School of Medicine, University of Cardiff, Cardiff, UK.
Helicobacter. 2023 Aug;28(4):e12982. doi: 10.1111/hel.12982. Epub 2023 Apr 27.
In the 1970s, 1% of the UK population consulted with dyspepsia; fiberoptic gastroscopy allowed biopsy specimens under direct vision enabling systematic histopathology. Steer et al described clusters of flagellated bacteria closely apposed to the gastric epithelium associated with chronic active gastritis. The first UK series of Helicobacter pylori following Marshall's 1983 visit to Worcester confirmed the association of H. pylori with gastritis. UK researchers completed much early helicobacter research as there were many UK campylobacteriologists. Steer and Newell proved the Campylobacter-like organisms grown on culture were the same as those seen in the gastric mucosa using antiserum raised by inoculating rabbits with H. pylori from cultures. Wyatt, Rathbone, and others showed a strong correlation between the number of organisms, type and severity of acute gastritis, immunological response, and bacterial adhesion similar to enteropathogenic E coli. Seroprevalence studies indicated H. pylori increased with age. Histopathologists also showed peptic duodenitis was in effect "gastritis in the duodenum" caused by H. pylori, unifying its role in the pathogenesis of both gastritis and duodenal ulceration. These bacteria were initially called Campylobacter pyloridis and then C. pylori. However, electron microscopy suggested that the bacteria were not campylobacters, and this was supported by differences in fatty acid and polyacrylamide electrophoresis profiles. In-vitro tests indicated that H. pylori was susceptible to penicillins, erythromycin, and quinolones, but not trimethoprim or cefsulodin allowing development of selective media for culture. Monotherapy with erythromycin ethylsuccinate was ineffective, and patients treated with bismuth subsalicylate initially responded with clearance of H. pylori and the associated gastritis, but then many relapsed. Thus, pharmacokinetic and treatment studies were important to direct suitable dual and triple treatments. Work optimized serology, and the rapid biopsy urease and urea breath tests. The link between H.pylori and gastric cancer was established in large seroprevalence studies, and H. pylori test and treat for dyspepsia became routine.
在 20 世纪 70 年代,英国有 1%的人口患有消化不良;纤维胃镜检查允许在直视下进行活检,从而实现系统的组织病理学检查。Steer 等人描述了与慢性活动性胃炎相关的紧密附着在胃上皮的鞭毛状细菌簇。在 Marshall 于 1983 年访问伍斯特之后,英国进行的第一个关于幽门螺杆菌的系列研究证实了幽门螺杆菌与胃炎的关联。由于有许多英国弯曲杆菌学家,英国研究人员完成了许多早期的幽门螺杆菌研究。Steer 和 Newell 证明,在培养物中生长的类似弯曲杆菌的生物体与用从培养物中接种幽门螺杆菌的兔子血清接种后在胃黏膜中看到的生物体相同。Wyatt、Rathbone 和其他人表明,生物体的数量、急性胃炎的类型和严重程度、免疫反应和细菌黏附之间存在很强的相关性,类似于肠致病性大肠杆菌。血清流行率研究表明,幽门螺杆菌的患病率随着年龄的增长而增加。组织病理学家还表明,十二指肠球部溃疡实际上是“十二指肠中的胃炎”,由幽门螺杆菌引起,统一了其在胃炎和十二指肠溃疡发病机制中的作用。这些细菌最初被称为幽门弯曲杆菌,然后称为 C. pylori。然而,电子显微镜表明这些细菌不是弯曲杆菌,这一点得到了脂肪酸和聚丙烯酰胺电泳图谱差异的支持。体外试验表明,幽门螺杆菌对青霉素、红霉素和喹诺酮类药物敏感,但对甲氧苄啶和头孢磺啶耐药,这允许开发用于培养的选择性培养基。红霉素乙琥酯单药治疗无效,最初用双水杨酸铋治疗的患者幽门螺杆菌清除和相关胃炎得到缓解,但随后许多患者复发。因此,药代动力学和治疗研究对于指导合适的双联和三联治疗非常重要。优化了血清学、快速活检尿素酶和尿素呼气试验。在大规模血清流行率研究中确立了幽门螺杆菌与胃癌之间的联系,对消化不良进行幽门螺杆菌检测和治疗成为常规。