Impact of <i>Helicobacter pylori</i> on the Development of Vitamin B<sub>12</sub> Deficiency in the Absence of Gastric Atrophy

Serin, Ender; Gümürdülü, Yüksel; Özer, Birol; Kayaselçuk, Fazi̇let; Yılmaz, Uğur; Koçak, Rikkat

doi:10.1046/j.1523-5378.2002.00106.x

Cited by 64 publications

(79 citation statements)

References 35 publications

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“…If H. pylori infection has any role in the development or severity of RAS by other mechanisms that we have not investigated in this study, then patients with genetic susceptibility to H. pylori and IL-6 polymorphisms should be evaluated for this infection. H. pylori gastritis, which has been reported by several studies (19,28,29). Low serum cobalamin level and H. Pylori gastritis have been reported to be strongly correlated via mechanisms suggested or reported by authors (18,19).…”

Section: Discussionmentioning

confidence: 78%

“…H. pylori gastritis, which has been reported by several studies (19,28,29). Low serum cobalamin level and H. Pylori gastritis have been reported to be strongly correlated via mechanisms suggested or reported by authors (18,19). In addition, several studies of nutritional deficiencies in patients with RAS have reported low levels of serum cobalamin (30,31).…”

Section: Discussionmentioning

confidence: 86%

“…RAS is improved by replacement therapies and patients with RAS have a higher rate of cobalamin deficiency, suggesting such a relationship. H. pylori has been proposed as a causative role for low levels of serum cobalamin (18,19). It is possible that H. pylori infection can trigger RAS in some patients through cobalamin deficiency.…”

Section: Introductionmentioning

confidence: 99%

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The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin

Yakar

Serin²,

Am³

et al. 2015

Turk J Gastroenterol

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Background/Aims: The aim of the present study was to investigate whether Helicobacter pylori causes or triggers recurrent aphthous stomatitis (RAS) through cytokine gene polymorphism and/or cobalamin deficiency. Materials and Methods: Thirty-six patients with RAS and 130 patients without RAS were genotyped for IL-1β (−511C/T) and IL-6 (−174G/C) and evaluated for H. pylori infection and serum cobalamin level. Results: The patient groups according to RAS had similar rates of H. pylori gastritis and interleukin genotypes/alleles, and there was a non-significant difference between serum cobalamin levels (p>0.05). RAS patients with H. pylori gastritis showed a higher frequency (51.9%) of GC IL-6 genotype than RAS patients without H. pylori gastritis (11.1%) (p=0.036). Non-GG genotype and C allele were increased in patients without RAS and with H. pylori gastritis (p<0.05). Patients with H. pylori gastritis showed a lower value of serum cobalamin without statistical significance, although this difference was more prominent in RAS patients (p=0.07). Conclusion: The carriage of the C allele of IL-6 may lead a susceptibility to chronic gastric inflammation after contamination with H. pylori. If H. pylori infection is justified as a predisposing factor for RAS and its severity by further studies, we can speculate that subjects with genetic susceptibility to this infection may benefit from H. pylori eradication treatment with respect to RAS.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 86%

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The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin

Yakar

Serin²,

Am³

et al. 2015

Turk J Gastroenterol

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“…For example, in patients with dyspepsia, a strong inverse association has been shown to exist between vitamin B 12 levels and H. pylori density, even in those with minimal or no gastric atrophy (Serin et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori infection does not influence the efficacy of iron and vitamin B12 fortification in marginally nourished Indian children

et al. 2010

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Background/Objectives: Helicobacter pylori infection and iron and vitamin B 12 deficiencies are widespread in economically disadvantaged populations. There is emerging evidence that H. pylori infection has a negative effect on the absorption of these micronutrients. The aim of this study was to evaluate the effect of H. pylori infection on the efficacy of micronutrient (including iron and vitamin B 12 )-fortified foods supplied for 1 year in marginally nourished children. Subjects/Methods: In all, 543 Indian children, aged 6-10 years, participated in a double-blind, randomized controlled intervention trial, receiving foods fortified with either high (100% Recommended Dietary Allowances (RDA)) or low (15% RDA) amounts of iron, vitamin B 12 and other micronutrients. The presence of H. pylori infection was diagnosed by the 13 C-labeled urea breath test at 11 months after the start of the intervention. Blood hemoglobin, serum ferritin (SF), total body iron and plasma vitamin B 12 were estimated at baseline and 12 months, and differences between these time points were assessed using an independent t-test. Results: Overall, the prevalence of H. pylori infection in this group of children was 79%. Baseline hemoglobin, SF, body iron and vitamin B 12 concentrations were not associated with H. pylori infection. The response to the intervention (either high or low amounts of iron and vitamin B 12 fortification) in terms of change in iron markers and vitamin B 12 status did not differ between children with and without H. pylori infection. Conclusions: This study shows that the presence of H. pylori infection did not affect the efficacy of long-term iron and vitamin B 12 fortification in these marginally nourished children.

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“…Incidence and baseline of asymptomatically infected population A conclusion regarding the incidence and baseline of an asymptomatically infected population was calculated to be approximately 14.3% (15/105) as represented by the high titer (>15 NTU/mL serum) of anti-H. pylori IgA among normal control subjects aged 18 to 50 years from the Hebron area. In an earlier study by Serin et al (24), 25% of healthy children were PCR-positive for H. pylori (24). Since some of the children were only transiently infected while others may have progressed to become symptomatic (25), it is likely that the percentage of asymptomatic subjects will decrease (i.e.…”

Section: Identification Of Contaminating Variables That Influenced Comentioning

confidence: 98%

Correlation between serum levels of vitamin B12 and anti-Helicobacter pyloriIgA antibodies in vitamin B12 deficient Palestinian patients

Hilu¹,

Dudeen²,

Barghouthi³

2015

Turk J Med Sci

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IntroductionHelicobacter pylori infections induce vigorous systemic and mucosal humoral responses that are predominantly mediated by IgA, IgG, and IgM. These immunoglobulins are detectable in sera, gastric aspirates, or stomach extracts (1,2). Humoral immunity against H. pylori can effectively prevent infection and reduce colonization but does not lead to eradication of H. pylori-induced gastritis (2).Absorption of dietary cobalamin (vitamin B 12 ; vB 12 ) depends on several factors, including acid-dependent deproteinization of vB 12 . Only free vB12 can form a complex with the intrinsic factor (IF). The vB12-IF complex is then absorbed by mucosal cells via its specific receptor (cubilin) in a calcium-dependent fashion. Gastric parietal cells are responsible for production of both hydrochloric acid and IF. Absorbed vB12 is then stored in the liver. Some H. pylori patients develop autoantibodies directed against gastric parietal H + /K + -ATPase cells (APCAs), resulting in achlorhydria and increased infection with H. pylori, which in turn contributes to gastric damage and atrophy of the corpus (2).Autoimmunity may destroy parietal cells that are responsible for hydrochloric acid and IF production, resulting in achlorhydria and failure to deproteinize vB 12 and/or failure to produce IF. Consequently, the vB 12 -IF complex fails to form, leading to malabsorption of vB 12 and, potentially, to pernicious anemia. Hence, patients diagnosed with vB 12 deficiency as a result of APCAs or anti-IF antibodies were excluded, since their vB 12 deficiency cannot be directly and solely attributed to H. pylori infection (3-6; see Section 2.2).In this work, we investigated the correlation between serum anti-H. pylori IgA antibodies and vB 12 . The role of contaminating variables on this correlation was explored as well. Methods and materials PatientsBlood samples were collected in 5-mL tubes from 133 vB 12deficient patients (60 males, 73 females) and 105 healthy volunteers (42 males, 63 females), aged 18-50 years (mean, 34.1 years). All 133 patients had vB 12 deficiency and Background/aim: H. pylori infection and vitamin B 12 (vB 12 ) deficiency have high prevalence rates among Palestinians. It was observed that most people who suffered from vB 12 deficiency were positive for H. pylori. Materials and methods:The correlation between H. pylori infection and vB 12 deficiency was investigated in a representative segment of the Palestinian population. ELISA was used to determine levels of vitamin B 12 (vB 12 ) and anti-H. pylori IgA in sera from 238 participants from Al-Khalil district (Hebron), Palestine.Results: There was a strong negative Pearson's correlation coefficient (r = -0.45; P = 0.00001) between levels of anti-H. pylori IgA and vB 12 levels in sera drawn from 238 participants (133 patients and 105 control subjects). Two important contaminating variables were identified in this study: healthy control subjects with elevated anti-H. pylori IgA titers and vB 12 -deficient patients testing negative for anti-H. pylori IgA antibodi...

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Impact of Helicobacter pylori on the Development of Vitamin B₁₂ Deficiency in the Absence of Gastric Atrophy

Abstract: The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.

Cited by 64 publications

References 35 publications

The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin

The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin

Helicobacter pylori infection does not influence the efficacy of iron and vitamin B12 fortification in marginally nourished Indian children

Correlation between serum levels of vitamin B12 and anti-Helicobacter pyloriIgA antibodies in vitamin B12 deficient Palestinian patients

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Impact of Helicobacter pylori on the Development of Vitamin B12 Deficiency in the Absence of Gastric Atrophy

Abstract: The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.

Cited by 64 publications

References 35 publications

The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin

The relationship of recurrent aphthous stomatitis and Helicobacter pylori, cytokine gene polymorphism and cobalamin

Helicobacter pylori infection does not influence the efficacy of iron and vitamin B12 fortification in marginally nourished Indian children

Correlation between serum levels of vitamin B12 and anti-Helicobacter pyloriIgA antibodies in vitamin B12 deficient Palestinian patients

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Impact of Helicobacter pylori on the Development of Vitamin B₁₂ Deficiency in the Absence of Gastric Atrophy