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* = Presenting author

P450 Poor recognition and management of iron deficiency anaemia in inflammatory bowel disease: a missed opportunity

S. Subramaniam*1, K. Besherdas2

1University College London Hospitals NHS Foundation Trust, Department of Gastroenterology, London, United Kingdom, 2Barnet & Chase Farm Hospitals, Royal Free London NHS Foundation Trust, Department of Gastroenterology, London, United Kingdom

Background

Iron deficiency anaemia (IDA) is a common complication of inflammatory bowel disease (IBD) that has an impact on the patient's quality of life. IDA is caused by inadequate dietary intake, malabsorption of iron and iron loss through intestinal bleeding. Current guidelines recommend that all patients with IBD should be assessed for IDA and that iron supplementation be given as indicated. The aim of this study was to ascertain the prevalence of IDA in our IBD cohort, to look at whether iron replacement therapy (and in what form) was given and to assess treatment response.

Methods

A single centre, retrospective analysis of IBD patients from a large district general NHS trust in North London was performed. The local IBD database and electronic patient records (blood results and outpatient clinic letters) were used to collect data on patient demographics, diagnosis, screening parameters for IDA (Hb, Ferritin/transferrin saturation, CRP) and iron replacement therapy. The WHO definitions of anaemia were used (Hb<13g/dL in men and Hb<12g/dL in non pregnant women). Iron deficiency was diagnosed if ferritin <30 ug/L in quiescent IBD or <100ug/L in active IBD (CRP elevated) or transferrin saturation <16%.

Results

333 IBD patients were identified in the database. 3 patients were excluded because of insufficient data as their care was transferred. 293/330 (88.8%) were checked for IDA using the screening parameters. 146/293 (49.8%) of this group were found to be anaemic. 101/146 (69.2%) had evidence of iron deficiency. 61/101 (60.4%) were treated using oral and/or intravenous (IV) iron preparations or blood transfusions. Most patients (50/61) received oral iron while 10 patients had IV iron (4 had failed oral therapy) and 6 had a transfusion. The recurrence rate of IDA was 21/50 with oral iron, 4/10 with IV iron and 4/6 with transfusions. We also noted that there were 39/184 patients (21.2%) with iron deficiency in the absence of anaemia. Only 3 of these patients were treated for iron deficiency.

Conclusion

The prevalence of IDA in our IBD group was close to 50%. Current practice in our trust does not comply with guidelines as only 60.4% of IDA patients were treated. Iron replacement therapy was mostly administered in the oral form. Recurrence of IDA was similar (about 40%) with both oral and IV iron therapy. There is little guidance on management of iron deficiency in the absence of anaemia and supplementation was not widespread in this group. Barriers to appropriate recognition of IDA including lack of routine monitoring and knowledge on iron data interpretation will need to be addressed to improve practice.