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J D de Korwin

Publications and source records attributed to J D de Korwin.

At least 19 recordsLinked to original sources
PubMed2001

[Eradication of Helicobacter pylori. Is it necessary to eradicate Helicobacter pylori in gastric reflux?].

POTENTIAL PROTECTIVE EFFECT OF H. PYLORI: Epidemiological studies have not demonstrated an association between H. pylori infection and symptoms of gastroesophageal reflux, reflux esophagitis, or Barrett's esophagus with or without dysplasia or esophageal adenocarcinoma. On the contrary, an apparently favorable negative association has been identified suggested a potential protective effect of H. pylori. An inverse association is also observed between the severity of reflux complications and infection by strains of H. pylori expressing certain virulence markers (cogA) associated with the more severe gastric lesions. The prevalence of gastroesophageal reflux-related disease has increased steadily for more than fifty years while the incidence of H. pylori infection has decreased in developed countries. This observation might suggest that H. pylori infection plays a protective role. In addition, eradication of H. pylori could favor he development of gastroesophageal reflux or reflux esophagitis. The degree of risk is unknown. Pangastritis with significant lesions of the gastric body leading to a reversible decrease in the secretion of acid after H. pylori eradication might lower the risk of gastroesophageal reflux. POTENTIAL PROMOTION EFFECT: The relations between H. pylori and gastroesophageal reflux are complex. Reflux associated with duodenal ulcer appears to be improved by eradication of H. pylori suggesting that infection might promote the development of reflux. The causal mechanism would be increased acid secretion induced by antral gastritis predominantly resulting from the H. pylori infection. Further work is needed to determine the exact role of gastritis and perturbed acid secretion. PERSPECTIVES: Data on the role of H. pylori in transient relaxation of the lower esophageal sphincter, implicated in the pathogenesis of gastroesophageal reflux, are lacking. Antisecretion treatments reduce the quantity of gastric acid favoring H. pylori colonization of the fundic mucosa and possibly aggravating fundic gastritis. The risk of progression from H. pylori gastritis to atrophy or intestinal metaplasia of the fundus under prolonged proton pump inhibitor treatment remains to be determined. Eradication of H. pylori reduces the efficacy of antisecretory drugs according to poorly understood mechanisms. The potential effect of gastroesophageal reflux on the transmission of H. pylori infection remains to be established. PRACTICAL ATTITUDE: Much remains to be learned concerning the beneficial or deleterious effects of eradication of H. pylori on the course of gastroesophageal reflux. In clinical practice, eradication of H. pylori is not useful for patients with gastroesophageal reflux.

Adenocarcinoma↗
PubMed2000

[Gastritis, dyspepsia and Helicobacter pylori].

Helicobacter pylori is a major culprit in chronic gastritis. Interactions between the infected host, the bacteria and the environment, influence the type of gastritis and the occurrence of specific diseases (peptic ulcer, gastric lymphoma and adenocarcinoma) associated with the infection in a minority of cases. The benefit of H. pylori eradication is not proved in isolated gastritis, except for rare forms such as hypertrophic or lymphocytic gastritis. In spite of a high prevalence in functional dyspepsia with normal gastroduodenal endoscopy, H. pylori is not the main cause of symptoms in dyspeptic patients, but the gastritis could be involved in the appearance of ulcer-like symptoms. Strategies for non-invasive H. pylori detection for primary eradication are developed to reduce the endoscopy workload in the management of uninvestigated dyspepsia.

Dyspepsia↗
PubMed1999

Evaluation of a new serologic test for diagnosis of Helicobacter pylori infection in children.

A new semiquantitative enzyme immunoassay (Platelia Helicobacter pylori; Sanofi Diagnostics Pasteur, France) was evaluated and compared with two other serological assays (Gap-test IgG; Bio-Rad, France; and Cobas Core; Roche, Switzerland) for the diagnosis of Helicobacter pylori infection in children. The three tests were compared with the examination of biopsy samples obtained from 160 dyspeptic subjects (mean age, 9 +/- 4.7 years). Discrepant results were studied using an immunoblot technique. The response obtained for the Platelia assay in children was significantly lower than that obtained in a previously described population of 92 adults (Helicobacter pylori-negative mean ratios, 0.376 vs. 0.504, P<0.000783; Helicobacter pylori-positive mean ratios, 1.95 vs. 2.67, P<0.000003). Thus, the optimal cut-off for children (0.80) was lower than the one recommended for adults (1.10). According to the Receiver Operating Characteristic (ROC) curve analysis and to the Wilcoxon value, the Platelia and Cobas Core assays showed the highest discriminatory properties (Wilcoxon value, 0.94 for both) compared with the Gap-test IgG (Wilcoxon value, 0.91). When the newly established cut-off value (0.80) was used, the performance of Platelia was equivalent to that of Cobas Core (sensitivity: 94.4% for each; respective specificities, 86.8% and 90.6%). The Gap-test IgG had a lower sensitivity (maximum, 79%) and a higher specificity (maximum, 95.3%), but there were difficulties in interpretation because its grey zone encompassed 12% of the sera. In conclusion, the results showed good performance of the Platelia Helicobacter pylori assay and confirmed the merit of a specific cut-off value for use of this test in children.

Adult↗
PubMed1999

Performance of native and recombinant antigens for diagnosis of Helicobacter pylori infection.

The aim of this study was to evaluate the performance of three antigenic preparations for serological diagnosis of Helicobacter pylori infection: (i) native antigens from Helicobacter pylori strain N6 or its aflagellated isogenic mutant N6flbA-, or an acellular extract (antigen AgFA) from a pool of six clinical strains; (ii) recombinant antigens consisting of CagA fused to MS2 polymerase and HspA or recombinant UreA and UreB fused to the maltose-binding protein, and (iii) the preparations provided with two commercial kits, the Cobas Core (Roche Diagnostic Systems, France) and the Pylori Stat (BioWhittaker, Belgium). All preparations were used in an enzyme immunoassay to test 92 sera from dyspeptic patients for whom the status of Helicobacter infection was established. Sensitivities were higher (90 to 100%) for the native antigens and the commercial kits than for the recombinant antigens. Specificities were higher than 90%, except with UreA + UreB (42%). The most useful antigens were those extracted from strains N6 and N6flbA-.

Adolescent↗
PubMed1997

Gastric diffusion of antibiotics used against Helicobacter pylori.

Only a few pharmacological studies have been carried out on men and guinea pigs to determine the gastric diffusion of antibiotics, which are active against Helicobacter pylori. The results of these studies have been analysed in considering the physicochemical nature, the mode of administration, the way of gastric diffusion (topic and/or systemic) and the pharmacological interactions. The correlation of these pharmacokinetic results with those obtained in clinical trials is difficult because of the heterogeneity of the pharmacological and pharmacodynamic data. The absence of a convenient and suitable animal or in vitro study model renders further standardized pharmacokinetic studies in infected man and at steady state necessary.

Animals↗
PubMed1996

[The treatment of Helicobacter pylori infection].

H. pylori causes inflammatory lesions of the stomach and duodenum. At the present time eradication is essentially recommended in case of gastric or duodenal ulcer. The choice of the appropriate drug depends on the characteristics of the H. pylori infection, the localization deep in the gastric mucosa, the physico-chemical properties of the gastric medium, especially the acidity which deactivates antibiotics, slow bacterial growth and the germ's sensitivity to antibiotics. Anti-infectious treatment is now based on a three-drug regimen combining an antisecretory drug (proton pump inhibitor or H2 receptor antagonist) and two antibiotics: clarithromycin associated with amoxicillin or an imidazol derivative (metronidazol or tinidazol) or tetracycline. Two antibiotics (clarithromycin, amoxicillin) as well as three anti-secretory agents (lansoprazole, omeprazole, ranitidine) have been authorized in France for three-drug regimens of 1 or 2 weeks leading to approximately 90% eradication. Special attention should be placed on the risk of resistance to antibiotics (macrolids and imidazol derivatives) and patient compliance required for successful eradication of H. pylori. Other therapeutic schemes are under assessment and a vaccine is being prepared. Eradication of H. pylori has totally changed the treatment of gastric and duodenal ulcers, eliminating the need for long-term treatment and avoiding complications.

Anti-Bacterial Agents↗
PubMed1995

[Ki-1 positive non-Hodgkin's lymphoma disclosed by mucocutaneous ulcerations and glomerulonephritis].

Malignant lymphoma particularly of T phenotype can be associated with specific or non specific cutaneous lesions. These cutaneous manifestations can occur at the onset of the disease being sometimes the revealing sign or they can appear during the course of the lymphoreticular malignancies. Glomerulonephritis was also described in lymphoma. Ki-1 positive large cell lymphoma was recently identified. A new case is reported with lymphadenopathy and intestinal localisation revealed by cutaneous and mucosal ulcerations principally in the mouth and a focal segmental glomerulonephritis with endo- and extracapillary proliferation. The absence of lymphoma in cutaneous and renal lesions and the clinical presentation support the hypothesis of paraneoplastic manifestations, may be related to a vasculitis.

Glomerulonephritis↗
PubMed1991

[Helicobacter pylori gastritis: a new infectious disease. Reflections from personal experience].

To determine the relationship of microscopic chronic antral gastritis to Helicobacter pylori, 69 consecutive patients were studied. In a prospective longitudinal study, at least 2 successive gastroscopies with antral biopsies were performed (177 investigations on the whole). Sixty six of the 69 patients were treated with various therapeutic regimens i.e. antiulcer drugs and/or antibiotics. The type and intensity of inflammation (as based on whole inflammatory infiltrate density, polymorphonuclear cells presence or absence and IgA and IgM plasma cells counts) were correlated with H. pylori status (Giemsa staining and/or biopsy culture). The presence of the organism (Hp) and the gastritis were significantly correlated (high grade of whole inflammatory infiltrate Hp + ve: 98/109 90 p. cent, Hp-ve: 9/61 15 p. cent, p less than 0.001--presence of neutrophil PMNC Hp + ve: 80/109 73 p. cent, Hp-ve: 1/61 2 p. cent; p less than 0.001--IgA and IgM plasma cells respectively Hp + ve: 7.6 +/- 6.6, 10.6 +/- 7.1, Hp-ve 1.9 +/- 2.9, 4.2 +/- 4.5; p less than 0.005). Clearance and/or eradication of H. pylori after antibiotic treatment were associated with the disappearance of chronic gastritis activity and a statistically significant decrease of whole inflammatory infiltrate density (p less than 0.001) and IgA (p less than 0.005) and IgM (p less than 0.01) plasma cells counts. Mucosal inflammation was unchanged in case of H. pylori persistence and inflammation worsening occurred in case of infection relapse. H. pylori gastric mucosa colonization seemed to be responsible for the antral chronic inflammation associated with its presence. This study documents that antral chronic gastritis is a microbial disease associated with infection by H. pylori, against which there is an inflammatory response characterized by a significant mucosal infiltration with granulocytes and IgA and IgM secreting plasma cells.

Antacids↗
PubMed1991

[Helicobacter pylori gastritis: a new infectious disease. Reflections from a personal experience].

To determine the relationship of microscopic chronic antral gastritis to Helicobacter pylori, 69 consecutive patients were studied. In a prospective longitudinal study, at least 2 successive gastroscopies with antral biopsies were performed (177 investigations on the whole). Sixty six of the 69 patients were treated with various therapeutic regimens i.e. antiulcer drugs and/or antibiotics. The type and intensity of inflammation (as based on whole inflammatory infiltrate density, polymorphonuclear cells presence or absence and IgA and IgM plasma cells counts) were correlated with H. pylori status (Giemsa staining and/or biopsy culture). The presence of the organism (Hp) and the gastritis were significantly correlated (high grade of whole inflammatory infiltrate Hp + ve: 98/109 90%, Hp-ve: 9/61 15%, p less than 0.001--presence of neutrophil PMNC Hp + ve: 80/109 73%, Hp-ve: 1/61 2%; p less than 0.001--IgA and IgM plasma cells respectively Hp + ve: 7.6 +/- 6.6, 10.6 +/- 7.1, Hp-ve 1.9 +/- 2.9, 4.2 +/- 4.5; p less than 0.005). Clearance and/or eradication of H. pylori after antibiotic treatment were associated with the disappearance of chronic gastritis activity and a statistically significant decrease of whole inflammatory infiltrate density (p less than 0.001) and IgA (p less than 0.005) and IgM (p less than 0.01) plasma cells counts. Mucosal inflammation was unchanged in case of H. pylori persistence and inflammation worsening occurred in case of infection relapse. H. pylori gastric mucosa colonization seemed to be responsible for the antral chronic inflammation associated with its presence.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗
PubMed1989

Isotype evolution in the follow-up study of patients with Campylobacter pylori associated gastritis.

Four sequential immuno-assays were performed from May to November 1988 to follow the levels of IgG, IgA and IgM to Campylobacter pylori in 16 infected patients with histologically proven gastritis, among which 12 received appropriate therapy. Histopathological examination of antral biopsies, bacteriological cultures and urease tests were performed on each occasion when serum was tested for antibodies to C. pylori. The detection and quantitative assessment of the various isotypes to this bacterium proved valuable to appreciate the response to therapy with, in case of success, a steady decrease of antibodies levels concomitant with clinical improvement.

Adult↗
PubMed1984

Ultrastructural study of the mast cells of the human duodenal mucosa.

The ultrastructure of the process of degranulation of mast cells of human duodenal mucosa was examined. In normal controls little degranulation was seen, but in persons with false food allergy (pseudo-allergy) considerable degranulation of mast cells was detected. This is consistent with the hypothesis that some persons have an abnormal fragility of duodenal mast cells in the presence of histamine-releasing substances. Incubation of duodenal biopsy material with various histamine-releasing agents (compound 48/80, Concanavalin A, the calcium ionophore A 23187, and anti-IgE) confirmed the susceptibility of duodenal mast cells for antigen non-specific release of histamine, or that mediated by IgE. In a group of patients with immediate-type, anaphylactic, food allergy, mast cells in the absence of antigen are in a normal state, but degranulation occurs on exposure in vitro or in vivo to specific antigen. The susceptibility to degranulation continues in persons cured of their food allergy. This suggests that a clinical cure is not due to a change of susceptibility of duodenal mast cells to release histamine, but is possibly associated with formation of blocking antibodies, and/or a modification in reactivity of basophils and mast cells of other organs.

Adolescent↗