Search PubMed⌕ Search

Biomedical subjects

M Deltenre

Publications and source records attributed to M Deltenre.

At least 19 recordsLinked to original sources
PubMed2000

How come I've got it? (A review of Helicobacter pylori transmission).

Numerous epidemiological studies have shown the two main risk factors for Helicobacter pylori acquisition: childhood and low socio-economic level both in developing and developed countries. Nevertheless, in the absence of ubiquitous extra-human reservoir(s), the route(s) for person-to-person transmission remains undetermined. Very recent data favour the oro-oral route: besides gastric mucosa, mouth might be a sanctuary site and the oro-oral transmission hypothesis seems applicable worldwide. Nevertheless, the gastro-oral route (vomiting, gastro-oesophageal reflux) is still possible and deserves further research. In developing countries, feco-oral transmission (perhaps through the water supply) might be a significant mechanism of human contamination both for primary infection in children and perhaps, reinfection in adults.

Adult↗
PubMed2000

Noninvasive antigen-based assay for assessing Helicobacter pylori eradication: a European multicenter study. The European Helicobacter pylori HpSA Study Group.

OBJECTIVE: In a recently published multicenter study involving 501 patients undergoing esophagogastroduodenoscopy (EGD) throughout Europe, we showed the high accuracy of a recently developed simple test (HpSA) to detect Helicobacter pylori (H. pylori) antigens in stools of untreated patients. The aim of this study was to assess the diagnostic usefulness of HpSA compared with 13C UBT shortly after H. pylori eradication treatment. METHODS: Of the 501 patients enrolled in the validation study, 279 were found to be H. pylori-positive. These patients were given H. pylori eradicating regimen and asked to return for follow-up EGD with biopsies, 13C UBT and HpSA testing 4 wk after therapy. Follow-up results were available for 235 patients. Of these, 162 consented to all testing and 73 consented only to 13C UBT and HpSA testing. We assessed sensitivity and specificity of both HpSA and 13C UBT compared with biopsy-based methods in the 162 patients, who accepted follow-up EGD. We also assessed sensitivity and specificity of HpSA compared with 13C UBT, arbitrarily chosen as the gold standard, in the whole population of 235 patients. RESULTS: Sensitivity and specificity in 162 patients who consented to a second EGD were 93.8% (CI: 85.4-100%) and 96.9% (CI: 93.9-99.9%) for HpSA, and 90.6% (CI: 80.5-100%) and 99.2% (CI: 97.7-100%) for UBT. Using EGD-based methods as the gold standard, 130 of the 162 treated patients' H. pylori infection were eradicated (125 HpSA-negative, one borderline, and four false-positive; 129 13C UBT-negative, one false-positive), and 32 remained H. pylori-infected (30 HpSA-positive, two false-negative, 29 13C UBT-positive, three false negative). The overall eradication rate was 80.2%. The sensitivity and specificity of HpSA relative to UBT as the gold standard in the overall population (n = 235) were 95.6% (CI: 89.6-100%) and 94.7% (CI: 91.5-97.9%), respectively. CONCLUSIONS: HpSA has proven to be a useful method in posttreatment eradication testing for H. pylori. Its ease of use, speed, and noninvasive nature make HpSA testing an ideal method for post-treatment monitoring where a second EGD may not be justified.

Adult↗
PubMed2000

[Dyspepsia in general medicine: current diagnostic approach].

Upper GI tract endoscopy remains a key investigation in dyspepsia. Nevertheless, since the development of non-invasive techniques for Helicobacter pylori (Hp) infection detection and the current trend for immediate prescription of anti secretary drugs in "endoscopy negative gastro-oesophageal reflux disease" (NORD), accurate indications for endoscopy must be reconsidered. Careful recording of the medical history of the patient is crucial. Personal antecedents (diseases and drugs), familial history (especially gastric cancer) must be evidenced and three symptomatic groups must be identified: patients with alarm symptom(s), typical ulcer pain and GORD. Beside those three categories, most patients must be classified in "non specific dyspepsia". Immediate endoscopy is highly recommended in all patients with either alarm symptom(s) or typical ulcer pain (except in suspected relapse of a well documented duodenal ulcer disease). Age is a key determinant in GORD: endoscopy is not necessary in patients under 45 years of age. In case of "non specific dyspepsia" in patients under 45 years, a non-invasive test for Hp infection will favour when positive endoscopic investigation ("test and scope" policy). Nevertheless, in all patients above 45 years and in all patients with either a personal history of gastric ulcer, or a familial history of gastric cancer (whatever the age), endoscopy with biopsies remains the first recommended investigation.

Adult↗
PubMed1999

Diagnosis of Helicobacter pylori infection with a new non-invasive antigen-based assay. HpSA European study group.

BACKGROUND: Helicobacter pylori is a common human pathogen implicated in certain gastrointestinal diseases. In the search for new non-invasive techniques to diagnose H. pylori infection, we evaluated an EIA for H. pylori antigen in stool (HpSA). METHODS: In a prospective multicentre study, stool specimens from 501 patients (276 men, 225 women; age range 17-88 years, mean 52) undergoing gastroscopy in 11 centres throughout Europe were tested with HpSA and the carbon-13-urea breath test. At endoscopy, four biopsy samples were taken for histology (haematoxylin and eosin) and H. pylori detection (giemsa in both antrum and corpus, culture and rapid urease test). Patients were defined as positive for H. pylori if histology (antrum, corpus, or both) and urease test were positive, or if culture was positive. Patients classified as having H. pylori infection received an eradication regimen; 107 were reassessed 4 weeks after therapy. FINDINGS: Of 272 patients with H. pylori infection by the predefined criteria, 256 were positive by HpSA (sensitivity 94.1% [95% CI 90.6-96.6]). Of 219 patients without infection, 201 were negative by HpSA (specificity 91.8% [87.3-95.1]). INTERPRETATION: The stool assay was a reliable and easy-to-use tool for diagnosis of H. pylori infection. The test was accurate even shortly after treatment.

Adolescent↗
PubMed1998

Eradication of Helicobacter pylori: why does it fail?

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.

Anti-Bacterial Agents↗
PubMed1997

Helicobacter pylori eradication in duodenal ulcer disease is cost-beneficial: a Belgian model.

The eradication of Helicobacter pylori in infected patients with gastroduodenal ulcer disease the allows to obtain a definite healing of this chronically relapsing condition for which the direct costs have been steadily increasing (while indirect costs were reduced) for the last two decades. Both short-term studies performed on real time, and prospective simulations using a Markov's model over periods of one, five and up to fifteen years, revealed a significant cost/benefit advantage of an eradication policy: according to the Belgian model, the eradication of HP in patients with peptic ulcer would save between 750,000 and one million US dollars by million inhabitants when compared to maintenance or episodic treatment with anti-secretory drugs. Nevertheless, models are very sensitive to several factors: eradication rate, costs of screening and HP status assessment, frequency of peptic ulcer disease.

Anti-Ulcer Agents↗
PubMed1996

Strategies for Helicobacter pylori eradication in 1995: a review of international and Belgian experience.

After a decade of research, Helicobacter pylori eradication is still a problem because of the steady increase of bacterial resistance (imidazole, macrolides), pH-dependent efficiency of antibiotics, poor compliance of patients and frequent side effects of the therapies. After the failure of various monotherapies and the unefficiency of Amoxicillin-Imidazole combination for Imidazole-resistant strains, the two weeks ¿Oral Triple Therapy' with a 85% mean eradication rate, was abandoned because of a mean 35% side effects rate. The current goal is to obtain 90% eradication rate and the excellent results of german studies with a 2 weeks regimen combining a Proton Pump Inhibitor (PPI) with Amoxicillin have not been confirmed elsewhere in Europe. PPI plus Clarithromycin (two weeks) gave a mean 72% eradication rate on an ITT basis. The short, low-dose combination PPI-Clarithromycin-Imidazole for one week proposed by Bazzoli is very efficient in a population where Imidazole resistant strains are rare. The recent result of one week with (Omeprazole 20-Clarithromycin 250-Tinidazole 500) BID or (Omeprazole 20-Clarithromycin 500-Amoxi 1000) BID reached a 95% eradication rate but these very promising results are not confirmed in Belgium in an on-going study including 147 patients.

Amoxicillin↗
PubMed1995

Omeprazole-based antimicrobial therapies: results in 198 Helicobacter pylori-positive patients.

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.

Amoxicillin↗
PubMed1994

Helicobacter pylori: the link with gastric cancer.

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)

Helicobacter Infections↗
PubMed1993

Gastric screening prospects.

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)

Helicobacter Infections↗
PubMed1991

Management of dysphagia in suspected esophageal motor disorders.

Fifty-three patients suffering from dysphagia because of suspected esophageal motor disorders were treated by pneumatic dilatation using the Rider-Moeller technique. Fifteen had achalasia demonstrated by manometric studies. Forty-nine of them had remarkable clinical improvement after the procedure. During the mean period of follow-up (average 5 years, range 1-11), 75% of the patients needed a new dilatation, with a delay of two years. The results of the dilatation were excellent or good in 80% of the cases. Early complications consisted in two esophageal perforations surgically treated. There was no mortality. We did not observe late complications of the procedure. We conclude that pneumatic dilatation should be the initial procedure in the treatment of dysphagia in suspected esophageal motor disorders.

Aged↗