Biomedical subjects
Publications and source records attributed to M Guslandi.
Since cimetidine in spite of its ulcer-healing properties was found to have a damaging effect on gastric mucus, the problem of the influence of anti-ulcer drugs on mucous barrier became of topical interest. The effects of various anti-ulcer drugs on gastric mucus secretion are briefly reviewed and the possible role of changes in cyclic AMP levels of gastric mucosa is discussed.
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Thirty outpatients suffering from duodenal ulcer of recent onset were given cimetidine 1 g/day or gefarnate 250 mg/day for 6 weeks in a double blind trial, randomly balances between the groups. Endoscopic assessment was carried out at 4 and 6 weeks; patients healed after 4 weeks were withdrawn from the trial. In all parameters considered, cimetidine showed a highly significant difference. The healing rate at 4--6 weeks was 67--93% after cimetidine treatment and 27--53% after gefarnate treatment. The effect of cimetidine on the disappearance of symptoms, mainly the nocturnal ulcer pain, and on antacid consumption was greater than that after medication wity gefarnate. After 4--6 weeks of a full dose cimetidine regimen, both basal and pentagastrin stimulated gastric acid secretion were reduced and peptone meal stimulated serum gastrin increased; the basal gastrinaemia remained unchanged.
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Mild to severe and persisting diarrhea and even colitis have been reported as a side effect of therapy with lincomycin and clindamycin. An alteration in the normal bowel flora with an overgrowth of coliforms and other antibiotic-resistant bacteria has been postulated as a mechanism for the development of diarrhea. Investigations were undertaken in men to observe whether the simultaneous administration of gentamicin was capable of preventing lincomycin-associated intestinal disturbances. Of the 30 subjects treated only with lincomycin 11 (36.6%) developed diarrhea. Of the 18 subjects treated with lincomycin and simultaneously with oral gentamicine, none developed diarrhea. Results of bacteriological examinations indicate that in subjects treated with lincomycin, some potentially pathogenic bacteria, like coliforms and clostridia, are still present in intestinal flora; the simultaneous absence of bifidobacteria and bacteriodes could result in the abolishment of the host resistance to the noxious activity of these endogenous bacteria, as some reported data of the literature suggest. Coliforms and the majority of clostridia strains are not present in subjects treated simultaneously with gentamicin.
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BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclo-oxygenase (COX), which leads to suppression of COX-1-mediated production of gastrointestinal-protective prostaglandins. Gastrointestinal injury is a common outcome. We compared the efficacy, safety, and tolerability of long-term therapy with celecoxib, a COX-1 sparing inhibitor of COX-2, with diclofenac, a non-specific COX inhibitor. METHODS: 655 patients with adult-onset rheumatoid arthritis of at least 6 months' duration were randomly assigned oral celecoxib 200 mg twice daily or diclofenac SR 75 mg twice daily for 24 weeks. Anti-inflammatory and analgesic activity and tolerability were assessed at baseline, every 4 weeks, and at week 24. We assessed gastrointestinal safety by upper-gastrointestinal endoscopy within 7 days of the last treatment dose at centres where the procedure was available. Analysis was by intention-to-treat. FINDINGS: 430 patients underwent endoscopy (celecoxib n=212, diclofenac n=218). The two drugs were similar in management of rheumatoid arthritis pain and inflammation. Gastroduodenal ulcers were detected endoscopically in 33 (15%) patients treated with diclofenac and in eight (4%) in the celecoxib group (p<0.001). The rate of withdrawal for any gastrointestinal-related adverse event, most commonly abdominal pain, diarrhoea, and dyspepsia, was nearly three times higher in the diclofenac-treated group than in the celecoxib group (16 vs 6%; p<0.001). INTERPRETATION: Celecoxib showed sustained anti-inflammatory and analgesic activity similar to diclofenac, with a lower frequency of upper gastrointestinal ulceration or gastrointestinal adverse events, and tolerability was better.
BACKGROUND: Elderly subjects are more prone to develop gastric injury, but human data on the state of mucosal protective mechanisms are scarce. The aim of the study was to assess gastric mucus and bicarbonate secretion as well as local microcirculation in elderly patients. METHODS: Fasting gastric juice was collected in 45 elderly patients and in 45 control subjects devoid of endoscopic gastric abnormalities. Total mucoproteins, 'mucoprotective index' (as qualitative expression of mucus secretion) and gastric bicarbonate (Feldman's method) were measured. In addition in 24 elderly patients, and in a matching group of younger subjects, gastric mucosal blood flow was measured by laser Doppler flowmetry. RESULTS: Mucus and bicarbonate production was significantly reduced (p < 0.01) in elderly patients, the quality of mucus secretion being unaltered. Gastric mucosal perfusion was also significantly decreased (p < 0. 01) in aged subjects. CONCLUSION: In the elderly gastric mucosal defences are impaired. This is in keeping with a reduced gastric prostaglandin biosynthesis and may account for the higher susceptibility of the mucosa to damaging agents. The possible role of atrophic gastritis and Helicobacter pylori infection as independent confounding factors remains to be determined.
The digestive system is one of the major sources of nitric oxide, which, due to its smooth muscle-relaxing and vasodilating properties, appears to play a key role in the regulation of gastrointestinal motility, mucosal blood flow and gastroprotection. In addition nitric oxide takes part in the control of pancreatic secretion and liver functions. Recent studies suggest that the substance may be involved in the pathogenesis of achalasia, toxic megacolon, Hirschsprung's disease and portal hypertension.
The effects on gastric mucus by two different H2-receptor antagonists, famotidine and ranitidine, have been investigated in 20 patients with duodenal ulcer. Before and after 4 weeks' treatment with either drug the quality of mucus secretion was assessed by means of a 'mucoprotective index'. A significant (P less than 0.01) decrease in the values of this index was observed in famotidine-treated subjects, whereas no changes were detected in those given ranitidine. The findings of this study with famotidine are in keeping with the results previously reported with cimetidine using the same method. It is suggested that blockade of gastric H2-receptors alters the composition of gastric mucus in man. This effect is not shared by ranitidine.
Evidence is accumulating that ursodeoxycholic acid (UDCA), an agent widely employed for gallstone dissolution, exerts therapeutic effects in chronic liver disease. UDCA is thought to act mainly by reducing the detergent properties of bile, making it less toxic for the liver cells. Confirming the results of preliminary observations double-blind, placebo-controlled trials have shown that UDCA significantly decreased serum concentrations of liver enzymes such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transferase in primary biliary cirrhosis and other cholestatic conditions, as well as in chronic active hepatitis. A substantial improvement in liver histology has also been detected in UDCA-treated patients with primary biliary cirrhosis. The effect of UDCA in chronic hepatitis is currently a matter of investigation.
Dyspeptic patients (n = 12) with endoscopic signs of chronic gastritis were treated orally for 28 days with a new gel formulation of sucralfate at a dose of 1 g twice daily. Before and after treatment, gastric blood flow was assessed during endoscopy by means of laser Doppler flowmetry. The sucralfate gel promoted a significant increase (P < 0.001) in blood perfusion in all patients, restoring normal levels of gastric microcirculation. The results are consistent with observations in animals, suggesting that the mechanisms responsible for the gastroprotective and therapeutic properties of sucralfate include enhancement of mucosal blood flow.
BACKGROUND/AIMS: Helicobacter pylori infection has a low prevalence in Crohn's disease, possibly because of sulphasalazine therapy. We investigated Helicobacter pylori seroprevalence in patients with Crohn's disease never treated with sulphasalazine in order to assess the possible role of antibiotic treatment. METHODOLOGY: Two groups of patients with Crohn's disease (group I: subjects treated with ciprofloxacin, metronidazole or both during the last six months; Group II: subjects who were not given antibiotics during the last six months) and a control group of 30 patients with irritable bowel syndrome were considered. IgG anti-H. pylori levels were measured in all patients. RESULTS: Serology was positive respectively in 16.6%, 13.3% and 36.6% of cases in the three groups. CONCLUSIONS: Our findings confirm the Helicobacter pylori infection is infrequent in Crohn's disease. Neither sulphasalazine nor antibiotics appear to play a role.