Effects of anti–TNF-alpha therapy on hemoglobin levels and anemia in patients with inflammatory bowel disease. Issue 4 (April 2020)

• Record Type: Journal Article
• Authors: Lucendo, Alfredo J; Roncero, Óscar; Serrano-Duenas, María Teresa; Hervías, Daniel; Alcázar, Luis Miguel; Miriam-Ruiz-Ponce, ; Verdejo, Cristina; Laserna-Mendieta, Emilio; Lorente, Rufo; Arias, Ángel
• Is Part Of: Digestive and liver disease. Volume 52:Issue 4(2020)
• Page Start: 400
• Page End: 407
• Publication Date: 2020-04
• Subjects: Anemia -- Crohn's disease -- Inflammatory bowel disease -- Ulcerative colitis; Digestive organs -- Diseases -- Periodicals; Liver -- Diseases -- Periodicals; 616.33005
• DOI: 10.1016/j.dld.2019.11.019
• Languages: English
• ISSNs: 1590-8658

Abstract

Abstract: Background: Tumor necrosis factor-α (TNF-α) is involved in inducing inflammatory anemia. The potential effect of anti–TNF-α agents on anemia in inflammatory bowel diseases (IBD) is still unknown. Methods: Analytical data and disease characteristics from 362 IBD patients [271 CD/91UC) treated with anti-TNF-α drugs were retrospectively collected. Effects on disease activity, blood markers and prevalence of anemia were assessed after 6 and 12 months of therapy. Results: 29.3% patients presented anemia at baseline, and significantly reduced to 14.4% and 7.8% after 6 and 12 months of therapy, respectively. Mean ± SD Hb levels increased significantly at month 6, and this increase was sustained at 12 months. Serum markers of iron metabolism increased significantly compared to baseline, as disease activity measured by C-reactive protein (CRP) was reduced. All these effects were observed independently for CD and UC, and were independent of iron supplementation during treatment. Anemia at baseline (OR 4.09; 95%CI 1.98–8.45) and elevated CRP (OR 3.45; 95CI 1.29–9.22) were independently associated with risk of persistent anemia, as well as iron replacement during therapy (OR 4.36; 95%CI 2.07–9.16). Conclusions: Controlling disease activity with anti-TNF- α therapy significantly and independently associated with resolution of anemia in IBD, with no relevant role for iron replacement therapy.