Alimentary Pharmacology and Therapeutics Letters to the Editors 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.
Letter: the irony of oral iron – not an underdog for post-gastrointestinal bleeding anaemia; authors’ reply P. Bager & J. F. Dahlerup Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus C, Denmark. E-mail: [email protected] doi:10.1111/apt.12619
SIRS, We thank Molina-Infante and colleagues for their interest in our investigation and their awareness on the topic of anaemia and iron supplementation after acute upper gastrointestinal bleeding (AUGIB).1, 2 We fully agree that the main consequence of our findings must be that no patient should be discharged after AUGIB without iron supplementation whenever anaemia is present. Furthermore, blood samples should be taken as a follow-up to monitor the effect of the iron supplementation given. A suggestion could be after 1 and 3 months. A switch from oral iron to intravenous iron supplementation could be done, if the expected effect does not appear. As described in our paper, there are only limited data on how anaemic patients are monitored after discharge following AUGIB. We conducted a retrospective study on the prevalence of anaemia in AUGIB patients, the post-discharge iron treatment recommended, and the quality of follow-up.3 We found that 80% of patients were anaemic at discharge, only 16% of the anaemic patients were recommended iron supplementation, and the follow-up of patients was scattered and irregular.3
Letter: effects of gastric microenvironment on the management of iron deficiency anaemia S. Kılıncalp*, F. Karaahmet*, Y. Ustun*, S. Coban* & I. Yuksel*,†
Aliment Pharmacol Ther 2014; 39: 547-553 ª 2014 John Wiley & Sons Ltd
2. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013; 368: 11–21.
Molina-Infante and colleagues also highlight that oral iron was found to be as effective as intravenous iron in treating anaemia and the use of proton pump inhibitors might have influenced these results.1 Several factors inhibit the enteral absorption of oral iron, such as proton pump inhibitors and inflammation in general.4, 5 We are currently analysing the patients’ levels of different markers such as C-reactive protein, ferritin, soluble transferrin receptor and hepcidin. We hope to be able to present a simple model in AUGIB patients to predict response and nonresponse to oral iron supplementation.
ACKNOWLEDGEMENTS The authors’ declarations of personal and financial interests are unchanged from those in the original article.2 REFERENCES 1. Molina-Infante J, Calvet X, Gispert JP. Letter: the irony of oral iron – not an underdog for post-gastrointestinal bleeding anaemia. Aliment Pharmacol Ther 2014; 39: 550–1. 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. Bager P, Dahlerup JF. Lack of follow-up of anaemia after discharge from an upper gastrointestinal bleeding centre. Dan Med J 2013; 60: A4583. 4. Ajmera AV, Shastri GS, Gajera MJ, Judge TA. Suboptimal response to ferrous sulfate in iron-deficient patients taking omeprazole. Am J Ther 2012; 19: 185–9. 5. von Drygalski A, Adamson JW. Iron metabolism in man. J Parent Ent Nutr 2013; 37: 599–606.
*Department of Gastroenterology, Dıskapı Yıldırım Beyazıt Educational and Research Hospital, Ankara, Turkey. † Department of Gastroenterology, Yıldırım Beyazıt University School of Medicine, Ankara, Turkey. E-mail: [email protected] doi:10.1111/apt.12622
551
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
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
Letter: the irony of oral iron – not an underdog for post-gastrointestinal bleeding anaemia; authors’ reply P. Bager & J. F. Dahlerup Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus C, Denmark. E-mail: [email protected] doi:10.1111/apt.12619
SIRS, We thank Molina-Infante and colleagues for their interest in our investigation and their awareness on the topic of anaemia and iron supplementation after acute upper gastrointestinal bleeding (AUGIB).1, 2 We fully agree that the main consequence of our findings must be that no patient should be discharged after AUGIB without iron supplementation whenever anaemia is present. Furthermore, blood samples should be taken as a follow-up to monitor the effect of the iron supplementation given. A suggestion could be after 1 and 3 months. A switch from oral iron to intravenous iron supplementation could be done, if the expected effect does not appear. As described in our paper, there are only limited data on how anaemic patients are monitored after discharge following AUGIB. We conducted a retrospective study on the prevalence of anaemia in AUGIB patients, the post-discharge iron treatment recommended, and the quality of follow-up.3 We found that 80% of patients were anaemic at discharge, only 16% of the anaemic patients were recommended iron supplementation, and the follow-up of patients was scattered and irregular.3
Letter: effects of gastric microenvironment on the management of iron deficiency anaemia S. Kılıncalp*, F. Karaahmet*, Y. Ustun*, S. Coban* & I. Yuksel*,†
Aliment Pharmacol Ther 2014; 39: 547-553 ª 2014 John Wiley & Sons Ltd
2. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013; 368: 11–21.
Molina-Infante and colleagues also highlight that oral iron was found to be as effective as intravenous iron in treating anaemia and the use of proton pump inhibitors might have influenced these results.1 Several factors inhibit the enteral absorption of oral iron, such as proton pump inhibitors and inflammation in general.4, 5 We are currently analysing the patients’ levels of different markers such as C-reactive protein, ferritin, soluble transferrin receptor and hepcidin. We hope to be able to present a simple model in AUGIB patients to predict response and nonresponse to oral iron supplementation.
ACKNOWLEDGEMENTS The authors’ declarations of personal and financial interests are unchanged from those in the original article.2 REFERENCES 1. Molina-Infante J, Calvet X, Gispert JP. Letter: the irony of oral iron – not an underdog for post-gastrointestinal bleeding anaemia. Aliment Pharmacol Ther 2014; 39: 550–1. 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. Bager P, Dahlerup JF. Lack of follow-up of anaemia after discharge from an upper gastrointestinal bleeding centre. Dan Med J 2013; 60: A4583. 4. Ajmera AV, Shastri GS, Gajera MJ, Judge TA. Suboptimal response to ferrous sulfate in iron-deficient patients taking omeprazole. Am J Ther 2012; 19: 185–9. 5. von Drygalski A, Adamson JW. Iron metabolism in man. J Parent Ent Nutr 2013; 37: 599–606.
*Department of Gastroenterology, Dıskapı Yıldırım Beyazıt Educational and Research Hospital, Ankara, Turkey. † Department of Gastroenterology, Yıldırım Beyazıt University School of Medicine, Ankara, Turkey. E-mail: [email protected] doi:10.1111/apt.12622
551
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
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
