Accelerated gastric epithelial proliferation.

Gray, Michael R.; Darnton, S. Jane; Hunt, John A.; Irlam, R W; Nemeth, Joe; Wallace, H M

doi:10.1136/gut.36.4.522

Cited by 13 publications

(4 citation statements)

References 28 publications

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“…The mouse monoclonal antiproliferating cell nuclear antigen (PCNA) antibody (antihuman, cross‐reacts with rat, IgG2a, kappa subclass; DAKO, Glostrup, Denmark) was used at a 1:100 dilution (diluted with 2% in phosphate‐buffered saline) 21–33 …”

Section: Methodsmentioning

confidence: 99%

“…20 The mouse monoclonal antiproliferating cell nuclear antigen (PCNA) antibody (antihuman, cross-reacts with rat, IgG2a, kappa subclass; DAKO, Glostrup, Denmark) was used at a 1:100 dilution (diluted with 2% in phosphate-buffered saline). [21][22][23][24][25][26][27][28][29][30][31][32][33] Immunohistochemical procedure Tissue sections, 4 mm thick, were mounted on slides precoated with ovalbumin. An immunohistochemical examination was then carried out by using the avidin-biotin-peroxidase complex (ABC) technique, 22 rabbit antihuman VEGF IgG and mouse antihuman PCNA IgG.…”

Section: Immunohistochemical Studymentioning

confidence: 99%

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Immunohistochemical localization of vascular endothelial growth factor in the rat portal hypertensive gastropathy

Tsugawa¹,

Hashizume²,

Tomikawa³

et al. 2001

J of Gastro and Hepatol

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The levels of SaO2 and PaO2 were lower in the PHT rats. There is a possibility that a kind of portal hypertensive gastric change may trigger an enhanced histochemical expression of VEGF. The increased activity of VEGF may have a possibility of the hypoxic gastric mucosal state caused by the presence of active congestion. This damaged mucosal state 'PHG' may thus facilitate the fragility in PHG and such lesions may be slow and insidious, which may therefore lead to sudden and severe anemia, thus causing massive and sometimes fatal hemorrhaging.

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Section: Methodsmentioning

confidence: 99%

Section: Immunohistochemical Studymentioning

confidence: 99%

Immunohistochemical localization of vascular endothelial growth factor in the rat portal hypertensive gastropathy

Tsugawa¹,

Hashizume²,

Tomikawa³

et al. 2001

J of Gastro and Hepatol

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“…To make NSAJD therapy safer, the use of coxibs and/or co-therapy with proton pump inhibitors (PPI) is recommended, in theory, for all patients but, in practice, at least for those with higher risk of bleeding or perforation (11)(12). PPJ therapy alone increases gastrin levels by suppressing acid production, the higher gastrin level increases cell turnover and in theory may promote gastrinoma formation (13). In clinical trials, however omeprazole did not alter cell turnover (14).…”

mentioning

confidence: 99%

Proton Pump Inhibitor Co-Therapy Normalizes the Increased Cell Turnover of the Gastric Mucosa Both in Nsaid and Selective Cox-2 Users

Hritz

Herszényi

Molnár

et al. 2005

Int J Immunopathol Pharmacol

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Proton pump inhibitor (PPI) co-therapy is considered the best strategy in preventing gastrointestinal complications during non-steroidal anti-inflammatory drug (NSAID) treatment, but there is limited information available on its effect on gastric mucosal cell kinetics. To evaluate the effect of PPI co-therapy on gastric mucosa we investigated epithelial cell proliferation, apoptosis, epithelial growth factor receptor (EGFR) and p53 expression in patients on chronic non-selective NSAID or cyclooxygenase-2 selective inhibitor (COX-2) treatment. Gastric biopsies of the antrum were taken from 10-10 patients on chronic NSAID and COX-2, therapy prior and after 6 months PPI co-therapy, and 10 controls without any treatment. Cell proliferation, apoptosis, EGFR and p53 expression were measured by immunohistochemistry. At least 600 glandular epithel cells were encountered and results were expressed as % of total cells counted. We found increased cell proliferation in patients on chronic COX-2 but not on NSAID therapy. Patients on either NSAID or COX-2 therapy had an increased p53 and decreased EGFR expression. PPI therapy reversed not only the increased cell proliferation and p53 expression, but also the suppressed EGFR expression when administered as co-therapy. The fewer gastrointestinal side effects observed during chronic COX-2 therapy may partially be the result of the higher cell proliferation. This effect is not mediated by the EGFR pathway. PPI co-therapy normalizes the disturbed cell kinetics irrespective of NSAID treatment used.

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“…10 Importantly, atrophic body gastritis as well as multifocal atrophic gastritis have been reported to be associated with an increased incidence of gastric cancer 1112 Studies in rats have suggested that hypergastrinaemia induced during omeprazole treatment causes persistent gastric epithelial cell proliferation 13. Furthermore, epithelial hyperproliferation has been reported in H pylori infected patients14 15; this can be reversed when the bacterium is eradicated 16-18…”

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confidence: 99%

Helicobacter pylori gastritis and epithelial cell proliferation in patients with reflux oesophagitis after treatment with lansoprazole

Hatlebakk

Maartmann-Moe

Berstad

et al. 1997

Gut

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Background-Helicobacter pylori gastritis may spread proximally in the stomach during profound acid inhibition. Aims-To examine histological gastric body changes and epithelial cell proliferation before and after treatment with lansoprazole. Patients and methods-Patients diagnosed as having reflux oesophagitis grade 1 or 2 were enrolled and treated for 12 weeks with lansoprazole (30 mg every morning). After 12 weeks, 103 of the 118 patients appeared endoscopically healed and were asymptomatic; they then received maintenance treatment with 15 or 30 mg lansoprazole daily. Biopsy specimens obtained from similar sites before and after treatment, were available from 90 patients after a median of 64 weeks (range 15-73 weeks). Epithelial cell proliferation was determined by the number of Ki-67 antigen positive cells per gland. Results-Of these 90 patients, 44 (49%) were found to be infected with H pylori. Their median inflammation score had increased from grade 1 before to grade 2 after treatment (p<0.0001). Initially, the number of Ki-67 antigen positive cells per gland was significantly higher in the H pylori infected than in the uninfected group and increased further after treatment (p<0.0001). In uninfected patients, no significant change in inflammation or proliferation occurred during treatment. Conclusions-A marked increase in body gastritis was observed in H pylori infected individuals during long term treatment with the proton pump inhibitor lansoprazole. Epithelial cell proliferation and atrophy also increased in infected but not in uninfected patients. (Gut 1997; 41: 740-747)

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Accelerated gastric epithelial proliferation.

Cited by 13 publications

References 28 publications

Immunohistochemical localization of vascular endothelial growth factor in the rat portal hypertensive gastropathy

Immunohistochemical localization of vascular endothelial growth factor in the rat portal hypertensive gastropathy

Proton Pump Inhibitor Co-Therapy Normalizes the Increased Cell Turnover of the Gastric Mucosa Both in Nsaid and Selective Cox-2 Users

Helicobacter pylori gastritis and epithelial cell proliferation in patients with reflux oesophagitis after treatment with lansoprazole

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