Parzecka Monika, Szaflarska-Popławska Anna, Gasiorowska Joanna, Gorzkiewicz Marta, Grzybowski Tomasz
Zakład Endoskopii i Badań Czynnościowych Przewodu Pokarmowego Wieku Rozwojowego, Uniwersytet Mikołaja Kopernika w Toruniu, Collegium Medicum im. Ludwika Rydygiera w Bydgoszczy.
Pol Merkur Lekarski. 2013 May;34(203):277-80.
The strains of Helicobacter pylori are described by many common features which determine their virulence. The genes which are connected with much higher virulence of some strains are vacA, cagA, oipA, dupA. Duodenal Ulcer Promoting Gene--dupA is the new virulence factor coexisting with a duodenum ulcer. There is a rationale that shows a protective character of dupA with reference to a stomach cancer. The dupA gene probably causes increasingly higher releasing of pro-infectious IL-8 via stomach cells and it influences the production of IL-12 and other cytokines. The aim of the study was to determine the frequency of dupA gene's appearance in the Polish children's group and in the Polish teenagers' group infected with H. pylori. The research was also aimed to determine the coexistence of dupA gene and duodenum ulcer disease or erosion infection of duodenum's mucous membrane.
The endoscopic examination of the upper part of digestive duct was performed in 119 qualified patients with dyspeptic symptoms and with suspicion of stomach and duodenum's mucous membrane infection. The segments were taken for histopathological identification of H. pylori and for genetic indicating via PCR method. To confirm the presence of H. pylori in the extract the amplification of DNA fragment sized 860 pz was used. The presence of dupA gene was detected by PCR reaction with using the starters which include the fragment of jhp0917-jhp0918 sequence in the plastic H. pylori's genome area. To confirm the infection the urea breathing test was taken.
88 patients confirm the infection of H. pylori. The presence of dupA gene was found in 20 patients--a group A (22.7%), whereas in 68 patients dupA gene was not found--a group B (77.2%). Pathological changes in duodenum was found in 20 patients infected with H. pylori (22.7%), included 4 patients in the group A (20%) and 16 in the group B (23.5%). There was an infection (swelling, redness, congestion) in duodenum was found in the group A in all cases and there was an erosion presented in 3 patients. In the group B in 2 patients the duodenum ulcer disease was diagnosed. The infectious changes in duodenum were found in 7 patients but they were not infected with H. pylori; 1 patient was diagnosed with the duodenum ulcer disease.
The presence of dupA gene in the Polish children population infected with H. pylori is quite frequent but there is no clinical correlation with the duodenum ulcer disease.
幽门螺杆菌菌株具有许多决定其毒力的共同特征。与某些菌株更高毒力相关的基因有vacA、cagA、oipA、dupA。十二指肠溃疡促进基因——dupA是与十二指肠溃疡共存的新毒力因子。有理论表明dupA对胃癌具有保护作用。dupA基因可能通过胃细胞导致促感染性白细胞介素-8的释放增加，并影响白细胞介素-12和其他细胞因子的产生。本研究的目的是确定dupA基因在波兰感染幽门螺杆菌的儿童组和青少年组中的出现频率。该研究还旨在确定dupA基因与十二指肠溃疡疾病或十二指肠黏膜糜烂感染的共存情况。
对119名有消化不良症状且怀疑胃和十二指肠黏膜感染的合格患者进行了上消化道内镜检查。取组织段进行幽门螺杆菌的组织病理学鉴定和通过聚合酶链反应（PCR）方法进行基因检测。为确认提取物中存在幽门螺杆菌，使用了对大小为860 pz的DNA片段进行扩增。通过使用包含幽门螺杆菌基因组区域中jhp0917 - jhp0918序列片段的引物进行PCR反应来检测dupA基因的存在。为确认感染进行了尿素呼气试验。
88名患者确认感染了幽门螺杆菌。在20名患者中发现了dupA基因——A组（22.7%），而在68名患者中未发现dupA基因——B组（77.2%）。在20名感染幽门螺杆菌的患者中发现了十二指肠的病理变化（22.7%），其中A组有4名患者（20%），B组有16名患者（23.5%）。A组所有病例的十二指肠均有感染（肿胀、发红、充血），3名患者出现糜烂。B组有2名患者被诊断为十二指肠溃疡疾病。在7名未感染幽门螺杆菌的患者中发现了十二指肠的感染性变化；1名患者被诊断为十二指肠溃疡疾病。
在波兰感染幽门螺杆菌的儿童人群中，dupA基因的存在相当频繁，但与十二指肠溃疡疾病无临床相关性。
