Duodenal gastric metaplasia and <i>Helicobacter pylori</i> infection in high and low duodenal ulcer‐prevalent areas in India

Tovey, F I; Hobsley, M; Kaushik, Soma; Pandey, Rakesh; Kurian, George; Singh, Kartar; Sood, Ajit; Jehangir, Ernest

doi:10.1111/j.1440-1746.2003.03320.x

Cited by 19 publications

(13 citation statements)

References 36 publications

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“…This might be due to the greater prevalence of duodenal ulcer in Odisha. 16 Variceal bleeding due to portal hypertension accounted for only a minority of cases (12.83%). This is in stark contrast to the reported spectra from Northern and Western India that create the impression that variceal bleeding is the most common cause of UGIB in India.…”

Section: Discussionmentioning

confidence: 99%

Spectrum of Upper Gastrointestinal Hemorrhage in Coastal Odisha

Singh

Panigrahi²

2013

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Section: Discussionmentioning

confidence: 99%

Spectrum of Upper Gastrointestinal Hemorrhage in Coastal Odisha

Singh

Panigrahi²

2013

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“…Researchers have reported the role of H. pylori infection in the pathogenesis of peptic ulcer and stomach cancer in India, and some have reported no association between stomach cancer and H. pylori infection. [7–12] These studies are criticized to have methodological pitfalls such as small sample size and inadequate description of sample size calculations, and case definitions. [1314] Several factors have been associated with the aggressiveness of H. pylori and hence implicated in epithelial damage, including the virulent East Asian CagA genotype, and environmental and dietary factors.…”

Section: Introductionmentioning

confidence: 99%

Assessment of risk factors of helicobacter pylori infection and peptic ulcer disease

Mhaskar

Izurieta

Azizan

et al. 2013

J Global Infect Dis

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Background:Helicobacter pylori (H. pylori) infection is a risk factor for peptic ulcer. There have been no studies addressing environmental and dietary risk factors in western India. We conducted a case control study enrolling peptic ulcer patients in Pune, India.Materials and Methods:Risk factors for peptic ulcer and H. pylori infection were assessed in a participant interview. H. pylori status was assessed from stool by monoclonal antigen detection.Results:We enrolled 190 peptic ulcer, 35 stomach cancer patients, and 125 controls. Fifty-one percent (180/350) of the participants were infected with H. pylori. Lower socioeconomic status (SES) [odds ratio (OR): 1.10, 95% confidence interval (CI): 1.02–1.39], meat consumption (OR: 2.35, 95% CI: 1.30–4.23), smoking (OR: 2.23, 95% CI: 1.24–4.02), eating restaurant food (OR: 3.77, 95% CI: 1.39–10.23), and drinking nonfiltered or nonboiled water (OR: 1.05, 95% CI: 1.01–1.23) were risk factors for H. pylori infection. H. pylori infection (OR: 1.70, 95% CI: 1.03–2.89), meat (OR: 1.10, 95% CI: 1.02-1.75), fish (OR: 1.05, 95% CI: 1.02–1.89) consumption, and a family history of ulcer (OR: 1.20, 95% CI: 1.08–1.60) were risk factors for peptic ulcer. Consumption of chili peppers (OR: 0.20, 95% CI: 0.10–0.37) and parasite infestation (OR: 0.44, 95% CI: 0.24–0.80) were protective against H. pylori infection.Conclusion:H. pylori infection is associated with peptic ulcer. Lower SES, consumption of restaurant food, meat, nonfiltered water, and smoking are risk factors for H. pylori. Consumption of meat, fish, and a family history of peptic ulcer are risk factors for peptic ulcer. Consumption of chili peppers and concurrent parasite infestation appear to be protective against H. pylori.

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“…More and more observations are consistent with the hypothesis that H pylori have both pathogenetic and symbiotic features, thus relatively balance their cost and benefit [23,24] . Changes in life style and sanitation conditions cause a probable disturbance of gastric microecology, which plays a more important role in the pathogenetic mechanism of H pylori in the modern era [25,26] . Therefore, eradiation of H pylori does not seem justified for all individuals, especially children.…”

Section: Viable Lbg or Lbg-s Inhibited H Pyloriss1-lps-induced Il-8 Pmentioning

confidence: 99%

Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4

Zhou¹,

Ma²,

Deng³

et al. 2008

WJG

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METHODS: S G C-7901 c el ls were t reat ed wi t h H pylori SS1-LPS in the presence or absence of pretreatment for 1 h with viable LBG or supernatant recovered from LBG culture MRS broth (LBG-S ). Cellular lysates were prepared for Western blot with anti-TLR4, anti-transforming growth factor β-activated kinase 1 (TAK1), anti-phospho-TAK1, anti-nuclear factor κB (NF-κB), anti-p38 mitogen-activated protein kinase (p38MAPK), and anti-phospho-p38MAPK antibodies. The amount of IL-8 in cell culture medium was measured by ELISA. R E S U LT S : H p y l o r i S S 1 -L P S u p -r e g u l a t e d t h eexpression of TLR4, stimulated the phosphorylation of TAK1, subsequently enhanced the activation of NF-κB and the phosphorylation of p38MAPK in a timedependent manner, leading to augmentation of IL-8 production in SGC-7901 cells. Viable LBG or LBG-S pretreatment attenuated the expression of TLR4, inhibited the phosphorylation of TAK1 and p38MAPK, prevented the activation of NF-κB, and consequently blocked IL-8 production.

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Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer‐prevalent areas in India

Abstract: The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.

Cited by 19 publications

References 36 publications

Spectrum of Upper Gastrointestinal Hemorrhage in Coastal Odisha

Spectrum of Upper Gastrointestinal Hemorrhage in Coastal Odisha

Assessment of risk factors of helicobacter pylori infection and peptic ulcer disease

Lactobacilli inhibit interleukin-8 production induced by Helicobacter pylori lipopolysaccharide-activated Toll-like receptor 4

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