Savarino V, Mela G S, Zentilin P, Mele M R, Lapertosa L, Patetta R, Dallorto E, Vassallo A, Mansi C, Vigneri S, Celle G
Dipartimento di Medicina Interna, Università di Genova, Italy.
Gut. 1996 Oct;39(4):508-12. doi: 10.1136/gut.39.4.508.
The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors.
To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia.
Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study.
Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959).
Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed.
The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.
胃化生的存在使幽门螺杆菌能够在十二指肠定植,这种情况被认为是对胃酸分泌过多的一种反应。然而,这种功能紊乱仅存在于一部分十二指肠溃疡患者中,此外,在正常人和非溃疡性消化不良患者的十二指肠近端也经常发现表面胃化生,而这些人不一定被认为是胃酸分泌过多者。
阐明胃酸在诱导十二指肠胃型上皮中的作用。本研究旨在评估有和没有十二指肠胃化生的幽门螺杆菌阳性十二指肠溃疡患者之间昼夜胃酸模式是否不同。
71例经内镜确诊为十二指肠溃疡且经胃窦活检标本组织学检查发现幽门螺杆菌感染阳性的患者纳入本研究。
71例溃疡患者中有49例(69%)在十二指肠发现胃型上皮。对50名健康受试者以及十二指肠有和没有胃化生的两个十二指肠溃疡患者亚组进行了连续24小时胃pH值测量。计算24小时(1700 - 1659)、夜间(2000 - 0759)和白天(0800 - 1959)的胃酸度。
在所有考虑的时间段内,没有胃化生的溃疡患者的胃酸度均显著高于对照组(p < 0.001),而有胃化生的溃疡亚组在整个24小时期间和白天比健康受试者胃酸更多(p < 0.001)。在分析的各个时间段内,有和没有胃化生的十二指肠溃疡患者两个亚组之间没有差异。
研究结果证实十二指肠溃疡患者的昼夜胃酸度高于对照组。由于有和没有胃化生的十二指肠溃疡患者之间胃pH值没有差异,胃酸过多并非十二指肠胃化生患者所特有。这种组织学变化可能是对各种因素导致的黏膜损伤的非特异性反应,而不仅仅是对酸的反应。