Tham K T, Peek R M, Atherton J C, Cover T L, Perez-Perez G I, Shyr Y, Blaser M J
Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Hum Pathol. 2001 Mar;32(3):264-73. doi: 10.1053/hupa.2001.21136.
From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P <.001) and epithelial degeneration (P =.004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non-Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and nonsteroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. HUM PATHOL 32:264-273. This is a US Government work. There are no restrictions on its use.
我们从183例接受上消化道内镜检查的患者中，采集胃窦和胃体活检组织进行细菌培养和组织病理学检查，采集血液样本检测抗幽门螺杆菌免疫球蛋白G抗体，并分析幽门螺杆菌基因组DNA的细胞毒素相关基因A（cagA）和空泡毒素（vacA）基因型。正如预期的那样，在幽门螺杆菌活检阳性的患者中，十二指肠溃疡（DU）患者（n = 34）胃窦部的慢性和急性炎症（P <.001）以及上皮变性（P =.004）明显比胃体部更严重。DU患者胃窦部的这3项指标以及幽门螺杆菌密度均显著高于胃溃疡（GU）患者或无溃疡患者。vacA s1/cagA阳性的幽门螺杆菌菌株定植与胃黏膜炎症和上皮变性以及消化性溃疡病（PUD）风险增加相关，而vacA s2m2/cagA阴性菌株定植与轻度胃组织病理学相关，且与PUD的任何显著风险均无关。非裔美国人中主要的幽门螺杆菌菌株为vacA s1bm1/cagA阳性，而在非西班牙裔白种人中所有基因型均有较好的代表性。多因素分析显示，幽门螺杆菌定植与DU显著相关（校正比值比[AdjOR]=3.2[1.4 - 7.2]），而使用非甾体抗炎药（NSAID）与之呈负相关（AdjOR = 0.3[0.2 - 0.7]）。使用NSAID（AdjOR = 4.3[1.02 - 18.5]）和非裔美国人种族（AdjOR = 10.9[2.6 - 50]）与GU显著相关。吸烟和年龄与DU或GU均无显著相关性。这些数据表明，DU与以胃窦为主的胃炎相关，幽门螺杆菌基因型和NSAID的使用独立地影响PUD的发病机制。《人类病理学》32:264 - 273。这是美国政府工作成果。其使用不受限制。
