Trial reportDigestive diseases and sciences2008
The effect of Helicobacter pylori eradication treatment on the MUC 1 and Lewis antigens level in human gastric juice: a preliminary study.
Trial report in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- The Role of Adhesion in Helicobacter pylori Persistent Colonization.Current microbiology · 2023Review
- Detection of digestive malignancies and post-gastrectomy complications via gastrointestinal fluid examination.Frontiers of medicine · 2017Review
- Influence of monoclonal anti-Lewis b, anti-H type 1, and anti-sialyl Lewis x antibodies on binding of Helicobacter pylori to MUC1 mucin.Molecular and cellular biochemistry · 2014Article
- Glycosylation of mucins present in gastric juice: the effect of helicobacter pylori eradication treatment.Clinical and experimental medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is considered as a causative agent of gastritis, duodenal and gastric ulcers, and gastric cancer. During inflammation, association of the pathogen of gastric epithelial cells and mucins is considered important. It was postulated that Lewis b structures of secretory MUC 5AC mucin can be a receptor for the bacterium. Some authors also suggest that epithelial MUC 1 mucin may be implicated in the mechanism of infection. The main aim of our work was to support this last suggestion by evaluation of the possible changes in MUC 1 and Lewis a and b levels in gastric juice before and at the end of eradication treatment. The gastric juices of ten examined patients were chromatographed on a Sepharose 4 B column, electrotransferred on Immobilon P membranes, and assessed for MUC 1 and Lewis a and b structures using monoclonal antibodies. In 90% of examined patients, higher amounts of MUC 1 mucin were observed at the end of eradication treatment. Similar results for Lewis a and b structures were found. In the case of MUC 1 and Lewis b, the differences were statistically significant. Helicobacter pylori influences expression of the soluble form of MUC 1 mucin and Lewis a and b structures present in gastric juice.
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Registered trials
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