[Endoscopic ligation: a new technic in the treatment of esophageal varices].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C Florent.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A randomized clinical trial was conducted to determine whether colonoscopy is useful in deciding how long to maintain steroid treatment in attacks of Crohn's disease involving the colon. One hundred forty-seven patients with acute attacks of colonic or ileocolonic Crohn's disease were treated by oral prednisolone, 1 mg.kg-1.day-1; 136 achieved clinical remission, but 96 of them still had active endoscopic lesions and were randomized either to immediate start of steroid tapering (group A; n = 46) or to continued prednisolone treatment at the same dosage for 5 more weeks before steroid tapering was begun (group B; n = 50). In the remaining 40 patients (already in endoscopic remission, group C), steroid tapering was begun immediately. After prednisolone discontinuation, patients were followed up for 18 months or until clinical relapse. Prolongation of prednisolone therapy significantly improved the endoscopic scores in group B (30% of endoscopic remission). The frequency of successful steroid weaning was almost identical in groups A and B (82% and 80%, respectively), as was the actuarially calculated relapse clinical rate after steroid withdrawal (P = 0.22). No factor predictive of clinical relapse could be found. The clinical course of patients in group C was similar to that of those in groups A and B. Overall, only 22% of the 147 patients were still in clinical remission and off steroids 18 months after prednisolone discontinuation, outlining the need for maintenance therapy. In conclusion, for patients who have achieved clinical remission, adjustment of steroid treatment duration on the basis of endoscopy results is of no benefit, and the endoscopic aspect has no prognostic value; thus, it appears unnecessary to repeat colonoscopy in such patients before steroid tapering is begun.
Explore the source record for details and available documents.
Upper gastrointestinal endoscopy (UGI) is now widely accepted as the first-line examination of the digestive tract. UGI provides the diagnosis of most oesophageal and gastroduodenal diseases such as ulcer, cancer or oesophagitis. It is also valuable in the diagnosis of chronic diarrhoea, immunodeficiencies (immunoglobulin deficiency) and in AIDS patients. Improvements in disinfection and anesthesia make UGI a safe and well-tolerated procedure. Finally, it is, of course, the gold standard for the diagnosis of upper gastrointestinal haemorrhages and in many cases requiring endoscopic therapy.
Prostaglandins (PGs) and aluminum-containing antacids (Al.AAs) are effective in preventing gastric and duodenal lesions induced by neutralizing agents. The efficacy of Al.AAs is thought to be due to neutralizing properties and to stimulation of endogenous PGs synthesis. Liquid Maalox has the same effect as cimetidine 400 mg on postprandial duodenal acid load. In numerous prospective studies, Al.AAs have been shown to be as effective as cimetidine in the short-term treatment of duodenal ulcer (DU). Maalox TC at a dosage of 3 tablets b.i.d. provides an effective method for preventing DU relapse. Its effect is similar to that of nighttime cimetidine. Meta-analysis of prospective trials suggests that Al.AAs prevent stress ulcers more effectively than does cimetidine. It has been suggested that Al.AA acts by inducing surface epithelial cell disruption. Al-induced mucosal protection could be caused by a stimulated release of endogenous PGs, induced by Al microcrystal penetration of cells. In a recent study, we showed that small amounts of Al were absorbed by human gastric mucosa and accumulated in lysosomes; however, we did not observe any histological or ultrastructural lesions of the gastric mucosa. Prostaglandins (enprostil, misoprostol, and rioprostil) are as effective as cimetidine, but less effective than ranitidine, in healing DU. Enprostil and rioprostil have been shown to be as effective as ranitidine in treating gastric ulcer (GU). Moreover, enprostil inhibits postprandial gastrin release, whereas H2-blockers increase gastrin levels. Coadministration of misoprostol with aspirin is highly effective in healing aspirin-induced gastroduodenal lesions. Moreover, cotreatment with misoprostol was associated with a marked decrease in GU in patients with osteoarthritis receiving NSAIDs chronically.(ABSTRACT TRUNCATED AT 250 WORDS)
On two occasions separated by seven days, 22 g mucin (hog gastric mucin) was infused into right and left colon of 12 healthy volunteers (6 CH4 producers and 6 non-producers) maintained on a controlled diet. In the six CH4 producers, excess volumes of H2 excreted in breath were 73.4 +/- 11.9 and 35.1 +/- 14.1 (SE) ml/8 h (P less than 0.05) in response to right and left colonic infusion of mucin, respectively; excess volumes of CH4 were, respectively, 6.7 +/- 1.7 and 38.9 +/- 11.1 ml/8 h (P less than 0.05). In the six CH4 nonproducers, excess volumes of H2 excreted in breath were 76.6 +/- 17.6 and 30.8 +/- 6.3 ml/8 h (P less than 0.02) in response to right and left colonic infusion of mucin, respectively; excess volumes of CH4 were, respectively, 0.0 +/- 0.0 and 0.1 +/- 0.1 ml/8 h (not significant). In a further experiment, 17 healthy volunteers (10 CH4 producers and 7 nonproducers) were given on 2 consecutive days an oral load and an enema of 10 g lactulose. In the 10 CH4 producers, excess volumes of H2 excreted in breath were 74.6 +/- 15.1 and 32.3 +/- 11.5 ml/6 h (P less than 0.001) in response to oral ingestion and lactulose enema, respectively; excess volumes of CH4 were, respectively, 7.7 +/- 3.0 and 38.2 +/- 7.2 ml/6 h (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
The formation of dental calculus in dogs is a major problem. Scanning electron microscopy of tartar specimens from dogs revealed on the outer surface of the plaque polymorphic configurations, more or less arranged as free filaments, corn-cobs or swab-like structures. Uninhabited bacterial recesses were found on the inner surface of the calculus. Calcification may occur between or within the bacteria. Elucidating the mechanisms of calculus formation should help in the development of prophylactic measures.
Diarrhea "with" bacterial fermentation is characterized by acidic liquid stools containing high amounts of organic acids. Disaccharide malabsorption is the main cause. The mechanism of diarrhea is osmotic, and colonic fermentations reduce diarrhea. It is unlikely that starch malabsorption induces significant diarrhea, whereas a high-fiber diet is responsible for "physiologic" diarrhea. Colonic fermentations increase diarrhea due to organic colitis and the "motor diarrheas". They may be responsible for some intestinal symptoms in patients with irritable bowel syndrome. This does not imply a "hyperfermentative" process due to a hypothetical disturbance of colonic microbial ecology.
After a meal, a single dose of enprostil, a synthetic dehydroprostaglandin E2, inhibits gastrin level in both normal subjects and patients with duodenal ulcer, whereas H2 blockers exaggerate the postprandial gastrin response. However, the effect of prolonged treatment with enprostil on the gastrin profile is unknown. The aim of this study was to compare serum gastrin levels over a 24-hr period before (day 0) and on the last day (day 14) of a two-week course of enprostil (35 micrograms twice a day). Nine healthy volunteers (four women and five men), ages 29 +/- 5 years (range 23-39) were studied twice during a 24-hr period. Serum gastrin was measured at 30-min intervals during the day and at 2-hr intervals during the night. Enprostil (35 micrograms) was taken after basal gastrin serum measurement at 8:00 AM and PM. Standardized meals were ingested at 8:30 AM, 12:30 PM, and 8:30 PM. The postprandial integrated serum gastrin response was calculated after the three meals (4-hr period). Fasting serum gastrin levels were similar for the two periods. Integrated postprandial gastrin response was significantly inhibited after breakfast and dinner (P less than 0.001). Average results are expressed as mean +/- SEM (pmol/min/liter). During the night, gastrin levels were significantly decreased by enprostil. After 14 days, the inhibition of gastric acid secretion, which induces an increase of gastrin release with other antisecretory drugs, remained counterbalanced by the antigastrin properties of enprostil.
Rates of hydrogen and methane production were compared in caecal and faecal homogenates in six methane producers. Faecal homogenates produced hydrogen and methane in the absence of and after the addition of lactulose, whereas caecal homogenates produced hydrogen but little methane.
Diarrhoea "whith" bacterial fermentation is characterized by acidic liquid stools containing high amounts of organic acids. Carbohydrate malabsorption is the main cause; the mechanism of diarrhoea is an osmotic one, and colonic fermentation does reduce the diarrhoea. It is unlikely that starch malabsorption induces significant diarrhoea, whereas the consumption of high amounts of fibers is responsible for a "physiologic" diarrhoea. Colonic fermentations increase diarrhoea due to organic colitis and the "diarrhées motrices". They can be responsible for some intestinal symptoms in patients with the irritable bowel syndrome. This does not imply a "hyperfermentative" process due to a hypothetical disturbance of colonic microbial ecology.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The amount of dietary starch released in the colon, its excretion in the stools, the hydrogen and methane resulting from its fermentation, were measured in six healthy volunteers, ingesting two diets, rich and low in starch (100 and 300 grams). Regardless of the diet, approximately 5% of the ingested starch was malabsorbed in the small bowel and completely metabolized in the colon. While the amount of malabsorbed starch was 2.5 times higher with 300 g than with 100 g, the volumes of hydrogen exhaled were not different. This suggests that the responsibility of alimentary substrates in the production of colic gas is overestimated.
Dietary starch delivery to the colon and excretion in stools and the ability of unabsorbed carbohydrates to promote hydrogen and methane release in breath were evaluated in 6 volunteers during two 8-day periods on starch diets of 100 and 300 g, respectively. Significantly less starch was recovered from the terminal ileum by aspiration per 24 h during the low-starch period (4.1 +/- 0.3 vs. 9.5 +/- 1.1 g, mean +/- SEM, p less than 0.01). Unabsorbed glucose tended to rise during the high-starch period (2.7 +/- 0.8 vs. 1.1 +/- 0.3 g). Fecal outputs of starch, glucose, volatile fatty acids, and lactic acid were not significantly different during the two periods. Daily breath hydrogen excretion was unchanged (181.2 +/- 22.7 vs. 193.7 +/- 19.8 ml for the low- and high-starch periods, respectively), whereas breath methane excretion increased markedly in the three methane producers during the high-starch period (217.2 +/- 80.9 vs. 32.4 +/- 7.3 ml). Starch malabsorption in the healthy small intestine was moderate even with a high-starch diet and less than that previously estimated by indirect methods. Unabsorbed starch catabolism by the colonic flora does not seem to explain most of the breath hydrogen excretion.