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IDA is commonly seen in IBD as a result of iron malabsorption and, ironically, chronic blood loss through disrupted mucosal surfaces.
This European review of the current state of the art for detecting and treating iron deficiency anemia (IDA) in the setting of inflammatory bowel disease (IBD) contains tremendous detail on workup and treatment that can’t be reasonably recounted here. I’ll summarize briefly and suggest reviewing the original material in the Journal of Crohn’s and Colitis when it’s available in July (it’s available online now for subscribers). But this article offers a larger message for those of us interested in holistic care of chronically ill patients.
It’s written by and for gastroenterologists, who exult in the delights of complex diagnosis within their specialty, but may find the details of general medicine and office hematology less exciting. The authors are clear on this, noting that IDA in IBD patients (whose care is almost always led by a gastroenterologist) is under-diagnosed and under-treated, and putting the responsibility squarely on the “gastroenterology community.”
The patient being well treated for IBD but struggling with symptomatic IDA is a perfect argument for superlative primary care. Although the authors don’t suggest this directly, it’s clear that primary care physicians could act as an extra safety net for patients in this situation. Their offices may be better equipped to handle intravenous treatment and the ongoing follow-up needed to detect and prevent recurrence of IDA in the setting of IBD. In a procedure-oriented gastroenterology office, these are exactly the kinds of activities that may fall through the cracks because those practices’ revenue streams depend on rapid and frequent performance of fiberoptic endoscopic procedures.
IDA is commonly seen in IBD because these patients often malabsorb iron, and chronically lose blood through disrupted mucosal surfaces. The most severe cases are seen in those with poorly treated or newly diagnosed IBD, for obvious reasons. The differential diagnosis includes anemia of chronic disease (ACD), but in anemic IBD patients, IDA is the culprit 90% of the time. Often, ACD is superimposed on a chronic iron deficiency, so careful workup is essential to tease out the relative contributions of both processes. Vitamin B12 deficiency (because of malabsorption) and folate deficiency (because methotrexate and sulfasalazine interfere with the absorption of folate) must be considered as possible contributors to a confusing picture in the anemia workup. Finally, sulfasalazine may induce hemolysis or bone marrow aplasia, and thiopurines and methotrexate can induce bone marrow toxicity in a minority of patients.
When iron deficiency with mild to moderate anemia is diagnosed, the authors recommend a course of oral iron (mostly available as inorganic ferrous salts and sometimes combined with vitamin C for improved absorption). But drawbacks abound: at typical tolerated doses of 50 to 200 mg/d, it may take several weeks before hemoglobin concentrations begin to increase, 2 months for them to normalize, and at least 6 months before iron stores are replenished. Oral iron has notoriously low bioavailability, and IBD lowers it further. There are even concerns that oral iron may increase IBD’s inflammatory process, but definitive data are lacking. And finally, oral iron therapy is often limited by poor GI tolerance by patients. When oral iron fails, IBD patients should be offered intravenous iron preparations. For severe anemia (Hgb <10 g/dL; ferritin <100 ng/mL; transferrin saturation < 20%), the authors recommend intravenous therapy as first-line treatment.
Three newer preparations have improved safety and simplified the administration of intravenous iron. Ferumoxytol, ferric carboxymaltose, and iron isomaltoside 1000 offer two important advantages: (1) a test dose is no longer required because immune-mediated reactions do not occur, and (2) higher doses of iron can be delivered in a single dose. Multiple studies have shown that intravenous iron is more effective and better tolerated that oral iron.
Primary care may be an ideal setting here, because continuous ongoing long-term follow-up care is needed. Hemoglobin and iron parameters must be repeated every 12 weeks after successful treatment because anemia frequently recurs-in short, these people need lots of careful follow-up and laboratory work. Chronically ill persons tend to use the primary care office as the hub for all their health care needs. If gastroenterologists’ offices aren’t optimal for this process, perhaps it’s time for primary care offices to step up and coordinate anemia detection, treatment, and prevention for IBD patients-a cohort that can do well when they receive superlative long-term care.
Reinisch W, Staun M, Bhandari S, Muoz M. State of the iron: how to diagnose and efficiently treat iron deficiency anemia in inflammatory bowel disease. J Crohns Colitis. 2013;7:429-440.