Alimentary Pharmacology and Therapeutics Letters to the Editors SIRS, We read with great interest the paper by Bager et al. about the comparison of oral iron treatment vs. intravenous (IV) iron treatment in patients with upper gastrointestinal haemorrhage.1 They reported that iron stores are replenished more effectively with IV iron compared with oral iron. The authors did not find any significant difference in Helicobacter pylori infection rates between the treatment groups at baseline. However, they did not mention the H. pylori treatment response rate, which could possibly influence the efficiency of oral iron treatment. Iron-deficient patients who have H. pylori do not seem to respond well to oral iron therapy until the bacterium has been eradicated. The possible pathogenic mechanisms include occult blood loss secondary to chronic erosive gastritis and decreased iron absorption secondary to atrophy-associated gastric hypochlorhydria.2 Gastric acid secretion is an important factor in iron absorption. An increase in the degree of alkalinity facilitates the oxidation of ferrous (Fe2+) iron to the ferric form (Fe3+), which is not absorbed. Thus, gastric hypoacidity should prolong the time to effectively treat iron deficiency anaemia. This is an important point for patients with bleeding ulcers, who are also iron deficient and require oral replacement therapies. Incidence of gastric atrophy strongly increases with age and is very low in the absence of H. pylori.3 After H. pylori eradication, inflammation decreases by 1–
3 months, whereas atrophy does not improve generally in all patients and requires a longer period for improvement of gastric hypoacidity.4 Helicobacter pylori and gastric atrophy should influence the oral iron treatment efficiency and extend the time for iron store replenishment. Therefore, we suggest that H. pylori and gastric atrophy should be considered before deciding the treatment route in iron deficiency anaemia.
Letter: effects of gastric microenvironment on the management of iron deficiency anaemia – authors’ reply
data on the response rate to H. pylori treatment. The primary aim of our study was to evaluate the effect of iron treatment in anaemic patients after AUGIB in a randomised controlled design, regardless of H. pylori infection and proton pump inhibitor (PPI) treatment. We are fully aware that several micro-environmental factors might influence the absorption of oral iron. A systematic review found a 2.8-fold increase in the relative risk of iron deficiency anaemia among H. pylori-infected patients.3 The infection itself consumes iron and decreases the concentration of gastric juice ascorbic acid.4, 5 As mentioned by Kilincalp et al., the presence of a gastric acidic environment is important for oral iron absorption.1 On the basis of our data, we cannot recommend a specific route of iron supplementation in anaemic patients after AUGIB with H. pylori infection. However, if intravenous iron is chosen, potential reduced iron
P. Bager & J. F. Dahlerup Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus C, Denmark. E-mail: [email protected] doi:10.1111/apt.12627
SIRS, We thank Kilincalp and colleagues for their interest in our investigation on patients with anaemia following acute upper gastrointestinal bleeding (AUGIB) and for highlighting the topic of oral iron absorption.1, 2 In our study, we measured the prevalence of Helicobacter pylori infection and found no difference between the treatment groups. Unfortunately, we do not have
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ACKNOWLEDGEMENTS Declaration of personal and funding interests: None. REFERENCES 1. Bager P, Dahlerup JF. Randomised clinical trial: oral vs. intravenous iron after upper gastrointestinal haemorrhage a placebo-controlled study. Aliment Pharmacol Ther 2014; 39: 176–87. 2. Sugiyama T, Tsuchida M, Yokota K, et al. Improvement of longstanding iron-deficiency anemia in adults after eradication of Helicobacter pylori infection. Intern Med 2002; 41: 491–4. 3. Weck MN, Stegmaier C, Rothenbacher D, et al. Epidemiology of chronic atrophic gastritis: population-based study among 9444 older adults from Germany. Aliment Pharmacol Ther 2007; 26: 879–87. 4. Ohkusa T, Fujiki K, Takashimizu I, et al. Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated. Ann Intern Med 2001; 134: 380–6.
Aliment Pharmacol Ther 2014; 39: 547-553 ª 2014 John Wiley & Sons Ltd
Letters to the Editors absorption due to H. pylori infection will be avoided. Use of intravenous iron supplementation furthermore solves the risk of a changed intestinal iron absorption in patients treated with PPI.6 Intravenous iron is still much more expensive than oral iron. Therefore, it would be desirable if we were able to allocate the anaemic AUGIB patients to the most effective iron treatment. This calls for large well-designed studies with a focus on iron absorption in patients with AUGIB, stratifying for PPI treatment, H. pylori status and eradication of H. pylori infection.
ACKNOWLEDGEMENTS The authors’ declarations of personal and financial interests are unchanged from those in the original article.2
Aliment Pharmacol Ther 2014; 39: 547-553 ª 2014 John Wiley & Sons Ltd
REFERENCES 1. Kilincalp S, Karaahmet F, Ustun Y, et al. Letter: effects of gastric microenvironment on the management of iron deficiency anaemia. Aliment Pharmacol Ther 2014; 39: 551–2. 2. Bager P, Dahlerup JF. Randomised clinical trial: oral vs. intravenous iron after upper gastrointestinal haemorrhage – a placebo-controlled study. Aliment Pharmacol Ther 2014; 39: 176–87. 3. Muhsen K, Cohen D. Helicobacter pylori infection and iron stores: a systematic review and meta-analysis. Helicobacter 2008; 13: 323–40. 4. Banerjee S, Hawksby C, Miller S, et al. Effect of Helicobacter pylori and its eradication on gastric juice ascorbic acid. Gut 1994; 35: 317–22. 5. Wang Z, Zhang L, Guo Z, et al. A unique feature of iron loss via close adhesion of Helicobacter pylori to host erythrocytes. PLoS ONE 2012; 7: e50314. 6. Hutchinson C, Geissler CA, Powell JJ, Bomford A. Proton pump inhibitors suppress absorption of dietary non-haem iron in hereditary haemochromatosis. Gut 2007; 56: 1291–5.
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3 months, whereas atrophy does not improve generally in all patients and requires a longer period for improvement of gastric hypoacidity.4 Helicobacter pylori and gastric atrophy should influence the oral iron treatment efficiency and extend the time for iron store replenishment. Therefore, we suggest that H. pylori and gastric atrophy should be considered before deciding the treatment route in iron deficiency anaemia.
Letter: effects of gastric microenvironment on the management of iron deficiency anaemia – authors’ reply
data on the response rate to H. pylori treatment. The primary aim of our study was to evaluate the effect of iron treatment in anaemic patients after AUGIB in a randomised controlled design, regardless of H. pylori infection and proton pump inhibitor (PPI) treatment. We are fully aware that several micro-environmental factors might influence the absorption of oral iron. A systematic review found a 2.8-fold increase in the relative risk of iron deficiency anaemia among H. pylori-infected patients.3 The infection itself consumes iron and decreases the concentration of gastric juice ascorbic acid.4, 5 As mentioned by Kilincalp et al., the presence of a gastric acidic environment is important for oral iron absorption.1 On the basis of our data, we cannot recommend a specific route of iron supplementation in anaemic patients after AUGIB with H. pylori infection. However, if intravenous iron is chosen, potential reduced iron
P. Bager & J. F. Dahlerup Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus C, Denmark. E-mail: [email protected] doi:10.1111/apt.12627
SIRS, We thank Kilincalp and colleagues for their interest in our investigation on patients with anaemia following acute upper gastrointestinal bleeding (AUGIB) and for highlighting the topic of oral iron absorption.1, 2 In our study, we measured the prevalence of Helicobacter pylori infection and found no difference between the treatment groups. Unfortunately, we do not have
552
ACKNOWLEDGEMENTS Declaration of personal and funding interests: None. REFERENCES 1. Bager P, Dahlerup JF. Randomised clinical trial: oral vs. intravenous iron after upper gastrointestinal haemorrhage a placebo-controlled study. Aliment Pharmacol Ther 2014; 39: 176–87. 2. Sugiyama T, Tsuchida M, Yokota K, et al. Improvement of longstanding iron-deficiency anemia in adults after eradication of Helicobacter pylori infection. Intern Med 2002; 41: 491–4. 3. Weck MN, Stegmaier C, Rothenbacher D, et al. Epidemiology of chronic atrophic gastritis: population-based study among 9444 older adults from Germany. Aliment Pharmacol Ther 2007; 26: 879–87. 4. Ohkusa T, Fujiki K, Takashimizu I, et al. Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated. Ann Intern Med 2001; 134: 380–6.
Aliment Pharmacol Ther 2014; 39: 547-553 ª 2014 John Wiley & Sons Ltd
Letters to the Editors absorption due to H. pylori infection will be avoided. Use of intravenous iron supplementation furthermore solves the risk of a changed intestinal iron absorption in patients treated with PPI.6 Intravenous iron is still much more expensive than oral iron. Therefore, it would be desirable if we were able to allocate the anaemic AUGIB patients to the most effective iron treatment. This calls for large well-designed studies with a focus on iron absorption in patients with AUGIB, stratifying for PPI treatment, H. pylori status and eradication of H. pylori infection.
ACKNOWLEDGEMENTS The authors’ declarations of personal and financial interests are unchanged from those in the original article.2
Aliment Pharmacol Ther 2014; 39: 547-553 ª 2014 John Wiley & Sons Ltd
REFERENCES 1. Kilincalp S, Karaahmet F, Ustun Y, et al. Letter: effects of gastric microenvironment on the management of iron deficiency anaemia. Aliment Pharmacol Ther 2014; 39: 551–2. 2. Bager P, Dahlerup JF. Randomised clinical trial: oral vs. intravenous iron after upper gastrointestinal haemorrhage – a placebo-controlled study. Aliment Pharmacol Ther 2014; 39: 176–87. 3. Muhsen K, Cohen D. Helicobacter pylori infection and iron stores: a systematic review and meta-analysis. Helicobacter 2008; 13: 323–40. 4. Banerjee S, Hawksby C, Miller S, et al. Effect of Helicobacter pylori and its eradication on gastric juice ascorbic acid. Gut 1994; 35: 317–22. 5. Wang Z, Zhang L, Guo Z, et al. A unique feature of iron loss via close adhesion of Helicobacter pylori to host erythrocytes. PLoS ONE 2012; 7: e50314. 6. Hutchinson C, Geissler CA, Powell JJ, Bomford A. Proton pump inhibitors suppress absorption of dietary non-haem iron in hereditary haemochromatosis. Gut 2007; 56: 1291–5.
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