Giris ve Amaç: Helikobakter pilori infeksiyonunun gastrointestinal motilite, pankreatik sekresyon ve gastrointestinal hormon salinimi üzerine etkileri oldugu bilinmekte olup, safra kesesi motilitesini de etkileyebilecegi düsüncesi söz konusudur. Bu çalismanin amaci da fonksiyonel dispepsili hastalarda Helikobakter pilori varliginin kese motilitesi üzerine etkisini arastirmaktadir. Gereç ve Yöntemler: Helikobakter pilori (+) 31 ve Helikobakter pilori (-) 19 olmak üzere toplam 50 fonksiyonel dispepsili olgu çalismaya alindi. Helikobakter pilori varligina histopatolojik yöntem ve üreaz testi ile bakildi. Histopatolojik yöntem esas alinarak olgular (+) ve (-) olmak üzere iki gruba ayrildi. Açlik ve postprandiyal 30, 60, 90, 120. dakikalarda kese volümleri ultrasonografi ile ölçüldü ve açlik plazma kolesistokinin seviyelerine bakildi. Bulgular: Açlik kese hacimleri ve postprandiyal 60. dakikada ölçülen kese hacmi Helikobakter pilori (+) olan grupta daha yüksek olarak bulundu. Postprandiyal 30, 90, 120. dakikalarda ölçülen kese hacimleri her iki grupta benzerdi. Plazma kolesistokinin seviyeleri Helikobakter pilori (+) olan grupta düsük olarak bulundu. Sonuç: Bu bulgular Helikobakter pilori infeksiyonunun safra kesesi motilitesini bozarak, biliyer diskinezi ve tas olusumunda rol oynayabilecegini düsündürmekle beraber, bu konuda yapilacak daha fazla çalismaya ihtiyaç duyulmaktadir.
Background and Aim: It is known that Helicobacter pylori infection affects gastrointestinal motility, pancreatic secretion and gastrointestinal hormones, and some authors have considered that the infection can also affect gallbladder motility. This study was undertaken to evaluate whether Helicobacter pylori has any effect on gallbladder motility in patients with functional dyspepsia. Material and Methods: Fifty patients with functional dyspepsia were studied, and 31 of them were Helicobacter pylori (+) and 19 were Helicobacter pylori (-).Helicobacter pylori was searched by histopathological method and rapid urease test. We separated the subjects as Helicobacter pylori (+) and (-) according to the histopathological method. In both groups, gallbladder volumes were measured by ultrasonographic method in fasting state and at postprandial 30, 60, 90 and 120 minutes, and ejection fraction values were calculated. All patients? fasting plasma cholecystokinin levels were determined by ELISA method. Results: Fasting volume and V60 were found significantly high in the Helicobacter pylori (+) group, while V30, 90, 120 were similar in both groups. Plasma cholecystokinin levels were found significantly low in the Helicobacter pylori (+) groups. Conclusion: These results suggest that Helicobacter pylori infection can play a role in gallstone formation and biliary dyskinesia by damaging gallbladder motility; therefore, more studies are needed to clarify this subject.