Browsing by Author "Kasirga, HE"

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    The Role of Fecal Calprotectin in Investigating Pediatric Ulcerative Colitis
    Unal, F; Semizel, E; Serdar, M; Ecevit, CÖ; Karaca, Y; Yilmaz, EM; Kocaefe, H; Kasirga, HE
    introduction: Fecal calprotectin (FCP) can be found in high concentrations in inflammatory bowel disease due to the increase in leucocyte turnover in intestinal wall or increase of migration of neutrophils into the lumen. In this study, we aimed to determine the FCP values of the ulcerative colitis (UC) patients at the time of diagnosis and to investigate the applicability and effectiveness of this non-invasive method in the diagnosis of the disease, routinely. Materials and Methods: A total of 19 patients with UC (10 females, 9 males, age: 11.5 +/- 3.5 years old) whoose stool samples collected during the diagnosis period and 20 healthy controls (10 female, 10 male, age: 10.3 +/- 4.5 years old) were included in the study. Stool samples were collected for FCP analysis by ELISA method at the time of diagnosis and before the treatment period. Results: FCP values of the UC group were statistically higher than the control group. FCP values of the UC and control groups were 398.4 mu g /gr stool (56.7-2450) and 19.4 mu g/gr stool (2-81), respectively (p<0.005). FCP values of the patient group with mild activity index (n=8), and moderate-severe activity index (n=11) according to the Pediatric Ulcerative Colitis Activity Index were 267.6-mu g/gr stool, and 435.2 mu g/gr stool, respectively (r2: 0.40, p<0.05). There was not statistical difference between the FCP values of the patients with pancolitis (422.6 mu g/gr stool) and with left-sided colitis, proctitis/sigmoiditis (371.7 mu g/gr stool) (p>0.05). High CRP values (89.4%), elevation of erythrocyte sedimentation rate (84.2%), leukocytosis (73.6%), thrombocytosis (68.4%), anemia (89.4%), and hypoalbuminemia (52.6%) were found. Conclusions: FCP values of the UC patients were found to be statistically higher than the control group, and increase in FCP values has been observed with increasing disease activity. Therefore, we believe that the determination of FCP could be useful at the time of diagnosis and during follow-up of the patients with UC.
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    Association of Helicobacter pylori-associated Duodenal Ulcer and Precancerous Findings with Toll-like Receptor-4 Asp299Gly and Toll- like Receptor-9123T/C Polymorphism and Cag-A, Vac-A in Children
    Tok, AC; Kasirga, HE; Gazi, H; Onay, H; Özkinay, F; Ayhan, S
    Objective: We aim to show whether endoscopic, histopathological and precancerous findings in childhood Helicobacter pylori (H. pylori) infection are associated with some changes in the host immune system and some virulence factors of the bacteria. For this purpose, we interpreted the changes in endoscopic and histopathological findings of TLR-4 and TLR-9 gene polymorphisms in the innate immune system of the host and cytotoxin associated gene A (Cag-A) and vacuolating cytotoxin A (Vac-A) positivity, the main virulence factors of the bacteria. Method: Between April 2009 and October 2010, 100 H. pylori-positive and 100 H. pylori-negative cases were cross-sectionally selected by retrospectively reviewing the files of patients admitted to a tertiary hospital with dyspepsia. After obtaining informed consent, blood samples from these patients were analysed for TLR-4 [Asp 299 Gly (rs4986790)] and TLR-9 [1237TC (rs574 3836)] gene polymorphisms and for the presence of Cag-A and Vac-A in isolates obtained from pathological specimens. Results: Poor socio-economic conditions were an important risk factor for H. pylori. The presence of Cag-A increased the likelihood of duodenal ulcer. There was no significant difference between TLR-4 [Asp 299 Gly (rs4986 790)] gene polymorphism and endoscopic and histopathological findings. However, TLR-9 [-1237TC (rs5743836)] polymorphism increased precancerous intestinal metaplasia and atrophy. Conclusion: The presence of Cag-A increases the risk of duodenal ulceration due to H. pylori infection. The TLR-9 [-1237TC (rs5743836)] polymorphism is associated with gastric atrophy and intestinal metaplasia in the pathogenesis of H. pylori infection. Studies in large groups of patients are needed.