Cases reported "Duodenal Ulcer"

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1/43. Relapse of duodenal ulcers after successful eradication of helicobacter pylori in gastric ulcer patients.

    Relapse of duodenal ulcers was observed endoscopically after helicobacter pylori eradication therapy for gastric ulcer patients in 2 of 32 successful cases. One patient, a 40-year-old woman, received dual therapy with lansoprazole 60mg and amoxicillin 1000mg for 2 weeks because of an intractable, easily-relapsing gastric ulcer accompanied by duodenal ulcer scars that had not relapsed for 5 years. The H. pylori status was assessed by a rapid urease test, light microscopy, culture, and anti-H. pylori antibody. At 24 months after the cure of H. pylori she had upper abdominal pain and showed relapse not of the gastric ulcer but of the duodenal ulcer. The H. pylori status remained negative. The other patient, a 44-year-old man, showed an active gastric ulcer and duodenal ulcer scars at the first endoscopy. He received the same regimen as described above. Ten weeks after completion of the eradication therapy, endoscopy showed healing of the gastric ulcer and relapse of the duodenal ulcer despite successful eradication. These two cases suggest that H. pylori eradication modifies the pathophysiological condition of gastric acid secretion and facilitates relapse of duodenal ulcers.
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keywords = gastric acid, acid
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2/43. Prevention of upper gastrointestinal hemorrhage in 582 burned children.

    In 582 burned children, neutralization of gastric acid and reduction of psychic stress were utilized to reduce upper gastrointestinal ulceration and hemorrhage. While receiving milk, diazepam, and psychologic support, two children required operation. Two of the children who died without clinically apparent gastrointestinal disease had ulcers discovered at autopsy. We conclude that a prophylactic regimen that reduced the amount of acid bathing the gastroduodenal mucosa, provides adequate calories, and minimizes psychic stress is useful in preventing gastrointestinal hemorrhage after burns.
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keywords = gastric acid, acid
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3/43. priapism as a complication of long-term intravenous nutrition.

    A case of priapism following prolonged intravenous nutrition is reported. The small amounts of heparin as received by our patient would tend to minimise a risk of hypercoagulability. However, the administration of intravenous feeding agents and the concomitant metabolic acidosis may have enhanced this risk.
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keywords = acid
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4/43. Reestablishing duodenal continuity after previous gastrectomy for peptic ulcer.

    Gastroduodenal anastomosis is not routine during reoperation for stomal ulcers after primary Billroth II gastrectomy. It nevertheless is a sure way to prevent an increased peptic potential which is brought about by a duodenal bypass. We have reviewed the published cases and added three more, bringing the total to 47. We analyzed the modalities, indications and results of this method. Gastroduodenal anastomosis can be accomplished more often than is thought, despite the often necessary large gastric resections. Separation of the duodenopancreatic block and liberation of the fundus allows suturing without traction. End-to-side anastomosis of the stomach on the anterior wall of the second portion of the duodenum avoids dissection of the duodenal stump. vagotomy is required when basal acidity is greater than 20 mEq/liter. Reestablishing a physiologic alimentary tract is particularly indicated in chronic obstruction due to stenosis associated with a proximal loop syndrome in young patients. Jejunal interposition becomes necessary when total gastrectomy is the result of repeated surgery. Such a method is the best solution for agastria. The excellent results obtained by gastroduodenal anastomosis after repeat gastrectomy should encourage wider use.
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keywords = acid
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5/43. Primary hyperparathyroidism with duodenal ulcer and H. pylori infection.

    A patient with duodenal ulcer and primary hyperparathyroidism was found to have an abnormally high intragastric pH. The pH level returned to normal after surgical removal of the parathyroid adenoma followed by normalization of parathyroid hormone (PTH) and serum calcium concentrations. The patient was positive for Helicobacter pylon (H. pylori) infection. Although the exact mechanism by which chronic hypercalcemia or high PTH level inhibited gastric acid secretion in this case remains unclear, our findings suggest that hypercalcemia may play some role in H. pylori associated gastroduodenal diseases through induction of proinflammatory cytokines or by enhancing the attachment of H. pylori to gastric epithelial cells.
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6/43. Evaluation of gastric acid secretion in two patients (each aged over 90 years) with helicobacter pylori-negative nonsteroidal anti-inflammatory drug-caused duodenal ulcers.

    We treated two patients (each aged over 90 years) with helicobacter pylori-negative nonsteroidal anti-inflammatory drug (NSAID)-caused duodenal ulcers, and had the opportunity to determine gastric acidity by means of 24-h pH monitoring. Endoscopic and histological examination showed no remarkable atrophic change in the gastric mucosa. The gastric pH was low throughout the day and night, and the gastric pH > or = 3 holding time ratio during 24 h was 17.1% and 25.8%, respectively in the two patients, so it was considered that they had gastric acid secretion of the same level as that in normal subjects of the same age or that in the young without H. pylori infection. Because of the complication of reflux esophagitis with a hiatal hernia, rabeprazole sodium, one of the proton pump inhibitors (PPIs), was administered and both patients made excellent progress. In conclusion, gastric acid secretion in patients with H. pylori-negative NSAID-caused duodenal ulcers is fully maintained even in the elderly, so PPIs may be the first choice of treatment.
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keywords = gastric acid, acid
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7/43. Congenital causes of duodenal ulcers in adults.

    In seven cases of congenital anomalies in adults, duodenal obstruction and peptic ulcer disease developed. There were two cases of congenital duodenal web, two of hypertrophic pyloric stenosis, two of annular pancreas, and one of a preduodenal portal vein. The diagnosis is seldom made preoperatively. In the four patients who had preoperative gastric analysis, the acid secretions were increased. Those patients who underwent endoscopy had changes consistent with hypertrophic secretory gastrophy and duodenitis. We believe that treatment should be directed toward relief of the duodenal obstruction and the reduction of basal acid secretion by truncal vagotomy in all such cases.
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ranking = 0.00040989436316359
keywords = acid
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8/43. Perforated duodenal ulcer at seven years after heart-renal transplantation: a case report.

    We experienced a rare case of perforated duodenal ulcer that occurred at seven years after heart-kidney transplantation. This patient is reported here together with a discussion of the etiology, the selection of treatment, and perioperative management. The patient was a 46-year-old man who presented with precordial pain. In 1995, he had undergone simultaneous heart and kidney transplantation in the united states and had been on long-term immunosuppressive and corticosteroid therapy. His precordial pain started from May 24, 2002. He was examined at our hospital on May 27 and underwent emergency surgery with a diagnosis of upper gastrointestinal perforation. A 4-mm perforation was observed on the anterior wall of the duodenal bulb and panperitonitis was also present. Patch closure of the perforation was performed by pulling the omentum over the defect. Perioperative management consisted of his usual immunosuppressants together with antacid therapy. The postoperative course was good and he was discharged on hospital day 15. In this patient, the mechanism of perforation was assumed to involve sudden irritation combined with poor circulation in the duodenum and tissue ischemia, as well as a decrease of mucosal protective factors based on long-term corticosteroid therapy. Perforated duodenal ulcer is a rare problem after heart transplantation. Because the time that elapses after perforation is an important determinant of the prognosis, early diagnosis and appropriate surgical repair are essential.
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ranking = 0.0002049471815818
keywords = acid
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9/43. Choledochoduodenal fistula from a penetrating duodenal ulcer. A case report.

    Choledochoduodenal fistula is an uncommon complication of duodenal ulcer disease. The role of medical therapy is unclear and surgical management has been recommended for the condition. A patient who was treated with ranitidine 150 mg twice daily for 8 weeks for a giant duodenal ulcer with a choledochoduodenal fistula is reported. Both the ulcer and the fistula completely healed on medical therapy. Medical therapy may now become the treatment of choice for this condition due to the availability of potent acid-reducing agents.
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keywords = acid
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10/43. Zollinger-Ellison phenotype in the absence of hypergastrinemia and islet-cell tumor.

    patients with the zollinger-ellison syndrome are characterized by islet-cell tumors, striking gastric acid hypersecretion, and peptic ulcer disease. They often experience severe abdominal pain, diarrhea, and gastrointestinal bleeding with potentially life-threatening consequences. It is a rare syndrome caused by non-beta cell islet-cell tumors (gastrinomas) located in or in proximity to the pancreas. These tumors freely secrete gastrin, a peptide hormone that serves as a powerful stimulant of gastric acid secretion. Exuberant secretion of gastrin from the gastrinomas produces severe gastric acid hypersecretion that often leads to impressive peptic ulcer disease and the constellation of symptoms listed above. We describe a patient presenting with clinical manifestations characteristic of the ZES with strikingly elevated gastric acid secretion,multiple ulcers in the first and second portions of the duodenum and diarrhea, but in absence of islet-cell tumor and/or hypergastrinemia.
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keywords = gastric acid, acid
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