Konturek P C, Ernst H, Konturek S J, Bobrzyński A J, Faller G, Klingler C, Hahn E G
Institute of Physiology, Jagiellonian University School of Medicine, Kraków, Poland.
Gut. 1997 Apr;40(4):463-9. doi: 10.1136/gut.40.4.463.
Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF alpha) are potent gastric acid inhibitors and stimuli of mucosal growth and protection but their involvement in Helicobacter pylori associated duodenal ulcer has been little examined.
To assess gastric acid secretion, plasma gastrin concentrations, mucosal content of EGF and TGF alpha, and mucosal expression of these peptides and their receptor (EGFr) as well as salivary and gastric luminal release of EGF under basal conditions and after pentagastrin stimulation in 10 healthy subjects and in 25 H pylori positive patients with duodenal ulcer before and after two weeks of triple anti-H pylori therapy and four weeks after the termination of this therapy.
Pentagastrin stimulation caused a significant increase in salivary and gastric release of EGF both in healthy controls and patients with duodenal ulcers but in the patients, the eradication of H pylori resulted in several fold higher gastric luminal (but not salivary) EGF release than before the anti-H pylori therapy. Mucosal contents of immunoreactive EGF and TGF alpha and mucosal expression of EGF, TGF alpha, and EGFr in H pylori positive patients with duodenal ulcer were significantly higher than those in healthy H pylori negative controls and this increase persisted after eradication of H pylori. Basal plasma gastrin was significantly reduced after two weeks of triple therapy and four weeks after the H pylori eradication all ulcers were completely healed.
(1) H pylori infection in patients with duodenal ulcer was accompanied by enhanced plasma gastrin and increased mucosal content and expression of TGF alpha, EGF, and EGFr; (2) H pylori eradication resulted in ulcer healing, reduction in plasma gastrin, and enhancement of gastric (but not salivary) luminal release of EGF, particularly after pentagastrin stimulation; and (3) enhanced mucosal content and expression of TGF alpha, EGF, and EGFr and increased luminal release of EGF may contribute to ulcer healing after eradication of H pylori.
表皮生长因子(EGF)和转化生长因子-α(TGFα)是强效胃酸抑制剂,也是黏膜生长和保护的刺激因子,但它们在幽门螺杆菌相关性十二指肠溃疡中的作用鲜少被研究。
评估10名健康受试者以及25名幽门螺杆菌阳性十二指肠溃疡患者在基础状态下以及在五肽胃泌素刺激后,胃酸分泌、血浆胃泌素浓度、EGF和TGFα的黏膜含量、这些肽及其受体(EGFr)的黏膜表达,以及EGF的唾液和胃腔释放情况。这些患者在接受两周三联抗幽门螺杆菌治疗前、治疗后以及治疗终止四周后进行上述评估。
五肽胃泌素刺激使健康对照组和十二指肠溃疡患者的唾液和胃腔EGF释放均显著增加,但在患者中,根除幽门螺杆菌后胃腔(而非唾液)EGF释放比抗幽门螺杆菌治疗前高出数倍。幽门螺杆菌阳性十二指肠溃疡患者中免疫反应性EGF和TGFα的黏膜含量以及EGF、TGFα和EGFr的黏膜表达显著高于幽门螺杆菌阴性的健康对照组,且在根除幽门螺杆菌后这种增加仍持续存在。三联治疗两周后基础血浆胃泌素显著降低,幽门螺杆菌根除四周后所有溃疡均完全愈合。
(1)十二指肠溃疡患者的幽门螺杆菌感染伴有血浆胃泌素升高以及TGFα、EGF和EGFr的黏膜含量和表达增加;(2)根除幽门螺杆菌导致溃疡愈合、血浆胃泌素降低以及胃(而非唾液)腔EGF释放增强,尤其是在五肽胃泌素刺激后;(3)TGFα、EGF和EGFr的黏膜含量和表达增加以及EGF的腔释放增加可能有助于根除幽门螺杆菌后的溃疡愈合。