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Biomedical subjects

B Desaint

Publications and source records attributed to B Desaint.

At least 19 recordsLinked to original sources

Familial adenomatous polyposis: prevalence of adenomas in the ileal pouch after restorative proctocolectomy.

OBJECTIVES: To determine the prevalence of adenomas in ileal pouches from patients with familial adenomatous polyposis (FAP) and to determine whether a correlation exists between the presence of pouch adenomas and duodenal adenomas and the site of the adenomatous polyposis coli gene mutation. SUMMARY BACKGROUND DATA: Restorative proctocolectomy can markedly reduce the risk of colorectal adenocarcinoma in FAP patients. However, adenomas with the potential to progress to adenocarcinoma can develop in the duodenum, ileum, and continent ileostomy after restorative proctocolectomy. More recently, adenomas have been described in the ileal pouch after ileoanal anastomosis. METHODS: Pouch endoscopy was offered to 167 patients with FAP who had undergone restorative proctocolectomy between January 1984 and December 1996. RESULTS: Adenomas were found in 35% of the 85 ileal pouches examined. No invasive carcinomas were noted. The risk of developing one or more adenomas at 5, 10, and 15 years was 7%, 35%, and 75%, respectively. Patients with adenomas were more likely to have duodenal and ampullary adenomas. No correlation was detected between adenoma development and the site of the adenomatous polyposis coli mutation. CONCLUSIONS: Adenomas are frequently found in the ileal pouch of patients after restorative proctocolectomy for FAP. Regular endoscopic surveillance of the pouch is recommended at a frequency similar to that of upper gastrointestinal endoscopy.

Adenomatous Polyposis Coli↗

Prevention of biliary stent occlusion by ursodeoxycholic acid plus norfloxacin: a multicenter randomized trial.

We report a prospective randomized multicenter trial that tested the efficacy of combining ursodeoxycholic acid and norfloxacin in the prevention of polyethylene stent clogging in patients with obstructive jaundice due to an unresectable malignancy at the level of the common bile duct. After insertion of a 10-Fr straight polyethylene stent, patients were allocated to receive oral treatment with ursodeoxycholic acid and norfloxacin, or conservative treatment. The primary outcome measure was stent blockage within six months. Thirty-three patients (group I) received ursodeoxycholic acid and norfloxacin, and 29 received conservative treatment (group II). At six months, cumulative stent patency rate did not differ significantly between group I (47+/-11%, mean +/- SE, median 149 days) and group II patients (24+/-10%, mean +/- SE, median 100 days, P = 0.23, log-rank test). Four stents were clogged by ursodeoxycholic acid. Survival did not differ between the two groups. Combined therapy with ursodeoxycholic acid and norfloxacin failed to improve stent patency. Moreover, ursodeoxycholic acid can cause stent obstruction.

Aged↗

Liver disease from surreptitious administration of urethane.

We report subacute necrosis, peliosis hepatis, venoocclusive disease and hepatic angiosarcoma after long-term administration of urethane. We take this to be the 12th case of urethane-induced hepatitis and the first associated with vascular liver tumor.

Chronic Disease↗

[Main indications for upper digestive endoscopy].

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.

Digestive System Diseases↗

Morphologic and ultrastructural effects of Maalox TC on human gastric and duodenal mucosa.

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)

Adult↗

Effect of two-week treatment with enprostil (35 micrograms twice a day) on 24-hour serum gastrin levels.

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.

Adult↗