C. ALKIM1, H. ALKIM2, M. BALCI3, F. ATAKAN ERKAL4, E. PARLAK5, U. DAGLI5,
A. ULKER5, G. SAYDAM4, B. SHAHİN5
1Gastroenterology Department of Sisli Etfal Training and Research Hospital, Istanbul, TURKEY.
2Gastroenterology Department of Bakırköy Dr. Sadi Konuk Training and Research Hospital, Istanbul, TURKEY.
3Laboratory of immunology and 4biochemistry, 5gastroenterology clinic of High Speciality Hospital, Ankara. TURKEY.
Aim: We aim to investigate whether microalbuminuria reflects the type and activity of the inflammatory bowel disease and is there any relation between microalbuminuria and serum levels of TH1/TH2 cytokines IFN-γ/IL-4.
Methods: Thirty-one ulcerative colitis and 18 Crohn’s disease patients together with 8 healthy controls were enrolled into the study. Serum creatinine, b-2 microglobulin, IL-4 and IFN-γ levels together with 24-hours urine creatinine, microalbumin and b-2 microglobulin levels were studied.
Results: Although the creatinine clearance level of the ulcerative colitis group was seemed lower than the healthy control group, any statistically important difference was not present between the renal functions of the ulcerative colitis, Crohn’s disease and healthy control groups. All of the 3 study groups’ urine b-2 microglobulin levels were found lower than the detectable level, so tubular damage was not present. Serum IL-4 level of the ulcerative colitis group was found significantly higher than the healthy control group (49.3±81.7 pg/ml, 1.6±0.0 pg/ml, p<0.01). Ulcerative colitis group microalbuminuria level was found minimally higher than the healthy control group, but the difference was insignificant. The serum IL-4 level of Crohn’s disease group (54.8±58 pg/ml) was found higher than both from ulcerative colitis and healthy control groups, but statistically significant difference was present only with healthy control group (p<0.01). Serum IFN-γ levels of all study groups was found lower than the detectable level. No difference was detected between the b-2 microglobulin levels of study groups.
Conclusion: Microalbuminuria and serum IFN-γ and β-2 microglobulin levels were insufficient in the diagnosis of inflammatory bowel disease and in determining the activation of the disease. Serum IL-4 levels were high in the inflammatory bowel disease without any relation with activation. But the number of patients having similar values with healthy control group was high, so it’s routine usage seems to be hard.
THROMBOSPONDIN-1 AND VEGF IN INFLAMMATORY BOWEL DISEASE
C. ALKIM 1, D. SAKIZ 2, H. ALKIM1, A. LIVAOGLU 2, T. KENDIR 1, H. DEMIRSOY 1,
L. ERDEM1, N. AKBAYIR1, M. SOKMEN1
Gastroenterology1 and Pathology2 Departments of Sisli Etfal Training and Research Hospital, Istanbul, TURKEY.
Background and Aim: Angiogenesis is an important process in the pathogenesis of chronic inflammation. We aimed to search the angiogeneic balance in inflammatory bowel disease via evaluating expression of vascular endothelial growth factor (VEGF) and thrombospondin-1 on colonic epithelial cells, together with expression of inducible nitric oxide synthase (iNOS).
Methods: Twenty-one ulcerative colitis, 14 Crohn’s disease, 11 colorectal cancer patients and 11 healthy controls colonic biopsy samples were evaluated immunohistochemically.
Results: The expressions of thrombospondin-1, VEGF and iNOS in ulcerative colitis and Crohn’s disease groups were higher than expression of healthy control group, all with statistical significance. However, in colorectal cancer group VEGF and iNOS expressions were increased importantly, but thrombospondin-1 expression was not statistically different from healthy control group’s expression. Both of thrombospondin-1 and VEGF expressions was correlated with iNOS expression distinctly, but did not correlate with each other.
Conclusions: Both of pro-angiogeneic VEGF and anti-angiogeneic thrombospondin-1 expressions were found increased in our inflammatory bowel disease groups but in colorectal cancer group only VEGF expression was increased. TSP-1 increases in inflammatory bowel disease patients as a response to inflammatory condition, but this increase was not enough to suppress pathologic angiogenesis and inflammation in inflammatory bowel disease.