@article{oai:twinkle.repo.nii.ac.jp:00019978,
 author = {NAKADA, Takuro and SUZUKI, Tadashi and KOBAYASHI, Makio and KAMEOKA, Shingo},
 issue = {10/11},
 journal = {東京女子医科大学雑誌},
 month = {Nov},
 note = {現在,十二指腸潰瘍とHelicobacter pylori (H. pylori)の関連が明らかにされているが,十二指腸潰瘍の穿孔に対するH. pyloriの関与については議論が分かれている.そこで,1981年1月～1989年3月に当院第二外科で行われた179例の穿孔性十二指腸潰瘍に対する胃切除手術症例のうち,潰瘍穿孔部と幽門腺領域の標本が存在する89例につき,病理形態学的所見とH. pyloriとの関連について検討した.ヘマトキシリン・エオジン染色,マッソン・トリクローム染色を行い,病理形態学的所見により急性潰瘍穿孔型(A群)と慢性潰瘍穿孔型(C群)に分け,臨床的背景を検討した.また,免疫組織化学染色により,潰瘍穿孔部周辺のH. pyloriの有無,幽門腺領域のH. pylori感染を定性的に評価し,病理形態学的所見との関連を検討した.C群は60例,A群は29例であった.臨床的背景では,潰瘍の既往,1週間以上の穿孔前症状,手術時の肉眼所見で両群に有意差を認めた.潰瘍穿孔部周辺にH. pyloriは観察されず,幽門腺領域では81例に感染を認め,レベル1が20例,レベル2が35例,レベル3が26例であった.H. pylori感染と病理形態学的所見の関連では,線維化や瘢痕形成,潰瘍周辺部の動脈璧の肥厚や線維化,好中球優位の炎症細胞浸潤,粘膜の炎症,浮腫,毛細管性出血について有意差が認められた.A群の55%がレベル1で,レベル2,3は28%であったが,C群は88%がレベル2,3であり,A群に比べ,有意にH. pyloriの感染レベルが高かった.両群は臨床的背景だけでなくH. pyloriの感染レベルも有意に異なっていた.潰瘍形成から穿孔に至る機序は,急性型と慢性型で異なると推測され,特に急性潰瘍穿孔症例は,H. pylori以外にも穿孔要因があることが示唆された., There is controversy concerning the contribution of Helicobacter pylori (H. pylori) to perforation by duodenal ulcers. We therefore investigated the association between the pathological findings and H. pylori infection in the 89 operated cases. We performed hematoxylin and eosin staining, Masson trichrome staining, and to observe the presence of H. pylori by immunohistochemical staining. We divided the cases into an acute ulcer perforation type (A group) and a chronic ulcer perforation type (C group). There were 60 cases in the C group and 29 cases in the A group. Infection was observed in the pyloric gland region in 81 cases without detection of H. pylori around the site of ulcer perforation. In the A group, 55% of the cases had up to 20 bacteria/gastric pit present in a few of gastric pits. However in the C group, 88% were almost all of or many gastric pits with more than 20 bacteria/gastric pits. Thus the infection was significantly higher in the C group than in the A group. The two groups differed significantly in level of H. pylori infection. The results suggested that the acute type and the chronic type differed in the mechanism that led from ulcer formation to perforation.},
 pages = {417--429},
 title = {Pathological Assessment of the Contribution of Helicobacter pylori Infection to Perforated Duodenal Ulcer},
 volume = {76},
 year = {2006}
}