Browsing by Subject "CagA protein"

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    The role of virulent Helicobacter pylori strains in the etiopathogenesis of coronary artery disease; [Virulan Helicobacter pylori suslarinin koroner arter hastaligi etyopatogenezindeki rolu]
    (1999) Yuceyar H.; Saruc M.; Arslan S.; Goksel G.; Ozbakkaloglu B.; Uyanik B.S.; Yigitoglu R.; Sengil A.Z.
    Epidemiological studies have shown a positive correlation between coronary artery disease (CAD) and gastric Helicobacter pylori (H. pylori) infection. The possible mechanism by which H. pylori could increase the risk of CAD is chronic inflammation. More virulent H. pylori strains bearing the cytotoxin associated gene-A (CagA) can induce much more inflammation than CagA negative strains. The aim of our study was to assess the role of virulent H. pylori strains and inflammatory response in the pathogenesis of CAD. We studied 30 patients with CAD, age and sex being matched with 30 controls of similar social class. We determined the presence of H. pylori infection by rapid urease test, histology and serology (anti-H. pylori IgG). CagA status, serum tumor necrosis factor-alpha (TNF-α), gastrin and fibrinogen levels were also studied. The presence of H. pylori infection was statistically equal in CAD group (93.3%) and controls (86.6%)(p = 0.705). Serum CagA titers were 28.13 ± 9.21 U and 18.32 ± 5.8 U in the CAD and control group respectively. Serum TNF-α levels were 15.21 ± 4.30 pg/ml in the CAD group and 5.36 ± 2.41 pg/ml in the control group. Serum CagA and TNF-α levels showed a significant difference between the two groups (p = 0.000). Patients with CAD had a higher prevalence of CagA-positive strains than controls (67.8% versus 42.3%; p = 0.021). The serum gastrin level was higher in CAD but there was no significant difference between two groups (p = 0.379). Fibrinogen levels of the CAD group were significantly higher than those of the control (370 ± 51 mg/ml and 247 ± 43 mg/ml, p = 0.001). Further more, numbers of occluded vessels in CAD patients were positively correlated with both cagA positivity and TNF-α levels. In conclusion, CagA bearing strains of H. pylori may increase the risk of CAD by inducing chronic inflammation and increasing the expression of cytokines and procoagulant substance.
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    The effect of CagA status on response to Helicobacter pylori eradication therapy in Western Turkey
    (Associacao Brasileira de Divulgacao Cientifica, 2001) Saruç M.; Goksel G.; Ozkaya S.; Guclu F.; Ozbakkaloglu B.; Yuceyar H.
    If cytotoxin-associated gene A (CagA) status affects the response rates of therapy, then it may be possible to predict Helicobacter pylori eradication rates. We aimed to evaluate the response to eradication treatment of H. pylori infection in CagA-positive and CagA-negative patients. A total of 184 patients (93 males, 91 females, mean age 42.6 ± 12.8 years) with H. pylori-positive chronic gastritis were studied. Subjects underwent a gastroscopy and biopsy specimens were taken from the gastric antrum, body, and fundus. Before the eradication therapy was given all patients were tested for CagA, TNF-α and gastrin levels. They were then prescribed lansoprazole (30 mg bid), clarithromycin (500 mg bid), and amoxicillin (1.0 mg bid) for one week. On the 8th week a second endoscopy was performed and further biopsy specimens were obtained from the same sites as in the initial endoscopy. One hundred and twenty-seven patients (69.1%) were found to be CagA positive and 57 patients (30.9%) were CagA negative. The total eradication rate was 82.6%. In the CagA-positive group this rate was 87.4%, and in the CagA-negative group it was 71.9% (P = 0.019). TNF-α levels were higher in the CagA-positive than in the CagA-negative group (P = 0.001). However, gastrin levels were not different between groups (P = 0.421). Our findings revealed that CagA-negative status might be a risk factor for failure of H. pylori triple therapies. The CagA pathogenicity island gives a growth advantage to H. pylori strains and has been associated with an increase in the inflammatory response at the gastric mucosal level. These properties could make CagA-positive H. pylori strains more susceptible to antibiotics.
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    Functional dyspepsia: Relationship between clinical subgroups and Helicobacter pylori status and Western Turkey
    (Associacao Brasileira de Divulgacao Cientifica, 2003) Saruc M.; Ozden N.; Turkel N.; Ayhan S.; Demir M.A.; Tuzcuoglu I.; Akarca U.S.; Yuceyar H.
    The etiology of functional dyspepsia is not known. The objective of the present study was to determine the characteristics of functional dyspepsia in Western Turkey. We divided 900 patients with functional dyspepsia into three subgroups according to symptoms: ulcer-like (UL), 321 (35.6%), motility disorder-like (ML), 281 (31.2%), and the combination (C) of these symptoms, 298 (33.1%). All patients were submitted to endoscopic evaluation, with two biopsies taken from the cardia and corpus, and four from the antrum of the stomach. All biopsy samples were studied for Helicobacter pylori (Hp) density, chronic inflammation, activity, intestinal metaplasia, atrophy, and the presence of lymphoid aggregates by histological examination. One antral biopsy was used for the rapid urease test. Tissue cagA status was determined by PCR from an antral biopsy specimen by a random sampling method. We also determined the serum levels of tumor necrosis factor-a (TNF-α) and gastrin by the same method. Data were analyzed statistically by the Kolmogorov-Smirnov test and by analysis of variance. Hp and cagA positivity was significantly higher in the UL subgroup than in the others. The patients in the ML subgroup had the lowest Hp and cagA positivity and Hp density. The ML subgroup also showed the lowest level of Hp-induced inflammation among all subgroups. The serum levels of TNF-α and gastrin did not reveal any difference between groups. Our findings show a poor association of Hp with the ML subgroup of functional dyspepsia, but a stronger association with the UL and C subgroups.