PubMed Health⌕ Search

Biomedical subjects

J Myren

Publications and source records attributed to J Myren.

At least 19 recordsLinked to original sources
PubMed1979

Endoscopic retrograde brush cytology in patients with primary and secondary malignancies of the pancreas.

Endoscopic retrograde brush cytology (ERBC) was performed in 29 patients with primary pancreatic malignancies verified later by histology. Results were positive in 21 patients, suspicious in five, and negative in three. ERBC performed in seven patients with uncertain findings at endoscopic retrograde cholangiopancreatography (ERCP) was positive for malignancy in six and suspicious in one. Endoscopic aspiration cytology (EAC) performed in 10 patients with primary tumours was positive for malignancy in three, suspicious in two, and negative in five cases. ERBC and/or EAC performed in five cases with secondary tumours were positive for malignancy in one and negative in four. It is concluded that ERBC gives a high rate of positive or suspicious (90%) diagnosis of malignancy in patients with primary pancreatic lesions. In secondary tumours cytology seems to be negative in most cases. The study further shows that many of the malignant tumours found by ERP are secondary lesions. Cytology is often able to detect malignancy when ERP has proved inconclusive.

Adenocarcinoma↗
PubMed1979

Comparison of glucagon, atropine, and placebo as premedication for endoscopy of the upper gastrointestinal tract.

The effects of 0.5 mg glucagon and 0.5 mg atropine given intravenously as premedication in upper gastrointestinal endoscopy have been examined and compared to those of placebo (0.9% NaCl) in a double-blind study involving 36 patients and 1 endoscopist. The results showed no difference between atropine, glucagon, and placebo with regard to vomiting, opening of the pylorus, feeling of discomfort, or the success of the examination. Glucagon significantly reduced peristalsis compared with both atropine (p less than 0.01) and placebo (p less than 0.01). The reflux was also significantly reduced by glucagon compared with both atropine (p less than 0.01) and placebo (p less than 0.01). No difference was found between glucagon and atropine with regard to secretion, but both drugs reduced the secretion compared with placebo (p less than 0.05). Glucagon also reduced the secretion of mucus compared with placebo (p = 0.05). No adverse effects occurred.

Aged↗
PubMed1979

Serum concentration of trimipramine (Surmontil) and gastric secretion of acid and pepsin following peroral administration of the drug in healthy humans.

Previous blind studies have shown an increased rate of healing of both duodenal and gastric ulcers following 4 weeks peroral administration of 50 mg trimipramine. The present study shows the effect of 50 mg trimipramine perorally on gastric secretion in relation to that of 25 mg of the drug and placebo. At regular intervals blood specimens were obtained for determination of the serum concentration of trimipramine. In 9 healthy young students it was found that the estimated stabilized values of volume and acid output following 50 mg trimipramine, 33 ml and 3.9 mmol/15 min, respectively, were significantly lower than those following the smallest dose, 37 ml and 4.6 mmol/15 min, respectively. On the other hand, no significant changes of gastric secretion were observed following the peroral administration of 25 mg trimipramine when compared to placebo. Following 50 mg trimipramine the output of pepsin was reduced by about 25%. The values of serum concentration of trimipramine were about 200 nmol/1 at 100 min after administration of 50 mg trimipramine and decreased gradually, whereas the values following the smaller dose were about half of those after the larger one. The results indicate that about 50 mg trimipramine is needed for obtaining a reduction of gastric secretions. Future studies may show whether 25 mg trimipramine, which does not suppress acid secretion when given perorally, is able to promote peptic ulcer healing.

Administration, Oral↗
PubMed1979

Maintenance treatment of duodenal ulcer patients with a single bedtime dose of cimetidine.

Fifty-eight patients with endoscopically verified duodenal ulcers were treated with cimetidine, 1 g/day, for 6--10 weeks. The ulcers healed in 52 out of the 54 patients completing the treatment (96.3%). Forty-seven of the patients with healed ulcer were randomly allocated to 1 year of maintenance treatment, 23 patients with cimetidine, 400 mg at night, and 24 patients with placebo tablets. In the cimetidine-treated group 2 out of the 20 patients (10%) completing the trial had recurrence of ulceration, whereas 16 out of the 23 patients (70%) completing the placebo treatment had ulcer recurrence (p less than 0.001). The drug was well tolerated and, except for a marked increase in serum transaminases in three patients, no serious side effects were seen.

Adult↗
PubMed1979

Comparison of gastric secretory response in man to duodenal and jejunal liver extract perfusion.

The stomachs of six healthy volunteers were intubated with a Levine tube. In addition, a thin polyethylene tube was placed in the proximal jejunum or in the proximal duodenum. After a 1-h period with no perfusion the intestine was perfused for 2 h with 7% liver extract (LE) (pH 5.5; 380 MOsm/kg water) at a rate of 100 ml/h. In control tests 200 ml of 0.9% physiologic saline solution were used as perfusate. Reflux to the stomach was determined by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin levels were measured in 15-min periods. During perfusion of the proximal jejunum only pepsin outputs were increased significantly. During duodenal perfusion of LE, gastric acid and pepsin outputs were increased to 31% and 73% of maximal pentagastrin stimulation, respectively. Controls showed no changes in gastric secretion. Plasma gastrin levels were not elevated after jejunal or duodenal perfusion. These results confirm that the intestinal phase of gastric secretory stimulation does exist in humans. Furthermore, it appears that the major portion of this stimulation originates from the duodenum and is not gastrin-dependent.

Adult↗
PubMed1978

A small dose of somatostatin inhibits the pentagastrin stimulated gastric secretion of acid, pepsin and intrinsic factor in man.

The effect of a small dose of somatostatin (0.05 mg/h) on the gastric secretion of acid, pepsin and Intrinsic Factor (IF) after stepwise increases in the dose of pentagastrin was examined in six healthy volunteers. The gastric secretion of acid, pepsin and IF in response to pentagastrin was significantly reduced by a continuous infusion of somatostatin. The pattern of inhibition indicates that somatostatin is a competitive inhibitor of pentagastrin in the stimulation of gastric secretion of both acid, pepsin and IF. This finding supports the hypothesis of a direct effect of somatostatin on the exocrine secretory cells of the stomach.

Blood Glucose↗