Lynch D A, Mapstone N P, Lewis F, Pentith J, Axon A T, Dixon M F, Quirke P
Centre for Digestive Diseases, General Infirmary at Leeds, England.
Helicobacter. 1996 Dec;1(4):219-26. doi: 10.1111/j.1523-5378.1996.tb00042.x.
Helicobacter pylori is the cause of chronic (type B) gastritis, duodenal ulceration (DU), and gastric ulceration (GU). Smoking is associated with delayed ulcer healing. Epidermal growth factor (EGF) is produced in the salivary and Brunner's glands of the upper gastrointestinal tract, inhibits gastric acid secretion, and is a powerful mitogen.
We sought to determine gastric luminal EGF (GL-EGF) in smokers and patients with Hp-associated DU and the effects of Hp eradication. Our aim was to determine GL-EGF in patients with GU and the effect of ulcer healing and to measure serum EGF in patients with Hp gastritis with or without DU disease.
GL-EGF was reduced in smokers compared to controls (p = .008). Subjects with HP gastritis had reduced GL-EGF compared to controls (p = .0002). There was no difference in GL-EGF between Hp-positive subjects who had DU and those with chronic gastritis alone. Eradication of Hp from those patients with DU had no effect on the low levels of GL-EGF. There was no difference between GL-EGF in Hp gastritis alone and in Hp-associated active GU. GL-EGF fell after ulcer healing (p = .04), a difference confirmed by analysis of paired samples from patients before and after ulcer healing (p = .03). There was no difference in serum EGF between controls and subjects with Hp infection. There was no difference in serum EGF in subjects with DU associated and non-ulcer-associated gastritis.
Subjects with Hp gastritis, or those who smoke, had low concentrations of GL-EGF regardless of whether DU was present. Eradication of Hp did not return the concentrations of GL-EGF to normal in DU subjects. Individuals and Hp gastritis and inactive GU had low levels of GL-EGF compared to non-ulcer Hp infection. The relative increase in GL-EGF that occurred with ulceration of the gastric mucosa may have resulted from the development of an ulcer-associated cell lineage. Serum EGF did not play a role in the pathogenesis of Hp gastritis or of associated DU ulcer disease.
幽门螺杆菌是慢性（B型）胃炎、十二指肠溃疡（DU）和胃溃疡（GU）的病因。吸烟与溃疡愈合延迟有关。表皮生长因子（EGF）在上消化道的唾液腺和Brunner腺中产生，抑制胃酸分泌，并且是一种强大的促有丝分裂原。
我们试图测定吸烟者以及幽门螺杆菌相关性十二指肠溃疡患者的胃腔内表皮生长因子（GL-EGF），以及根除幽门螺杆菌的效果。我们的目的是测定胃溃疡患者的GL-EGF以及溃疡愈合的效果，并测量幽门螺杆菌胃炎伴或不伴十二指肠溃疡疾病患者的血清表皮生长因子。
与对照组相比，吸烟者的GL-EGF降低（p = 0.008）。幽门螺杆菌胃炎患者的GL-EGF较对照组降低（p = 0.0002）。患有十二指肠溃疡的幽门螺杆菌阳性受试者与仅患有慢性胃炎的受试者之间的GL-EGF没有差异。根除这些十二指肠溃疡患者的幽门螺杆菌对低水平的GL-EGF没有影响。单纯幽门螺杆菌胃炎患者与幽门螺杆菌相关性活动性胃溃疡患者的GL-EGF没有差异。溃疡愈合后GL-EGF下降（p = 0.04），通过对溃疡愈合前后患者的配对样本分析证实了这一差异（p = 0.03）。对照组与幽门螺杆菌感染受试者的血清表皮生长因子没有差异。十二指肠溃疡相关性胃炎和非溃疡相关性胃炎受试者的血清表皮生长因子没有差异。
幽门螺杆菌胃炎患者或吸烟者，无论是否存在十二指肠溃疡，GL-EGF浓度均较低。根除幽门螺杆菌并没有使十二指肠溃疡患者的GL-EGF浓度恢复正常。与非溃疡幽门螺杆菌感染相比，幽门螺杆菌胃炎和非活动性胃溃疡患者的GL-EGF水平较低。胃黏膜溃疡时GL-EGF的相对增加可能是由溃疡相关细胞谱系的发展所致。血清表皮生长因子在幽门螺杆菌胃炎或相关十二指肠溃疡疾病的发病机制中不起作用。
