Persistent or recurrent anemia is associated with severe and disabling inflammatory bowel disease (IBD), researchers report in the October issue of Clinical Gastroenterology and Hepatology. Persistent or recurrent anemia could be used as a marker of severe disease and to identify patients who require aggressive management.
Anemia is a well-recognized but underestimated problem in patients with IBD that can significantly reduce their quality of life. IBD causes anemia via blood loss and iron malabsorption, as well as by disrupting iron distribution from the enterocytes to the circulation, due to high levels of hepcidin and inflammatory cytokines.
Ioannis E. Koutroubakis et al investigated the presence and duration of anemia, and its association with aggressive disease, in a longitudinal study of 410 patients with IBD (245 with Crohn’s disease and 165 with ulcerative colitis).
They found that 33%–37% of patients with IBD also had anemia during the study period (2009–2013), with no significant differences between patients with Crohn’s disease vs ulcerative colitis. Patients with IBD and anemia required significantly more health care and had higher indices of disease activity, as well as a lower average quality of life, than patients without anemia.
Anemia for 3 or more years correlated with hospitalization, visits to gastroenterology clinics, telephone calls to the doctor, surgeries, higher levels of C-reactive protein (in patients with ulcerative colitis), and higher erythrocyte sedimentation rates. There was a negative correlation between anemia and quality-of-life scores.
In contrast to other studies, Koutroubakis et al found only a small decrease in the prevalence of anemia among patients with IBD over time (37.1% in 2009 and 33.2% in 2013), despite IBD treatment and iron supplementation.
IBD treatment did not differ significantly between patients with anemia vs those without anemia, except for the more frequent use of thiopurines in patients without anemia than patients with anemia. This might be related to differences in the tolerability of these medications in patients with anemia.
Clinical and serologic markers are needed to stratify patients with IBD and determine their prognoses. Although red cell parameters have been used in diagnosis of anemia or assessment of disease activity, anemia is not used as a marker of severity or predicted course. The authors propose that the presence of persistent or recurrent is an important parameter in making therapeutic decisions for patients.
In an editorial, Gionata Fiorino et al state that anemia is untreated in as many as 50% of patients with IBD. This might be because the anemia is believed to be caused by inflammation, and that IBD treatment will normalize iron levels. However, iron deficiency might actually induce and maintain chronic inflammation, by P-selectin-mediated activation of platelets. Fiorino et al say that studies are needed to determine whether iron replacement could reduce inflammation, especially in patients with secondary thrombocytosis.
Patients with IBD should be checked carefully and routinely for anemia and iron deficiency. Koutroubakis et al state that intravenous iron replacement should be the first-line treatment, followed by erythropoiesis-stimulating agents in patients with persistent anemia. Fiorino et al provide an algorithm for management of iron-deficiency anemia in patients with IBD (see figure).
The Crohn’s and Colitis Foundation of America recently incorporated assessment and treatment of anemia in IBD as one of its quality improvement efforts.