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Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

Background : Although large hiatal hernia may cause bleeding from Cameron erosions, its role in iron deficiency anaemia has been debated, and no data are available on the treatment of these patients with proton pump inhibitors.

Aims : To determine the prevalence of large hiatal hernia in out-patients with iron deficiency anaemia and the role of proton pump inhibitors in the prevention of recurrence of anaemia.

Methods : Two hundred and twenty-eight out-patients underwent upper/lower endoscopy. Those with large hiatal hernia were given an oesophagogram, discontinued iron supplementation and received proton pump inhibitor treatment with (group 1) or without (group 2) surgery. Anaemia was re-assessed during 1 year of follow-up.

Results : Large hiatal hernia was the likely cause of anaemia in 21 patients (9.2%). The median haemoglobin and ferritin values at the diagnosis of anaemia were 7.9 g/dL and 6 µg/L, respectively. Cameron erosions were found in 33% of patients. Ten and eleven patients were included in groups 1 and 2, respectively. Haemoglobin values were 13.8 g/dL and 13.4 g/dL at 3 months of follow-up, and 13.4 g/dL and 13.8 g/dL at 1 year of follow-up, in groups 1 and 2, respectively.

Conclusions : Large hiatal hernia may cause iron deficiency anaemia, even without Cameron erosions. Surgery in combination with proton pump inhibitor therapy is no better than proton pump inhibitor therapy alone in preventing the recurrence of anaemia.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

Large hiatal hernia is a known cause of iron deficiency anaemia, owing to the presence of erosions at the waist of the hernia (Cameron erosions), which can produce chronic blood loss.1, 2 Although the association between large hiatal hernia, Cameron lesions and iron deficiency anaemia has long been recognized,2 the pathophysiological mechanism causing the erosions is unclear, and it is probable that both mechanical trauma and gastro-oesophageal acid reflux are involved.3 It is therefore feasible to hypothesize that an optimal therapeutic approach to this blood-loss anaemia would include surgical repair of the hernia and inhibition of gastric acid secretion. Moskovitz et al. were the first to demonstrate that short-term inhibition of gastric acid secretion, using an H2-antagonist, and long-term iron supplementation were effective in promoting the healing of Cameron erosions and in correcting anaemia which, however, could relapse when iron was withdrawn.3 However, the therapeutic approach of the inhibition of gastric acid secretion in patients with both large hiatal hernia and iron deficiency anaemia has not been investigated further, not even after the introduction of proton pump inhibitors, which are currently considered to be the optimal antisecretory therapy in acid-related disorders.4

The reported prevalence of large hiatal hernia in patients with iron deficiency anaemia is 6–7%,3, 5 and a recent epidemiological study investigating hospitalized patients with oesophagitis and/or hiatal hernia confirmed a close correlation between iron deficiency anaemia and hiatal hernia.6 The American Gastroenterological Association position statement included large hiatal hernia with Cameron erosions as a possible cause of obscure bleeding, i.e. in the case of recurrent or persistent iron deficiency anaemia after an initial negative endoscopy (upper and/or lower).7 However, few studies have focused on the role of large hiatal hernia as the source of bleeding.3, 6 Furthermore, large hiatal hernia was not listed amongst the causes of this condition in the British Society of Gastroenterology guidelines8 or in the majority of studies performed to investigate the possible causes of iron deficiency anaemia.9–12 Thus, the true impact of large hiatal hernia in causing iron deficiency anaemia remains controversial, and its prevalence in out-patients with iron deficiency anaemia has rarely been investigated.

The aims of this study were to determine, in a consecutive series of out-patients with iron deficiency anaemia, the prevalence of large hiatal hernia as a likely cause of anaemia, and to evaluate the efficacy of proton pump inhibitor therapy, alone or associated with surgical repair of the hernia, after withdrawal of iron supplementation, in the prevention of recurrence of iron deficiency anaemia during 1 year of follow-up.

Patients

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

From March 1999 to May 2002, of the 2580 consecutive out-patients referred to the University Haematology Department, those referred to the Out-patient Unit of the Digestive and Liver Disease Department with iron deficiency anaemia were considered as possible candidates for the study. The 2580 patients were derived from the general population, and were referred to the Haematology Department by their primary care physicians owing to the presence of iron deficiency anaemia. Iron deficiency anaemia was defined as follows: a haemoglobin concentration of 14 g/dL for males and 12 g/dL for females; a mean corpuscular volume of < 80 fL; and a ferritin level of < 30 µg/L.5 The following exclusion criteria were used: age < 21 years; history of alcoholism or drug addiction; use of non-steroidal anti-inflammatory drugs (NSAIDs) or anticoagulants, at least twice a week; previous diagnosis of gastrointestinal disease that may possibly have caused iron deficiency anaemia; pregnancy, heavy menstrual loss or menorrhagia/metrorrhagia for pre-menopausal women (metrorrhagia for post-menopausal women); haematological diseases other than iron deficiency anaemia; cancer or other chronic diseases; anorexia; vegetarian or iron-deficient diet. On the basis of these criteria, 274 patients (49 males, 225 females; median age, 50 years; range, 21–89 years) were enrolled in the study, which was approved by the local Ethics Committee. Full informed consent was obtained from all patients.

Part A.  Part A of the study aimed to investigate the cause of iron deficiency anaemia in the 274 enrolled patients, and thus to determine the prevalence of large hiatal hernia as a likely cause of iron deficiency anaemia in this series of patients. It comprised baseline evaluations, consisting of a clinical examination and an interview based on a detailed structured questionnaire to define private data, lifestyle, history of anaemia, previous medical history and/or surgery, obvious causes of blood loss and/or anaemia, and family history of gastrointestinal diseases and gastrointestinal tract symptoms. Gastrointestinal tract investigation was performed by gastroscopy and colonoscopy. The endoscopists were not aware of the patients' clinical history, and were asked to perform gastroscopy with biopsies taken from the antrum (n = 3), body (n = 3) and second portion of the duodenum (n = 2) (additional biopsies were taken from any suspicious lesions), as described elsewhere.5 The lower gastrointestinal tract was investigated by colonoscopy, or double-contrast barium enema if the patient refused colonoscopy or if the caecum had not been reached at previous colonoscopy. The indication for the diagnostic procedures was the presence of iron deficiency anaemia. In patients aged < 50 years (n = 140), as reported elsewhere,13 lower gastrointestinal tract investigation was deemed necessary only in the presence of positive faecal occult blood test, and this was the case in 22% of these patients. On the basis of clinical and blood count features, patients underwent, if necessary (or continued if it had already been prescribed by other physicians), supplementation therapy with iron and/or red blood cell transfusions. Patients presenting with a hiatal hernia of ≥ 4 cm at gastroscopy (defined as a large hiatal hernia)5 also underwent lower gastrointestinal tract investigation (if not previously performed) and double-contrast barium oesophagogram, which was performed by the evaluation of patients in the fasting condition using a standard double-contrast barium technique.

The following conditions, revealed during part A, were considered as exclusion criteria for entry into part B of the study: duodenal/gastric/colonic ulcer, gastric/colonic carcinoma, gastric/colonic adenomatous polyps, gastric/colonic vascular ectasia, erosive gastritis, coeliac disease, atrophic body gastritis or histologically proven inflammatory bowel disease. Patients with a large hiatal hernia and concomitant Helicobacter pylori-positive chronic gastritis underwent standard eradication treatment and were included in part B only if iron deficiency anaemia persisted 3 months after successful H. pylori eradication. Patients were also excluded if they were considered to be unsuitable for a possible laparoscopic Nissen procedure due to a poor general condition.

Part B.  Patients entered part B of the study if a large hiatal hernia, confirmed by radiology, was considered to be the only cause of iron deficiency anaemia, and no other concomitant likely cause of iron deficiency anaemia was present (see part A). In order to exclude possible small bowel bleeding lesions, these patients also underwent small bowel follow through, with a negative result. These patients discontinued iron supplementation therapy as soon as haemoglobin values returned to normal limits, started therapy with a proton pump inhibitor at a standard dose (lansoprazole 30 mg/day per os), and were assigned by a simple randomization model (random number generator) to undergo laparoscopic reduction of the hernia plus Nissen fundoplication (group 1), or to continue medical treatment only with a proton pump inhibitor (group 2). Proton pump inhibitor was continued for the entire duration of the study.

All patients were operated on by the same surgeon. Blood count and plasma ferritin were assessed on entry into part B (baseline evaluation), and thereafter follow-up was performed at 3 and 12 months with clinical evaluation, haemoglobin and ferritin assessment. Group 1 patients also underwent barium oesophagogram and gastroscopy at 1 and 6 months of follow-up, respectively.

Working definitions

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

During gastroscopy, the size of the hernia was assessed, after inspection of the oesophagus, stomach and proximal duodenum, with the stomach inflated by air, evaluating the distance between the oesophago-gastric junction and the diaphragm. The hernia was defined as a large hiatal hernia when this distance was ≥ 4 cm. Diagnoses of chronic gastritis, atrophic body gastritis and coeliac disease were obtained by histological examination, as described previously.14–16H. pylori chronic superficial gastritis was included amongst the possible causes of iron deficiency anaemia, owing to the increased intragastric pH and decreased intragastric ascorbic acid levels which occur in these patients.17 However, it was considered to be the likely cause of iron deficiency anaemia only after exclusion of other possible concomitant causes.18 Oesophagitis was classified as reported previously,19 and was considered as a possible cause of iron deficiency anaemia only if mucosal erosions were present (grade ≥ 2). The presence of Cameron lesions was defined if linear erosions were identified on the crests of the mucosal folds, at or near the level of the diaphragm, during gastroscopy.2

Statistical analysis

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

Statistical analysis was performed by MedCalc (MedCalc Software, Mariakerke, Belgium), and the unpaired Wilcoxon test was used to compare variables in the subgroups of patients. A P value of < 0.05 was considered to be statistically significant.

Prevalence of large hiatal hernia (part A)

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

Of the 274 patients enrolled in part A, 10 refused to enter the study and 36 were lost during follow-up. Thus, 228 patients were evaluated. The most frequent causes of iron deficiency anaemia were H. pylori chronic gastritis (18.9%) and atrophic body gastritis (16.7%). In 44 patients (19.3%), no gastrointestinal finding, as a probable cause of iron deficiency anaemia, was detected (Table 1). Twenty-one of the 228 patients (9.2%) (including 19 females; median age, 67 years; range, 44–88 years) had a diagnosis of large hiatal hernia as the likely cause of iron deficiency anaemia and entered part B of the study. In these patients, the median duration of iron deficiency anaemia, before the diagnosis of large hiatal hernia, was 36 months (range, 10–120 months). At the time of diagnosis of iron deficiency anaemia, the median haemoglobin value was 7.9 g/dL (range, 4.7–11.5 g/dL) and the median ferritin value was 6 µg/L (range, 1–29 µg/L).

Table 1.  Probable causes of iron deficiency anaemia in the 228 patients evaluated
FindingsNo. patients (%)
  • Considered as probable cause of iron deficiency anaemia only if no other diseases were found.

Helicobacter pylori chronic gastritis*43 (18.9)
Atrophic body gastritis38 (16.7)
Coeliac disease21 (9.2)
Large hiatal hernia21 (9.2)
Colon cancer12 (5.3)
Duodenal ulcer9 (3.9)
Previous gastric surgery8 (3.5)
Gastric cancer4 (1.7)
Other bleeding gastrointestinal findings28 (12.3)
Normal endoscopic/histological findings44 (19.3)

During baseline evaluation, all 21 patients had complained of fatigue and/or dyspnoea, whereas no patient had complained of dysphagia, heartburn or acid regurgitation. However, during follow-up visits, performed after the diagnosis of large hiatal hernia, 57% (n = 12) of patients (eight treated with a proton pump inhibitor only, and four with a proton pump inhibitor plus surgery) reported being aware of dysphagia and/or pyrosis long before entering the study. Six patients had reported taking NSAIDs during the 3 months prior to enrolment in the study (less than twice per week).

Faecal occult blood test data were available in 13 patients, being positive in three (23%). Cameron erosions were detected by gastroscopy in seven patients (33%). The median size of the hernia, measured during gastroscopy, was 6 cm (range, 4–10 cm); however, the median size was 10 cm (range, 6–15 cm) on evaluation by barium oesophagogram images (P < 0.01) (a case is shown in Figure 2). Concomitant findings were H. pylori gastritis in 13 patients (61.9%), reflux oesophagitis in eight (38%) and colonic diverticular disease in six (28.6%). However, these were not considered to be the causes of iron deficiency anaemia in the 21 patients with large hiatal hernia because: (i) in patients with concomitant H. pylori infection, iron deficiency anaemia was still present despite successful eradication; (ii) in patients with oesophagitis, the severity was grade 0–1 (absence of mucosal erosions).19

image

Figure 2. A case of large hiatal hernia.

Download figure to PowerPoint

Treatment of large hiatal hernia (part B)

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

Ten patients were randomized to group 1 (treated with proton pump inhibitor and surgery) and 11 to group 2 (treated with proton pump inhibitor only) (Table 2). The size of the hernia was similar in the two groups of patients, being 11 cm and 10 cm in groups 1 and 2, respectively (measurement by barium oesophagogram). The median haemoglobin value on entry into part B of the study (baseline evaluation) was 12.8 g/dL in both groups of patients. Iron treatment was withdrawn in all patients during part B of the study.

Table 2.  Patients' general features (values are median [range])
 OverallGroup 1Group 2
  • IDA, iron deficiency anaemia.

  • At first diagnosis of IDA.

  • † 

    P = N.S. vs. group 2.

  • ‡ 

    P = 0.03 vs. group 2.

Male/female2/191/91/10
Age (years)67 [44–88]66[54–77]69 [44–88]
Body mass index (kg/m2)26.9 [23.8–35.2]28.7[24.8–35.2]25.8 [23.8–28.0]
Duration of IDA (months)36 [10–120]24[10–84]48 [13–120]
Haemoglobin* (g/dL)7.9 [4.7–11.5]8.3[4.7–10.9]7.9 [5.2–11.5]
Ferritin* (µg/L)6 [1–29]12[1–29]4.5 [1–27]

During the 1 year of follow-up, no significant decrease in haemoglobin or ferritin values was observed in either group of patients (Table 3). Indeed, the haemoglobin values were 13.8 g/dL and 13.4 g/dL at 3 months of follow-up (P = N.S.), and 13.4 g/dL and 13.8 g/dL at 1 year of follow-up (P = N.S.), in groups 1 and 2, respectively. The ferritin values were 14 µg/L and 7 µg/L at 3 months of follow-up (P = N.S.), and 27 µg/L and 18 µg/L at 1 year of follow-up (P = N.S.), in groups 1 and 2, respectively. Furthermore, although iron supplementation had been stopped, a progressive amelioration of anaemia was observed in most patients during follow-up. Indeed, at baseline evaluation, nine patients (four in group 1 and five in group 2) had mild to moderate anaemia, whereas, at 3 months of follow-up, eight patients had anaemia (four in each group). Of these, five (two in group 1 and three in group 2) still had mild anaemia, despite the increase in ferritin values, at 1 year of follow-up.

Table 3.  Effect of therapy on iron deficiency anaemia (values are median [range])
 Baseline3 months1 year
Haemoglobin (g/dL)Ferritin (µg/L)Haemoglobin (g/dL)Ferritin (µg/L)Haemoglobin (g/dL)Ferritin (µg/L)
Group 112.8 [9.5–15.2]18 [9–40]13.8 [10.7–15.2]14 [6–85]13.4 [10.5–15.7]27 [14–71]
Group 212.8 [8.7–15.0]16 [5–38]13.4 [11.2–15.5]7 [6–21]13.8 [11.2–15.5]18 [8–27]

Barium oesophagogram, performed at 1 month of follow-up in patients who had undergone surgery, showed no recurrence of hiatal hernia (in one patient, slow transit of barium through the gastro-oesophageal junction, with no evidence of stopping, was demonstrated). Patients in whom Cameron erosions were detected at baseline evaluation (five patients in group 1 and two patients in group 2) underwent gastroscopy at 6 months of follow-up, but no Cameron lesions were detected.

Discussion

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

This study investigated prospectively, in a large series of consecutive out-patients, the role of large hiatal hernia as a cause of iron deficiency anaemia, and the efficacy of proton pump inhibitor, alone or associated with surgical reduction of the hernia, in preventing the recurrence of iron deficiency anaemia after withdrawal of iron supplementation. The first important finding emerging from this study is that large hiatal hernia has a relatively high prevalence in patients not presenting obvious causes of iron deficiency anaemia; it was the probable cause of iron deficiency anaemia in 9.2% of patients.

This prevalence is higher than the value of 5.9% reported by Moskovitz et al.,3 and the difference is probably due to various factors, such as the different referral of patients. In the study by Moskovitz et al., the patients were selected from a clinical community-based gastroenterology practice; furthermore, different inclusion criteria were used, as all patients evaluated had large hiatal hernia with erosions. Other authors have also investigated the association between hiatal hernia and iron deficiency anaemia.1, 20, 21 However, they used the presence of hiatal hernia as an inclusion criterion, and then determined the prevalence of iron deficiency anaemia. In contrast, in this study, the aim was to assess the prevalence of large hiatal hernia in a homogeneous series of patients enrolled due to the presence of iron deficiency anaemia, who underwent upper and lower gastrointestinal tract evaluation in order to find possible sources of bleeding or non-bleeding disease. Furthermore, the patients included in our series were not referred to the gastroenterologist with gastrointestinal symptoms, evidence of blood loss or positive faecal occult blood test, but originated from a Haematology Department to which they had been referred by their primary care physicians due to the presence of iron deficiency anaemia. Thus, our findings confirm that an epidemiological association exists between large hiatal hernia and iron deficiency anaemia, and suggest that large hiatal hernia can be considered as an important and often neglected cause of iron deficiency anaemia.

We observed a higher prevalence of females amongst those with large hiatal hernia (19 females/two males), probably as a result of the higher prevalence of females in the population investigated in part A of the study. Indeed, females represented 82% (225/274) of all enrolled patients.

Cameron erosions were found in only 33% of patients with large hiatal hernia-related iron deficiency anaemia. This finding is surprising, as these lesions, which are considered to be the source of the slow chronic bleeding responsible for the development of iron deficiency anaemia, were lacking in 67% of patients. However, this prevalence of 33% probably underestimates the proportion of patients with large hiatal hernia-related iron deficiency anaemia who develop Cameron lesions during the course of the disease. Indeed, in this study, the lack of erosions in the majority of patients with large hiatal hernia-related iron deficiency anaemia could be attributed to various factors, such as the possibility that erosions may heal and recur, possible failure of gastroscopy to detect them, their misinterpretation as stomach lesions in the context of erosive gastritis rather than erosions at the waist of the hernia, and the lack of importance attached to these lesions in patients undergoing upper endoscopy due to the presence of iron deficiency anaemia, in whom the first aim of the endoscopist is to exclude the presence of malignancies or peptic ulcers. Finally, as pointed out previously by Morrisey concerning the poor awareness of endoscopists with regard to Cameron erosions: ‘you see what you look for’.22 However, one finding that corroborates the lack of erosions at endoscopy in many patients is the positive faecal occult blood test at baseline evaluation in only 23% of patients; this confirms, as suggested earlier,3 that bleeding from Cameron erosions is probably intermittent and small in volume. However, we were unable to better define the role of faecal occult blood testing in these patients, as it was not part of the study design and was thus not assessed prospectively.

One important finding was that the median size of the hernia was statistically larger following the evaluation of images obtained by barium oesophagogram relative to endoscopic measurement (10 cm vs. 6 cm, P < 0.01). This difference in the size of the hernia is probably a result of the difficulties encountered by endoscopists when measuring the width of a hernia, such as the physiological displacement of the squamocellular junction during swallowing, respiration or changes in posture, the need to use more than minimal air insufflation, the frequent belches occurring during gastroscopy in these patients, and the sliding feature of the hernia.23 Radiologists, on the other hand, can make use of changes in the patient's position and increased amounts of barium to better characterize and visualize the hernia. Thus, we suggest that barium oesophagogram should be included in the evaluation of patients with large hiatal hernia diagnosed by gastroscopy, otherwise endoscopic evaluation alone could lead to an underestimation of the size of the hernia and to the missing of a possible cause of iron deficiency anaemia.

With regard to treatment, both proton pump inhibitor alone and proton pump inhibitor in combination with surgical repair of the hernia plus Nissen fundoplication were effective during the 1-year follow-up period in preventing the recurrence of iron deficiency anaemia. Indeed, the haemoglobin and ferritin values did not decrease during follow-up, despite the lack of iron supplementation, which had been discontinued before patients entered part B of the study. That similar findings were observed, irrespective of the type of treatment, emphasizes the role of gastric acid in the pathogenesis of erosions, and confirms that long-term gastric acid inhibition is necessary in these patients, as it contributes to the resolution of iron deficiency anaemia. Furthermore, the mortality and morbidity associated with surgery, although low, should be considered during the evaluation of patients with large hiatal hernia-related iron deficiency anaemia, in whom treatment with proton pump inhibitor alone should be proposed as an initial therapeutic approach. Surgery can be considered as an option in patients with non-healing Cameron ulcers who are persistently iron deficient and have bleeding after the failure of medical treatment. Proton pump inhibitors are safe drugs.24 In the past, it has been considered possible that an increased intragastric pH due to antisecretory therapy could impair iron adsorption and cause anaemia.25 However, this hypothesis has not been confirmed by more recent observations in patients with Zollinger–Ellison syndrome, who underwent long-term treatment with proton pump inhibitors.26 Moreover, proton pump inhibitor treatment leads to the relief of reflux symptoms related to the presence of a large hiatal hernia. Although patients did not complain of pyrosis, regurgitation or dysphagia during baseline evaluation, probably due to poor awareness of these symptoms, during follow-up visits, 57% of patients reported that dysphagia, regurgitation and pyrosis had been present for a long time before entering the study. The discrepancy between baseline and follow-up evaluation is probably due to both an increased patient awareness of these symptoms as a result of taking part in the study, and the benefits of treatment on gastro-oesophageal reflux symptoms.

One limitation of this study concerns the small number of patients included in part B; this is probably related to the features of the patients evaluated, who were all from the Haematology Department, and had not been referred to the Gastrointestinal Department with gastrointestinal symptoms or evident bleeding. A further limitation is that a complete gastrointestinal tract investigation, including lower gastrointestinal tract, was not performed in all patients, and thus some lesions could, potentially, have been missed. However, in our opinion, from the criteria used in the study design, this risk can be considered to be negligible, particularly with regard to malignancies. An additional limit of this study is the lack of a control arm of patients who received neither surgery nor proton pump inhibitor therapy.

In conclusion, the results of this study suggest that large hiatal hernia should always be taken into consideration as a possible cause of iron deficiency anaemia. In these patients, Cameron erosions should always be sought during initial gastroscopy. Long-term inhibition of gastric acid secretion by a proton pump inhibitor is an effective tool in preventing the recurrence of iron deficiency anaemia, and is feasible as a single therapeutic approach, particularly in patients who, due to a poor general condition or advanced age, are not amenable to surgical reduction of the hernia. However, further multi-centre randomized trials, evaluating larger series of patients, are necessary in order to better determine the optimal therapeutic approach in patients with large hiatal hernia-related iron deficiency anaemia.

Acknowledgements

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References

The authors thank Mrs M. Shields for help with the English.

This work was supported by grant 02/12/01/10 1999–2002 from the Italian Ministry for the University (MIUR).

References

  1. Top of page
  2. Summary
  3. Introduction
  4. Patients and methods
  5. Patients
  6. Study design
  7. Working definitions
  8. Statistical analysis
  9. Results
  10. Prevalence of large hiatal hernia (part A)
  11. Treatment of large hiatal hernia (part B)
  12. Discussion
  13. Acknowledgements
  14. References
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    Annibale B, Aprile MR, D'Ambra G, et al. Cure of Helicobacter pylori infection in atrophic body gastritis patients does not improve mucosal atrophy but reduces hypergastrinemia and its related effects on body ECL-cell hyperplasia. Aliment Pharmacol Ther 2000; 14: 62534.
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