Dwyer B, Sun N X, Kaldor J, Tee W, Lambert J, Luppino M, Flannery G
Clinical Pathology Laboratory, Fairfield Hospital, Australia.
Scand J Infect Dis. 1988;20(1):63-8. doi: 10.3109/00365548809117218.
The association between duodenal ulcer, gastritis and gastroduodenal colonization with Campylobacter pylori suggests a causal role for this newly described bacterium. In an attempt to challenge the verity of this association we studied a group of people in whom duodenal ulcer is apparently absent. Serological evidence of infection was sought with a sensitive, specific ELISA assay for C. pylori specific IgG and was compared with results from control sera from teenagers referred for respiratory viral serology, volunteer blood bank donors, patients with duodenal ulcers and patients in whom the presence or absence of C. pylori had been determined by histological and microbiological examination of gastric tissue. A relatively isolated group of Australian Aborigines in whom peptic ulceration is virtually unknown, was observed to possess age-specific mean C. pylori antibody levels comparable those found in a group of white Australian dyspeptic patients without microbiological evidence of infection with this organism. The antibody levels of Aborigines were lower than those found in an aged-matched group of 'healthy' white Australians, both of these groups having levels which were significantly lower than the levels found in culture positive white Australian dyspeptic patients. It was found that 21/144 'healthy' white Australians (14.6%) had antibody levels greater than or equal to the lower 99% confidence interval of the mean level found in culture positive patients, while only 2/274 Aborigines (0.7%) had such elevated levels. By contrast, 89/142 (62.7%) patients with endoscopically proven duodenal ulcer had similarly elevated specific antibody levels. These differences were highly significant. We consider these findings to be consistent with the hypothesis that C. pylori is important in the pathogenesis of duodenal ulcer.
十二指肠溃疡、胃炎与幽门弯曲菌在胃十二指肠定植之间的关联表明,这种新发现的细菌具有致病作用。为了验证这种关联的真实性,我们对一组显然没有十二指肠溃疡的人群进行了研究。采用一种灵敏、特异的酶联免疫吸附测定法(ELISA)检测幽门螺杆菌特异性IgG,以寻找感染的血清学证据,并将结果与因呼吸道病毒血清学检查前来就诊的青少年、志愿献血者、十二指肠溃疡患者以及通过胃组织组织学和微生物学检查确定是否存在幽门螺杆菌的患者的对照血清结果进行比较。观察到一个相对隔离的澳大利亚原住民群体,他们几乎没有消化性溃疡,其年龄特异性幽门螺杆菌平均抗体水平与一组没有该生物体感染微生物学证据的澳大利亚白人消化不良患者相当。原住民的抗体水平低于年龄匹配的“健康”澳大利亚白人组,这两组的水平均显著低于培养阳性的澳大利亚白人消化不良患者的水平。结果发现,21/144名“健康”澳大利亚白人(14.6%)的抗体水平大于或等于培养阳性患者平均水平的99%置信区间下限,而只有2/274名原住民(0.7%)有如此升高的水平。相比之下,89/142名(62.7%)经内镜证实有十二指肠溃疡的患者有类似升高的特异性抗体水平。这些差异具有高度显著性。我们认为这些发现与幽门螺杆菌在十二指肠溃疡发病机制中起重要作用的假说一致。