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P316. Stored body iron serum markers are modulated by anti-TNF therapy in inflammatory bowel disease patients

L. Pastorelli1,2, C. Testa2, R. Rigolini3, P. Giubbilini3, L. Spina2, G.E. Tontini2, N. Munizio2, C. De Salvo2,4, B. Rampoldi3, E. Costa3, M. Vecchi1,2

1University of Milan, Milan, Italy; 2Gastroenterology and Gastrointestinal Endoscopy Unit, IRCCS Policlinico San Donato, San Donato Milanese, Italy; 3Laboratory Medicine Service, IRCCS Policlinico San Donato, San Donato Milanese, Italy; 4Department of Pathology, Case Western Reserve University, Cleveland, OH, United States

Aim of the study: Chronic intestinal inflammation, characterizing Inflammatory Bowel Diseases (IBD), may cause profound changes in gut tissue architecture, resulting eventually in nutrient malabsorption and chronic loss of blood from gut mucosa. Moreover, the chronic inflammatory state is able to induce the activation of the reticuloendothelial system, and consequent iron sequestration. Thus, IBD patients often present iron deficiency and alterations of iron markers leading to anemia or other clinical conditions. Infliximab (IFX) is a chimeric anti-TNFα monoclonal antibody, currently used as a therapeutic option in moderate to severe IBD. Indeed effective in inducing remission or reducing disease activity, the blockade of TNFα acts at different levels, which are yet to be fully characterized. Aim of the present study is to evaluate if IFX therapy exerts direct effects of on stored body iron in IBD patients.

Materials and Methods: 42 sera were collected from 14 IBD patients (8 CD, 6 UC), before each IFX infusion, for the first 3 infusions of the therapeutic regimen. Serum ferritin was determined by a solid-phase two-site chemiluminescent immunometric assay (IMMULITE 2000 – SIEMENS), instead transferrin and CRP levels were measured by a immunoturbidimetric and iron by a colorimetric assay (COBAS c – ROCHE/HITACHI SYSTEMS).

Statistical analysis was performed by means of paired Student's t test.

Results: Serum iron significantly increased between the first and the third IFX infusion (36.71±11.98 vs. 48.14±19.51 μg/dl, p < 0.05), as well as serum total transferrin (202.57±43.11 vs. 252.29±39.90 mg/dl, p < 0.01); CRP was significantly reduced (2.06±2.26 vs. 0.49±0.52 mg/dl, p < 0.05), while a trend towards ferritin decrease was detectable, although not significant (64.14±71.50 vs. 27.50±30.80 ng/ml, p = 0.06).

Conclusions: Taken together, our data show that anti-TNFα therapy significantly modifies serum markers of stored body iron, suggesting that, inducing mucosal healing, IFX may restore iron absorption and reduce intestinal iron loss, but also it may directly modulate the cytokine network regulating iron metabolism in the reticuloendothelial system.