Gastric acid secretion in a child with postbulbar duodenal ulcer

A 14-year-old case was reported with a primary postbulbar duodenal ulcer, which was confirmed by barium meal study and duodenoscopy. In the preoperative study, the patient showed marked gastric hyperacidity: maximal and peak acid output were 0.980 and 1.434 mEq/kg/hr, respectively. As previously described, hyperacidity appears to be a main factor in the pathogenesis of postbulbar duodenal ulcer. Fasting and postprandial serum gastrin secretion was not thought to be responsible for gastric hyperacidity in the present case. Upon histological investigation, the operatively resected stomach did not suggest a possible relationship between hyperacidity and an enlarged parietal cell mass.     

Gastric acid secretion in a child with postbulbar duodenal ulcer

A 14-year-old case was reported with a primary postbulbar duodenal ulcer, which was confirmed by barium meal study and duodenoscopy. In the preoperative study, the patient showed marked gastric hyperacidity: maximal and peak acid output were 0.980 and 1.434 mEq/kg/hr, respectively. As previously described, hyperacidity appears to be a main factor in the pathogenesis of postbulbar duodenal ulcer. Fasting and postprandial serum gastrin secretion was not thought to be responsible for gastric hyperacidity in the present case. Upon histological investigation, the operatively resected stomach did not suggest a possible relationship between hyperacidity and an enlarged parietal cell mass.     

Postmortal coronarography by means of a roentgen double contrast method]

In the conventional postmortem coronary angiogram and vessels are illustrated by a "compact" filling with contrast medium. In the case of the double contrast technique, a thin film of contrast medium is brought about the inner surface of the arteries. Gas injected under controlled pressures into the vessels acts as a further control against the surrounding media. The method is suitable for a more precise illustration of the subepicardial and large intramural coronary arteries. Of particular advantage is the high transparency of the x-ray pictures and the possibility to make the coronary ostia visible. The evaluation of x-ray pictures produced at different controlled pressures permits conclusions about pressure-volume relations of defined vessel sections, which then can be analysed histologically.     

Compression of the duodenum and postbulbar duodenal spasms

Summary and conclusions X-ray examination of the gastrointestinal tract showed a constant, string-shaped streak of barium at the site of the descending portion of the duodenum in 6 patients. The pathogenesis is discussed, the post-bulbar duodenal spasm syndrome described, and various therapeutic suggestions are advanced.We feel that the syndrome is caused by isolated spastic contraction of the descending portion of the duodenum. This syndrome may be present as a component of the symptom complex malrotation or mesenteric root compression, but evidently it may also occur as a diseasesui generis.Rational treatment in uncomplicated cases is administration of spasmolytics, possibly combined with dietetic measures. In cases of X-ray signs showing obstruction around the duodenojejunal junction, primary treatment should be surgery to cut the adhesions, possibly combined with duodenojejunostomy in the most severe cases.     

Acid perfusion of duodenal ulcer craters and ulcer pain: a controlled double blind study

Although early studies attributed an important role to acid in the pathogenesis of duodenal ulcer pain, recent reports are conflicting. The aim of the present study is to determine whether direct acidification of the duodenal ulcer crater in symptomatic patients reproduces ucler pain. Patients with endoscopically diagnosed duodenal ulcers were studied. No premedication or sedation was given. A washing tube was passed via the endoscope and 0.1 N hydrochloric acid as well as normal saline were sequentially administered on to the ulcer crater, the sequence of infusion being randomised and double blind. Forty patients were studied. Sixteen developed typical ulcer pain during acid infusion compared with four with saline (p less than 0.005). Ten patients who developed pain on acid were rechallenged with acid after their pains disappeared. Typical pain recurred in all. Twenty patients without duodenal ulcer did not develop pain when 200 ml of 0.1 N hydrochloric acid was infused into the duodenum. Acid therefore appears to have a definite role in the pathogenesis of duodenal ulcer pain although other factors may also be important.