Duodenal bulb acidity in patients with duodenal ulcer

Intraluminal pH was measured simultaneously in the human stomach and proximal duodenum with six small glass electrodes tied together at 1.5-cm intervals. Twenty-four healthy control subjects and 44 patients with duodenal ulcer disease were studied under fasting conditions and for 3 h after a standard liquid meal. Mean and median hydrogen ion activity, percentage of time with pH below 2 and 3, and the frequency of pH fluctuations were calculated from digital pH data sampled at a frequency of once per second from each electrode. None of these measurements of acidity differed significantly between the two groups or between subgroups of normosecretor controls and hypersecretor ulcer patients. At the time of pH study 15 of the patients had endoscopically verified active ulcer disease and 13 patients were without disease activity. Gastric as well as duodenal bulb acidity was the same in these two subgroups. We conclude that even though duodenal ulcer patients deliver more acid into the duodenum, this does not cause increased luminal acid aggression.     

Postbulbar duodenal ulcer in a patient with pentagastrin-fast achlorhydria

This report describes the clinicopathologic features of a 55-yr-old man found to have a bleeding, postbulbar duodenal ulcer and fasting hypergastrinemia. Gastric analysis revealed pentagastrin-fast achlorhydria. Healing of the ulcer was documented 8 wk after vagotomy, antrectomy, gastrojejunostomy, and a course of sucralfate therapy. The etiology of the postbulbar ulcer was uncertain. This is the first documented case of a duodenal ulcer with pentagastrin-fast achlorhydria.     

Gastric metaplasia in duodenal bulb andCampylobacter-like organisms in development of duodenal ulcer

Multiple biopsies were taken from 50 patients with endoscopic appearance of duodenitis in order to study the relationship between gastric metaplasia in duodenum and the presence ofCampylobacter-like organisms (CLOs) and the development of duodenal ulcer disease. Metaplasia was found in at least one biopsy specimen from 46 of the 50 patients; CLOs were seen in 25 of the 50 patients, only in metaplastic areas. In four cases a transitional epithelium with the presence of cells containing few apical mucoid granules and absorbent-type brush border as well as goblet cells was seen. In two cases, this epithelium was colonized by a small number of CLOs. Gastric heterotopia appears to be a rare condition.     

Effect of a single dose of antacid on gastric and duodenal bulb pH in duodenal ulcer patients

Gastric and duodenal bulb pH was measured simultaneously with a multiple pH electrode system in 15 duodenal ulcer patients. A single dose of 10 ml antacid was given 120 min after a liquid standard meal, and the pH was measured for another 90 min. The effect of antacid on duodenal pH, expressed as the time pH is kept above 3.0, was on an average 60 min--shorter in patients with a high gastric acid secretion and longer in normosecretors (p less than 0.01). Regression analysis of simultaneously measured gastric and duodenal bulb pH after antacid showed a highly significant linear correlation with a slope of 1.43, which is significantly greater than 1.0 (p less than 0.01), indicating that antacid has a more pronounced effect on duodenal pH than on gastric pH.     

Intestinal obstruction due to antacid treatment for duodenal ulcer: Report of a case

Summary A case of mechanical obstruction of the large intestine resulting from the injudicious self-overadministration of an antacid mixture by a patient with a chronic duodenal ulcer is presented. The literature relating to this subject is briefly reviewed and several differences regarding the course and the outcome in the case described are noted.     

The influence of severe bulb deformity on duodenal ulcer relapse

In order to evaluate the prognostic role of duodenal bulb deformation in the recurrence of peptic ulcer, duodenal bulb morphology and the complete healing of duodenal ulcer were endoscopically evaluated in sixty patients, who were subsequently allocated at random to either maintenance therapy with ranitidine or no treatment. Endoscopic checkups were done at regular intervals, up to the first ulcer recurrence. As expected, long-term ranitidine treatment significantly reduced the relapse rate (12 month cumulative relapse rate was 32% versus 86% in the untreated). A set of prognostic factors which might interfere with this result (sex, age, alcohol consumption, history of ulcerous relatives, duration of the disease, previous H2-blocking treatment, previous complications, smoking and morphology of the duodenal bulb) were evaluated by multivariate analysis using the Cox regression model. Only duodenal bulb morphology appeared to have any independent prognostic value. In the untreated group ulcer recurrence seemed to occur earlier (median relapse time = 2 months) in the patients with severe non-stenosing bulb deformity, and later in those with normal or mildly deformed bulb (median relapse time = 8 months); ranitidine treatment delayed relapse in deformed bulb patients (median relapse time = 14 months) and almost eliminated it in those with normal duodenal bulb morphology. No association was found between the presence of duodenal bulb deformity and the above-mentioned covariates. Our study confirms the primary importance of anti-H2 treatment and suggests that anatomical characteristics of the duodenal bulb also influence the occurrence of ulcer relapse.     

Intramural duodenal hematoma after endoscopic therapy for a bleeding duodenal ulcer in a patient with liver cirrhosis

We report a case of intestinal obstruction due to intramural hematoma of the duodenum following therapeutic endoscopy for a bleeding duodenal ulcer in a patient with liver cirrhosis. A 44-year-old man was admitted to our hospital with severe epigastralgia, nausea and tarry stool. Two years previously he had undergone endoscopic sclerotherapy for esophageal varices caused by alcoholic liver cirrhosis. Endoscopy revealed an open ulcer with a bleeding vessel in the duodenal bulb, and sclerotherapy was performed by clipping the vessel and injecting 20 ml of 0.2% epinephrine. His platelet count was 3.5x10(4)/mul. Twelve hours later, he again developed epigastralgia and hypotension. Emergency computed tomography and ultrasonography revealed an intramural hematoma, 15x18 cm in diameter, at the dorsal and lateral duodenum. Endoscopy and upper gastrointestinal series revealed severe stenosis of the duodenal lumen caused by intramural hematoma. He received parenteral feeding for 22 days and within 8 weeks the hematoma was gradually absorbed using conservative management. Intramural duodenal hematoma may be diagnosed as a complication of the endoscopic procedure in a patient with a bleeding tendency, such as liver cirrhosis.     

Choledochoduodenal fistula at the anterior wall of the duodenal bulb: a rare complication of duodenal ulcer

A 38 year-old man was admitted to our hospital with the chief complaint of epigastralgia. His laboratory data revealed leukocytosis and increased serum amylase, and abdominal ultrasonography revealed diffuse swelling of the pancreas. Thus, he was diagnosed as having acute pancreatitis. Moreover, abdominal computed tomography showed pneumobilia in the gallbladder and the common bile duct. Gastroduodenal fiberscopy demonstrated peptic ulcer scars around a foramen with smooth margins at the anterior wall of the duodenal bulb. The bile juice flowed from the bottom of the foramen. Endoscopic retrograde cholangiopancreatography revealed the fistula between the common bile duct and the anterior wall of the duodenal bulb, but not the posterior wall. However, there was no pancreatico-biliary maljunction and no stones in the gallbladder or bile duct. This is a rare case of choledochoduodenal fistula at the anterior wall of the duodenal bulb caused by duodenal peptic ulcer disease.