目的:幽門桿菌與慢性胃炎、胃潰瘍及十二指腸潰瘍等疾病息息想關。而幽門桿菌感染胃的上皮細胞後是否會引起疾病,一般認為與幽門桿菌本身所帶有的致病基因如vacA、 vagA、 iceA和 babA基因有關。因此我們希望了解東部幽門桿菌所帶來的致病基因在疾病和不同族群之間是否有差異,材料與方法:在東部的慈濟醫院取得病患胃切片,經過CLO檢驗為陽性者,以聚合?連鎖反應(PCR)檢驗幽門桿菌所帶有的致病基因vacA-(s1,s1a,s1b,s2,m1和m2)、cagA和flaA在不同族群間之異同。結果:經過兩個月的臨床內視鏡胃切片共收集102件切片。男女比例為39:63。CLO檢驗陽性結果為47.5%(男:女 = 21:27) 。臨床疾病的分佈上,CLO檢驗的、陰性兩組之間沒有顯著差異(p = 0.103)。在兩性之間的疾病分佈上,統計上也沒有顯著差異。48位CLO test陽性的檢體利用PRC檢驗,有3個案例無任何幽門桿菌之基因存在,因此被認為是偽陽性(false positive),所以CLO test診斷率為93.75%。東部地區幽門桿菌致病基因陽性率為:vacA-s1+;93.3%,vacA-s1a+;80.0%,vacA-m-/m1m2;22.2%/28.9%/48.9%;和vagA+;86.7%,但原住民族群的vacA-m1/m2:6/6(n=12)和漢人vacA-m-/m1/m2:7/16(n=23)(p=0.144)的比較中,雖然沒有達到統計之差異,但很明顯的漢人的vacA-m2較多,而原住民族群之vacA-m1與m2相同,此外兩族群之間,包括平均年齡、疾病分怖、致病基因:vacA-(s-type,)和cagA在統計上都沒有顯著差別。而幽門桿菌中帶有vacA-s1a-/m-和vacA-m-/cagA-基因組合,在臨床觀察上以引起胃炎的疾病較多,但並未達到統甫的顯著差異(p值分別是0.182和0.199),推測可能是個案數不足。結論:在兩個族群之間,幽門桿菌感染所引起的消化性疾病和幽門桿菌菌種無顯著統計差異。臨床觀察上幽門桿菌帶有vacA-s1a-/m-和vacA-m-/cagA-基因組合以胃炎表現較多。
Objective: Helicobacter pylori infection cause peptic ulcers, gastritis, and distal gastric cancer. It carries virulent genes, such as vacA, cagA, iceA and BabA, is more toxic to epithelial cells, and induces more-severe clinical disease, such as peptic ulcers and distal gastric cancer. We investigated the status of virulent genes, such as vacA and its suballele (s1, s2, s1a, s1b, m1, and m2), and the cagA gene in eastern Taiwan. We also studied whether any difference exists in virulent genes between Aboriginals and Han Chinese. Material and Methods: Using polymerase chain reaction (PCR), gastric biopsy specimens with positive CLO examination from symptomatic patients were examined for H. pylori virulent genes, such as vacA-(s1, s2, s1a, s1b, m1, and m2) and cagA. The genetic status was studied in association with the clinical diagnosis between Aboriginal and Han Chinese. Results: Endoscopic gastric biopsies of 102 patients (39 males, 63 females) were obtained from Tzu Chi General Hospital. Positive rates of the CLO test were 47.5% (n=48, male: female=21:27) . There was no difference in the clinical diagnosis between CLO-positive and negative cases (p= 0.103). Only 45 patients with CLO positive results had a positive PCR product. Three cases were CLO false positive with a diagnostic rate of 93.75%. The percentage of patients carrying virulent genes was as follows: cagA, 86.7%, vacA-s1: 93.3%, vacA-s1a, 80.0%; and vacA-m-/m1/m2, 22.2%/28.9%/48.9%. When comparing the genetic status of H. pylori and the clinical diagnosis between Aboriginals and Han Chinese, there was no statistically significant difference. Although not reaching statistical significance, H. pylori carrying vacA-sla-/m- and vacA-m-/ cagA- was predominantly present with gastritis (p=0.182 and 0.199 respectively). Conclusions: There was no statistically significant difference in the vacA and cagA genetic statuses between Aboriginals and Han Chinese at Taiwan. In addition, clinical observations indicated that patients with H. pylori infection who were carrying virulent genes such as vacA-sla-/m- and vacA-m-/cagA- may have a less-toxic infection and may experience gastritis more frequently.