Con Sergio A, Valerín Ana L, Takeuchi Hiroaki, Con-Wong Reinaldo, Con-Chin Vicky G, Con-Chin Gil R, Yagi-Chaves Sachiko N, Mena Fernando, Brenes Pino Fernando, Echandi Guillermo, Kobayashi Michiya, Monge-Izaguirre Mario, Nishioka Mitsuaki, Morimoto Norihito, Sugiura Tetsuro, Araki Keijiro
Department of Tumor Surgery, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku, 783-8505, Japan.
J Gastroenterol. 2006 Jul;41(7):632-7. doi: 10.1007/s00535-006-1812-3.
We evaluated several risk factors for gastric cancer in Costa Rican regions having contrasting gastric cancer incidence rates, despite the small dimensions of the country.
A total of 180 dyspeptic patients were classified into two groups according to the gastric cancer incidence (GCI) rate in their Costa Rican region: group A, with a high GCI rate (n = 91) and group B, with a low GCI rate (n = 89). Helicobacter pylori infection was detected by rapid urease test, Gram staining, and histological observation. Antral and corpus specimens were obtained to assess the grade of inflammation, topography of gastritis, gastric atrophy, and intestinal metaplasia by histological examination. Serum CagA antibody was measured by an antigen-specific enzyme-linked immunosorbent assay.
There was no significant difference in H. pylori prevalence between groups A (73%) and B (63%); however, serum CagA antibody was more frequently detected in group A (79%) than in group B (54%) [P = 0.02; odds ratio (OR), 2.68]. Among patients under 60 years of age, serum CagA antibody was even more frequently detected in group A (81%) than in group B (49%) (P < 0.01; OR, 4.50). The prevalence of corpus-predominant gastritis, atrophic gastritis, and moderate/severe grades of neutrophilic infiltration was higher in serum CagA antibody-positive patients than in CagA antibody-negative patients (P = 0.003, 0.04, and 0.002, respectively).
Infection with H. pylori possessing the cagA gene is associated with the development of severe gastric damage such as gastric atrophy, leading to gastric cancer, and probably influences the differences in GCI between Costa Rican regions.
尽管哥斯达黎加国土面积不大，但我们对该国胃癌发病率不同的地区的几种胃癌风险因素进行了评估。
根据哥斯达黎加地区的胃癌发病率（GCI），将180例消化不良患者分为两组：A组，GCI率高（n = 91）；B组，GCI率低（n = 89）。通过快速尿素酶试验、革兰氏染色和组织学观察检测幽门螺杆菌感染。获取胃窦和胃体标本，通过组织学检查评估炎症程度、胃炎类型、胃萎缩和肠化生情况。采用抗原特异性酶联免疫吸附测定法检测血清CagA抗体。
A组（73%）和B组（63%）的幽门螺杆菌感染率无显著差异；然而，A组（79%）血清CagA抗体检测阳性率高于B组（54%）[P = 0.02；比值比（OR），2.68]。在60岁以下的患者中，A组（81%）血清CagA抗体检测阳性率甚至高于B组（49%）（P < 0.01；OR，4.50）。血清CagA抗体阳性患者的胃体为主型胃炎、萎缩性胃炎和中度/重度中性粒细胞浸润的发生率高于CagA抗体阴性患者（分别为P = 0.003、0.04和0.002）。
携带cagA基因的幽门螺杆菌感染与胃萎缩等严重胃损伤的发生有关，进而导致胃癌，并且可能影响哥斯达黎加不同地区之间的GCI差异。
