Prophylactic treatment with gabexate reduced pancreatic damage related to ERCP, as reflected by reductions in the extent but not the frequency of elevated enzyme levels and in the frequency of pancreatic pain and acute pancreatitis.
Esophageal manometry was performed in 45 cirrhotics with varices, in 15 cirrhotics without varices, and in 20 normal subjects, to define the effect of varices on esophageal motility. Cirrhotics with varices showed a decreased amplitude of motor waves in the lower half of the esophagus (p less than 0.01), an increased duration of primary peristaltic waves along the entire length of the esophagus (upper esophagus, p less than 0.05; lower esophagus, p less than 0.01), and an increased peak-to-peak speed of primary peristaltic waves (p less than 0.01). Resting lower esophageal sphincter pressure and duration of sphincter relaxation were similar in patients and controls. The above-mentioned abnormalities might be due to the mechanical effect of the presence of varices.
In ten patients with mild to moderate clinical relapses of ulcerative colitis during treatment with mesalazine (1 g t.i.d.) and with a previous history of poorly tolerated steroid courses, transdermal nicotine (15 mg daily) was added for 4 weeks. Clinical findings were assessed by employing Rachmilewitz's activity index. In 7 of the patients, clinical remission was achieved, the results persisting for up to 3 months after nicotine withdrawal. Endoscopic and histological examination, when performed, confirmed the clinical findings. Nicotine patches may represent a good alternative to steroids in selected patients with mild to moderate relapses of ulcerative colitis. The precise mechanism of action remains unknown.
In order to investigate some pathophysiological aspects of the two diseases, 15 patients with congestive gastropathy and 15 with chronic gastritis have been studied and compared with 15 healthy controls. Gastric blood flow as determined during endoscopy by means of laser Doppler flowmetry was found to be significantly increased (p < 0.001) in congestive gastropathy, whereas a significant reduction (p < 0.001) was noted in chronic gastritis. On the other hand, Helicobacter pylori was detected in 80% of cases in chronic gastritis, while the prevalence of the microorganism in congestive gastritis was similar to that in healthy controls. It is concluded that chronic gastritis and congestive gastropathy are related to different pathogenetic factors and require different therapeutic approaches.
The data collected in the study showed that, in general, there is compliance with the Società Italiana di Endoscopia Digestiva (SIED) and Società Italiana di Gastroenterologia (SIGE) guidelines, although with some important exceptions.
The effects of the antidopaminergic drug sulpiride on gastric acid secretion and gastrin release have been evaluated in 42 healthy individuals. Basal and submaximal pentagastrin (0.5 micrograms/kg-h)-stimulated gastric acid secretion, as well as basal and meal-induced gastrin secretion, were studied after acute intramuscular administration of racemic sulpiride (100 mg) and its L-(50 mg) D-(50 mg) isomers. Racemic and L-sulpiride significantly decreased stimulated serum gastrin concentration, but they did not affect fasting serum gastrin or basal and stimulated gastric acidity. D-sulpiride significantly decreased gastric acid secretion, without affecting serum gastrin levels. While the effects of racemic and L-sulpiride are analogous to those of other antidopaminergic drugs, D-sulpiride mimics the action of dopamine, at least at gastric level. These data support the hypothesis that the D-isomer may possess agonist-antagonist activity at dopamine receptors. Since racemic sulpiride has been used with conflicting results in the therapy of patients with peptic ulcer, in the light of the present results it would be of interest to study separately the efficiency of the D- and L-isomers of the drug in healing peptic ulcer.
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