Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations

INT RO DUCT IO NHelicobacter pylori (H.pylori) infection is now recognized as the cause of type B gastritis, as a critical factor in the development and the recurrence of duodenal ulcer disease, and as an essential co-factor in the development of gastric carcinoma and gastric MALTlymphoma 1 -5 ) .Although estimation of the lifetime risk of developing an ulce r in people with H. pylori infection is difficult, it is believed that approximatley 10 -15 % of individuals with H. pylori infection may deve lop an ulcer.6 , 7 ) The link between H. pylori a nd the developme nt of peptic ulcer disease may be related to the inappropriate release of gastrin observed in H. pylori-positive patients.One of the most notable H.Eff e ct o f He lic o b a ct e r p y lo ri in f e ct io n o n a n t r a l g a s t r in a n d s o m a t o s t a t in c e lls a n d o n s e r u m g a s t r in c o n c e n t r a t io n s S ill Mo o P a rk*, Hy o Ra n g Le e *, J a e Gy u Kim *, J o o n g W o n Pa rk* Gy u J u n g *, S e o n g Hy u c k Ha n *, J o o n Hy u n g C h o * a n d M i Ky u n g Kim + *De p a rt m e nt o f Int e rna l M e d ic in e a n d + De p a rt m e nt o f Pat h o lo g y , Co lle g e o f M e d ic ine , C h u ng -A ng U n iv e rs ity , S e o u l, Ko re a O bj e c t iv e s : He lic o b act e r py lo ri inf e ct io n ind uc e s s e le ct iv e re d uct io n o f t he n u m b e r o f a nt ra l D-ce lls a nd re s u lt s in a b no rm a l re g u lat io n o f s e ru m g a s t rin s e c re t io n .T h e p u rp o s e o f t h is s t udy w as t o inv e s t ig at e t h e re lat io ns h ip b e tw e e n H. py lo ri inf e ct io n a nd t he n u m b e rs o f G -ce lls a nd D-ce lls .M e t h o d s : T he n u m b e rs o f a nt ra l G -ce lls a nd D-ce lls , t he rat io o f G -ce lls t o D-ce lls a nd f as t ing s e ru m g a s t rin c o nc e nt rat io ns w e re c o m p a re d b e tw e e n 3 7 p at ie nt s w it h ( 2 9 w it h d uo d e n a l u lc e rs a nd 8 w it h g a s t ric u lce rs ) a nd 3 3 w it h o ut H. py lo ri inf e ct io n ( 2 2 w it h d uo d e n a l u lc e rs a nd 1 1 w it h g as t ric u lc e rs ) .S e ru m g as t rin c o nce nt rat io ns w e re m e a s u re d us ing t he ra d io im m u no a s s ay t e c h n iq ue .A nt ra l m u co s a l b io p s y s p e c im e ns w e re e x a m ine d us ing im m u no h is t o c he m ic a l s t a in ing w it h a nt ib o d ie s s p e c if ic f o r g a s t rin a nd s o m at o s t at in a nd t h e n u m b e rs o f G -c e lls a nd D-ce lls p e r g a s t ric g la nd w e re c o u nt e d .Re s u lt s : Fas t ing s e ru m g a s t rin co n ce nt rat io ns w e re s ig n if ica nt ly h ig he r in p at ie nt s w it h H. py lo ri inf e ct io n c o m p a re d t o p at ie nt s w it h o ut inf e ct io n (8 0 .3±23 .5 v s 4 7 .6±14 . 1 p g/ m l, p <0 .0 0 1) .T h e n u m b e r o f G -c e lls p e r g as t ric g la nd w a s s im ila r in inf e ct e d a nd u n inf e ct e d p at ie nt s ( 7 .1±3 . 1 v s 7 .3±3 .9 , re s p e ct iv e ly , p >0 .5) .T he n u m b e r o f D-ce lls w as s ig n if ic a nt ly lo w e r in p at ie nt s w it h H. py lo ri inf e ct io n t ha n in u n inf e ct e d p at ie nt s in b o t h d uo d e n a l a nd g as t ric u lce r p at ie nt s ( 1 .3±0 .4v s 2 .5± 1.6 , re s p e ct iv e ly , p <0 .00 1) .T he rat io o f G -ce lls t o D-c e lls w a s a ls o s ig n if ica nt ly h ig he r in inf e ct e d p at ie nt s co m p a re d w it h u n inf e ct e d p at ie nt s f o r b o t h g a s t ric a nd d uo d e na l u lce rs ( 5 .7± 2 .7 v s 3 .5±1. 9 , re s p e ct iv e ly , p <0 .00 1) . Co nc lu s io n s : T h e s e re s u lt s s t ro ng ly s ug g e s t t h at He lico b a ct e r py lo ri inf e ct io n ind uc e s re d uct io n o f t h e n u m b e r o f a nt ra l D-ce lls . T h e re s u lt ing re lat iv e hy p o f u nct io n o f t he in h ib it o ry act io n o f D-ce lls ag a ins t G -ce lls m ay b e re s p o ns ib le f o r in c re a s e d s e ru m g a s t rin s e c re t ion.