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et al. about the comparison of oral iron treatment vs. intravenous (IV) iron treatment in patients with upper gastrointestinal haemorrhage. 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. Gastric acid secretion is an important factor in iron absorption. An increase in the degree of alkalinity facilitates the oxidation of ferrous (Fe) iron to the ferric form (Fe), 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. 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. 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.

We agree that all effects of a certain intervention need to be evaluated from a broad perspective. The effect of iron supplementation after a non-variceal acute upper gastrointestinal haemorrhage (AUGIB) is no exception. As mentioned in our paper, the topic of anaemia treatment after AUGIB was unenlightened at the time we performed our study. The primary outcome measurement when investigating anaemia and the effect of iron supplementations were naturally haemoglobin levels and markers for iron stores respectively. The results for these parameters, as well as adherence to oral iron therapy and considerations on the health economic aspects, are described in our paper. 2 Bounford and Ford ask for further data on the clinical impact on anaemia after AUGIB. We did measure patient-reported outcomes both during the study period (13 weeks) and in a 3-month follow-up period after the end of treatment. We used the EuroQol 5-item questionnaire and the Multidimensional Fatigue Inventory questionnaire to measure health-related quality of life and fatigue respectively. The results have been stratified for the presence or absence of anaemia at week 13, and we have compared the groups with each other and with a general population. The results are almost ready and a manuscript will be submitted to an international journal.