Biomedical subjects
Publications and source records attributed to E De Koster.
The article gives an overview of the current status of treatment of AP. The different therapeutical strategies are described and compared. The basic treatment for severe AP remains a medical therapy in an Intensive Care Unit. Surgical therapy is indicated in case of infection of necrotizing areas or other severe complications. The potential benefit of antiprotase agents and other new molecules is discussed.
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Currently, the first therapeutic attempt to eradicate Helicobacter pylori fails in one case out of six in intention to treat analysis. The main causes of failure are bad compliance, partly because of side effects that are severe in 1 to 4% of cases, absence of local validation of the treatment scheme, since some differences do exist between regions and countries, primary and secondary resistance of the strain (stable for Imidazole-derivates, but increasing for Macrolides), and, to a lesser extent, smoking and pre-treatment with proton pump inhibitors. Moreover, in routine medicine, inappropriate treatment cocktails are still prescribed, even by gastroenterologists. Obviously, there is a need for careful medical education and information both as far as concerns doctors and patients, for well-designed prescription, based on local experience and the precise previous history of every patient, as well as for continuous monitoring of the bacterial resistance to antibiotics. Culture of the strain is recommended after eradication failure with the classic one-week triple therapy, but if reliable culture and resistance testing are not available, the quadruple therapy as a second-line treatment is, so far, the best choice.
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AIM: To compare the efficacies of omeprazole-based antimicrobial therapies in Helicobacter pylori-positive patients. PATIENTS AND METHODS: We report the results of seven therapeutic trials combining omeprazole, clarithromycin, amoxycillin, colloidal bismuth subcitrate and tinidazole in 198 patients (peptic ulcer disease/non-ulcerative dyspepsia, 137/61) to eradicate H. pylori infection. The diagnosis of infection was performed by Sydney system biopsies, compliance was checked after a pill count at the end of the treatment and eradication was assessed at least 4 weeks after the end of the treatment either by the Sydney system for peptic ulcer disease or the urease breath test for non-ulcerative dyspepsia. RESULTS: When results were analysed on a protocol basis, the only significant difference in eradication (P = 0.006) was found between the total population of patients treated with amoxycillin-based combinations (27 eradications out of 48 patients) and those given a treatment that included clarithromycin (84 eradications out of 108). Forty-two patients (21%) dropped out either because of side effects (10 among patients taking clarithromycin and two taking amoxycillin) or because they were lost to follow-up (27 patients). Out of 64 patients with active ulcers, 43 (67%) were both H. pylori-negative and ulcer-free 4-8 weeks after the end of therapy, 12 out of 64 (19%) were ulcer-free but remained H. pylori-positive and nine out of 64 (14%) were H. pylori-positive and had active ulceration.
Gastric cancer is the world's overall second most common cancer, and carries a bad prognosis. In the Correa model of gastric carcinogenesis, environmental factors (salt, nitrate, a lack of vitamin C and beta-carotene, bile reflux, bacterial overgrowth in atrophic gastritis with nitrosamine formation) are related to the evolution from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma. The incidence of H. pylori decreases with progressing preneoplastic lesions. In several studies, the prevalence of H. pylori was elevated in patients with gastric cancer, with a trend for a higher prevalence in intestinal type gastric cancer vs diffuse type. Family members of patients with gastric adenocarcinoma have a higher H. pylori prevalence than controls; patients infected with H. pylori have more family members with gastric cancer. Several epidemiological studies showed a higher H. pylori prevalence in regions or populations with high gastric cancer risk vs low-risk populations. Large-scale studies in China and Europe showed a correlation between H. pylori seroprevalence and gastric cancer incidence and mortality. Three prospective nested case-control studies showed that infection with H. pylori increased the risk of further development of gastric adenocarcinoma, showing that H. pylori infection precedes the development of gastric cancer. Several pathways can be identified explaining the association between H. pylori and gastric adenocarcinoma. We showed that gastric cell proliferation is increased in parallel with inflammation. The ascorbic acid concentrating mechanism is abolished in gastritis. Ammonia, generated by H. pylori's urease, gives rise to gastric mucosal atrophy. We showed that salt increases the gastric cell proliferation only in H. pylori-infected individuals. The organism's toxin may play a role in gastric cancer. Besides H. pylori, other environmental factors are important in determining the gastric cancer risk. For instance, we showed that in Belgium, Maghreb immigrants have a high prevalence of H. pylori infection but a low prevalence of intestinal metaplasia and gastric cancer. Gastric lymphoma is rare (about 5% of all gastric tumours), but its incidence is steadily increasing. It was shown that H. pylori also increases the risk for low-grade as well as high-grade gastric lymphoma. Eradication of H. pylori has been shown to cure several cases of unequivocally proven gastric low-grade lymphoma.(ABSTRACT TRUNCATED AT 400 WORDS)
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The incidence of gastric cancer is rapidly declining in the Western world, but it remains high in the Third World and in Japan. Systematic screening for gastric cancer has been undertaken in Japan, where barium X-ray is used in people over the age of 40. Evaluation data suggest a benefit in reduced mortality, but biases cannot be ruled out. A similar screening programme has been started in Venezuela. Currently, stomach cancer screening programmes cannot be recommended as public health policy, except in high-risk areas where they have already started. The Correa model of gastric carcinogenesis states that environmental influences cause a normal gastric mucosa to undergo successive stepwise changes, through superficial gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, carcinoma and, finally, invasion. Incriminated environmental influences include irritant, antibodies, gastrectomy, nutritional deficits, intake of nitrogen compounds and Helicobacter pylori. These bacteria cause a chronic superficial gastritis, which may develop into atrophic gastritis. H. pylori is less frequently found in advancing preneoplastic lesions, and seldomly in gastric carcinoma tissue (it may, however, be identified more readily in the surrounding non-cancerous tissue). Several lines of evidence suggest that H. pylori may play an important role in human gastric carcinogenesis. We found that in some patients with H. pylori infection and without preneoplastic lesions, the gastric cell turnover was increased; this was correlated with the intensity of the inflammatory changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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Worldwide Campylobacter pylori is a major cause of active chronic gastritis in man. This curved spiraled microorganism can readily be detected within the mucusgel especially in the antrum, in particular in patients suffering from peptic ulcer disease or non-ulcer dyspepsia, rarely in individuals with normal gastroduodenal mucosa. Increasingly arguments are being presented in support of a pathogenetic role of C. pylori in non-ulcer dyspepsia and in peptic ulcer disease. There is a striking discordance between in vitro antibiotic sensitivity, and in vivo efficacy with respect to suppression or eradication of the organism. At present the combination of colloidal bismuth subcitrate and amoxicilline or tinidazole appears to be encouraging with respect to longterm eradication of this peculiar microorganism. Eradication by antibacterial treatment ultimately may result in histologic normalization of the gastric mucosa. To what extent peptic ulcer disease. There is a striking discordance between in vitro antibiotic sensitivity, and in.
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A putative pathogenetic role has been ascribed to Helicobacter pylori in several extradigestive diseases, including vascular (atherosclerosis and ischaemic heart disease, primary Raynaud phenomenon, primary headache), autoimmune (Sjögren's syndrome, Henoch-Schönlein purpura, autoimmune thyroiditis, idiopathic arrythmias, Parkinson's disease, nonarterial anterior optic ischemic neuropathy), and skin diseases (chronic idiopathic urticaria, rosacea, alopecia areata), sideropenic anemia, growth retardation, late menarche, extragastric MALT lymphoma, diabetes mellitus, hepatic encephalopathy, sudden infant death syndrome, and anorexia of aging. We examine critically the strength of the evidence linking these diseases to Helicobacter pylori, using ischaemic heart disease as an example of epidemiological techniques, and skin diseases as an example of treatment studies. By the standards of evidence-based medicine, studies have been often of low quality. The best evidence usually is not indicative of a role for Helicobacter pylori in these diseases.
Both juxtapapillary duodenal diverticula and colon diverticula are acquired lesions, the pathogenesis of which is believed to involve the influence of high intraluminal pressure on loci minoris resistentiae in the gastrointestinal wall. We wanted to investigate whether juxtapapillary duodenal diverticula and colon diverticula occur independently, or whether they are part of a hypothetical general "gastrointestinal diverticular disease". 239 patients with juxtapapillary duodenal diverticula were identified in 2231 patients undergoing ERCP. Complete radiology data were available in 119/239 patients. Double contrast barium enema had been performed in 28/119 patients. In these patients, colon diverticula were present in 9/20 women and 1/8 men. The frequency of colon diverticula in these patients was compared with randomly chosen age- and sex-matched controls, for whom barium enema results were available. In these controls, 9/20 women and 1/8 men also had colon diverticula (n.s.). We conclude that after stratification for age and sex, the occurrence of colon diverticula is not higher in patients with juxtapapillary duodenal diverticula than in the general population. Juxtapapillary duodenal diverticula and colon diverticula thus occur independently. These data are not in favor of the existence of a general gastrointestinal diverticular disease.
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In a retrospective study of 702 consecutive colonoscopies, the authors observed 185 cases of diverticulosis or moderate diverticulitis. They studied the colonic diseases associated with the presence of diverticula (78 cases) and discussed the role of endoscope in the approach of colonic diverticulosis.
In order to explore the relationship between duodenal diverticula and biliary stone disease, we reviewed 2231 endoscopic retrograde cholangio-pancreatography procedures. We found at least one juxtapapillary diverticulum per 239 patients (10.8%). The occurrence of duodenal diverticula increases with age. Patients with duodenal diverticula were older, had more gallbladder stones, more common bile duct stones, had undergone cholecystectomy more frequently, and experienced more frequently common bile duct stone recurrence after cholecystectomy. We thus confirm an association between the presence of diverticula of the second part of the duodenum, and biliary stone pathology, including gallbladder stones, common bile duct stones, and recurrent stones after cholecystectomy. We discuss the aetiopathogeny of this affection.
The efficacy of various antimicrobial and anti-ulcer agents on the eradication of Campylobacter pylori in patients with antral gastritis or duodenal ulcers was investigated by several open studies or double-blind, placebo-controlled protocols. Among the anti-ulcer agents, ranitidine, cimetidine or sucraflate had no effect on C. pylori. Colloidal bismuth subcitrate achieved clearance of C. pylori in 40% of treated patients at the end of therapy but a high relapse rate (14/16 patients) was observed after a 6-month follow-up period. The antibacterial agents doxycycline, minocycline, ofloxacin, clindamycin, paromomycin and nifuroxazide failed to eradicate C. pylori in most patients. By contrast, short term elimination of C. pylori could be achieved in more than 90% of patients treated with amoxycillin. However, relapse occurred as a rule in all amoxycillin-treated patients within one month after therapy. Overall, we observed no correlation between the in-vitro activity of the different antibacterial agents and their in vivo efficacy. Development of resistance during therapy does not seem to account for this discrepancy since it occurred only with ofloxacin. On the basis of these results, we conclude that long term eradication of C. pylori from the gastric antrum cannot be achieved after monotherapy either with antibiotics or with bismuth salts.