and chronic duodenal ulcer disease is reported. Antral G-cell hyperplasia (AGCH) appeared to be the cause of his underlying hypergastrinaemia. Differentiation between AGCH (pseudo-Zollinger-Ellison syndrome) and an extragastric gastrin-secreting tumour (true Zollinger-Ellison syndrome) was made on the basis of the gastrin responses to stimulation with intravenous secretin as compared to an oral protein test meal. The localisation of the source of hypergastrinaemia determined the appropriate operative procedure for this patient. Vagotomy and gastric antrectomy is recommended for AGCH. The possible familial nature of this disease and the pathway to diagnosis and management are emphasised.

Early myoelectrical activity changes during gastric or duodenal ulceration in dogs.

Antroduodenal myoelectric activity and gastric transmural potential difference were recorded before and during fundic, antral, or duodenal ulceration in dogs. Gastric injury was obtained by electrocoagulation of the fundic or antral mucosa. Duodenal ulceration was induced by cysteamine injection which was accompanied by nausea or vomiting. Both antral electrocoagulation and cysteamine injection were also accompanied by antral dysrhythmia and a transient decrease of the gastric transmural potential difference. Effects of antral electrocoagulation were prevented by selective vagotomy. Since antral dysrhythmia disappeared as soon as the antral or duodenal ulcers became active, ie, within three days and 24 hr respectively, it is suggested that antral dysrhythmia is the result of antroduodenal stimulation and could thus not be assessed as a criterion of active ulceration.

Antral gastritis and ulceration in a patient with secondary syphilis

A 35-year-old black male was admitted to the Medical College of Georgia Hospital in Augusta, Georgia, with a 2week history of epigastric pain radiating to the right scapula. Initially the pain was relieved by antacids or meals, but 1 week prior to admission the pain became constant and food aggravated it. Three days before admission he experienced a single episode of hematemesis and melena. Seven years and again 3 years before this episode he had been treated for several weeks for undocumented peptic ulcer disease. On physical examination there was a diffuse maculopapular, hyperpigmented rash in a malar distribution which had been present for several months. There was also a painful, raised, erythematous, 2-cm lesion with sharp borders on the foreskin of his penis. The VDRL test was positive in a titer of 1:32. All other laboratory tests were normal or negative. Two days after admission, when intravenous cimetidine and oral antacids failed to relieve the epigastric pain, he underwent esophagogastroduodenoscopy. The entire antrum, which was poorly distensible, showed a diffuse, friable, nodular, dark red lesion with multiple small ulcers abruptly ending at the pylorus (Fig. 1). A 2-cm ulcer on the angularis was biopsied at the edge and center, and random biopsies were taken from the antrum. These biopsies all showed actively ulcerated granulation tissue with intense plasmacytosis; a Warthin-Starry stain failed to show spirochetes. Biopsies of the penile lesion showed intense plasmacytosis, and again the Warthin-Starry stain failed to show spirochetes. Unfortunately, the results of the VDRL test were not available prior to endoscopy and syphilis was not suspected; therefore, fresh biopsy material was not sent for flourescent antibody staining. The patient refused lumbar puncture to rule out neurosyphilis and was empirically treated with 2.4 million units of penicillin intramuscularly daily for 10 days. Thirty-six hours after beginning the penicillin, the patient's abdominal pain completely resolved and his penile lesion began to recede. Four days after beginning penicillin, a repeat gastroscopy showed that the superficial ulcerations and nodularity had resolved and the intense red-brown hue had disappeared. The ulcer on the angularis was unchanged, but