ABSTRACT
Introduction: Anemia is a common extraintestinal manifestation in IBD patients and considerably impacts disease prognosis, hospitalization rates and time lost from work. While iron deficiency anemia is predominant, combinations of hematimetric and biochemical markers enable detection and targeted therapy of other etiologies including vitamin B12/folic acid deficiencies, hemolysis, myelosuppression and pharmacotherapies.
Areas covered: Current literature was searched for articles focusing on etiology, diagnostics and therapy of anemia in IBD. In the light of their own experience, the authors describe the physiology of anemia in IBD and present current evidence endorsing diagnostic and therapeutic options, focusing particularly on non-iron-related etiologies.
Expert commentary: Anemia in IBD is polyetiological, reaching far beyond iron deficiency anemia. While clinicians need to be aware of the increasing pallet of diagnostic tools and therapeutic options, detailed studies are needed to develop more convenient test procedures, long-term treatment and monitoring strategies, and unified guidelines for daily practice.
Acknowledgments
The authors thank Janet Collins (Interdisciplinary Crohn-Colitis Centre Rhein-Main, Frankfurt, Germany) for writing assistance, editing and proofreading the manuscript.
Declaration of interest
J. Stein has received consultancy fees from AbbVie, Fresenius-Kabi, Immundiagnostik, MSD, Pharmacosmos, Takeda, and Vifor. Dr. Stein has also received payment for lectures from Abbvie, Falk Foundation, Ferring, Immundiagnostik, MSD, Pharmacosmos, Takeda, Thermofischer and Vifor. Additionally, Dr. Stein has received payment for manuscript preparation from Abbvie, Falk Foundation and MSD. A. U. Dignass has received consultancy fees from Abbott, MSD, Ferring, UCB, Otsuka, Roche/Genentech, Takeda, Pharmacosmos, Holystone Biotech and Falk Foundation. Dr. Dignass has also received grants from Institut für Gemeinwohl and Stiftung Leben mit Krebs as well as payment for lectures including service on speakers’ bureaus from Falk Foundation, Ferring, MSD, Abbott, Otsuka, Vifor, Stiftung Leben mit Krebs, Kompetenznetz CED, Takeda and Pharmacosmos. Additionally, A. Dignass has received payment for manuscript preparation from Falk Foundation and payment for development of education presentations from Abbott, Pharmacosmos, Falk Foundation and Ferring. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.