Serum and gastric luminal epidermal growth factor in Helicobacter pylori-associated gastritis and peptic ulcer disease.
BACKGROUND
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Lynch
D A
DA
Centre for Digestive Diseases, General Infirmary at Leeds, England.
Mapstone
N P
NP
Lewis
F
F
Pentith
J
J
Axon
A T
AT
Dixon
M F
MF
Quirke
P
P
D000328:Adult; D000368:Aged; D001706:Biopsy; D004381:Duodenal Ulcer / Q000209:etiology / Q000382:microbiology / Q000473:pathology; D004815:Epidermal Growth Factor / Q000032:analysis* / Q000097:blood / Q000502:physiology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005750:Gastric Juice / Q000737:chemistry; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000378:metabolism* / Q000382:microbiology; D005766:Gastrointestinal Contents / Q000737:chemistry*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D010295:Parietal Cells, Gastric / Q000378:metabolism; D010437:Peptic Ulcer / Q000209:etiology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D012907:Smoking / Q000009:adverse effects / Q000378:metabolism
D004815:Epidermal Growth Factor