A Follow-Up Is Necessary To Accurately Assess The Incidence Rate Of Inflammatory Bowel Diseases (Ibd) In Population Registries.

Background: Crohn s disease (CD) is characterized by bacterial invasion of the mucosa and the development of fistulae.Both phenomena point towards a disturbed immune reaction and reduced granulocyte function.This hypothesis is supported by results of antibiotic therapy in CD and case reports on healing of fistulae after treatment with G-CSF (N Engl J Med 340:239;1999).The Aim of this study was therefore to compare granulocyte function in CD patients with healthy controls.Methods: Phagocytic function of granulocytes was tested by assessing the uptake of opsonized E.coli using flow cytometry and the Phagotest kit (Orpegen Pharma, Germany) in 16 patients with Crohn's disease (7 fistulizing, 9 non fistulizing, age range 19-51 years) and 10 healthy volunteers (age 20-42).Additionally, secretion of pro-and contra-inflammatory cytokines was determined after whole blood LPS stimulation (50 pg/ml, Milenia Ex vivo stimulation kit, DPC Biermann, Germany) for 4 h (TNF-a) and 24 hours (ILlO), respectively.Results: Granulocytic phagocytosis was not impaired in CD as compared to healthy controls (77.0% vs. 82.2%E. coli positive cells; 849.1 vs. 967.6mean fluorescence intensity [mJ.i.]).The subgroup analysis of patients with versus without fistulae also showed no difference (69.8% vs. 82.1% E.coli positive cells; 760.4 vs. 911.2m.f.i.).CD patients had higher LPS-induced TNF-a secretion than controls (550.1 vs. 286.8pg/ml, not significant).Again no significant difference between fistulizing vs. non fistulizing patients was found (716.2 vs. 431.4pg/ml).Furthermore, CD patients showed significantly lower IL-lO secretion after LPS stimulation than controls (63.4 vs. 150.5 pg/ml, p=0.023).However, no significant difference between patients with fistulizing and non-fistulizing CD was seen (34.5 vs. 85.9 pg/ml).In conclusion, our data do not support the hypothesis that a defect in granulocyte phagocytic function is involved in the pathogenesis of CD or the development of fistulae.Effects of antibiotic or GCSF therapy must be explained by a different mechanism.