Helicobacter pylori gastritis and gastric physiology

被引:93
作者
McColl, KEL [1 ]
El-Omar, E
Gillen, D
机构
[1] Western Infirm & Associated Hosp, Dept Med & Therapeut, Glasgow G11 6NT, Lanark, Scotland
[2] Univ Aberdeen, Dept Med & Therapeut, Aberdeen, Scotland
关键词
D O I
10.1016/S0889-8553(05)70138-2
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
It is now recognized that Helicobacter pylori infection exerts profound and diverse effects on gastric acid secretory function and that the alterations in acid secretion depend on the pattern of gastritis caused by the infection. In patients with an antral predominant nonatrophic gastritis, there is acid hypersecretion leading to duodenal ulcer disease. In patients with an atrophic pangastritis, there is markedly reduced acid secretion and increased risk for gastric cancer. It is now recognized that acid secretion also modifies H. pylori gastritis and a person's premorbid acid secretory status may be an important factor in determining the pattern of gastritis that an individual develops. This two-way interaction between H. pylori gastritis and gastric acid secretion is important in understanding the role of H. pylori infection in the response to proton-pump inhibitor therapy: It explains the more profound control of gastric acid secretion in H. pylori-positive patients and why rebound acid hypersecretion is confined to H. pylori-negative subjects.
引用
收藏
页码:687 / +
页数:18
相关论文
共 60 条
[41]   Gastrin induces heparin-binding epidermal growth factor-like growth factor in rat gastric epithelial cells transfected with gastrin receptor [J].
Miyazaki, Y ;
Shinomura, Y ;
Tsutsui, S ;
Zushi, S ;
Higashimoto, Y ;
Kanayama, S ;
Higashiyama, S ;
Taniguchi, N ;
Matsuzawa, Y .
GASTROENTEROLOGY, 1999, 116 (01) :78-89
[42]   The gastric enterochromaffin-like cell: An enigmatic cellular link [J].
Modlin, IM ;
Tang, LH .
GASTROENTEROLOGY, 1996, 111 (03) :783-810
[43]   EFFECT OF HELICOBACTER-PYLORI ON GASTRIC SOMATOSTATIN IN DUODENAL-ULCER DISEASE [J].
MOSS, SF ;
LEGON, S ;
BISHOP, AE ;
POLAK, JM ;
CALAM, J .
LANCET, 1992, 340 (8825) :930-932
[44]   HELICOBACTER-PYLORI RELATED HYPERGASTRINEMIA IS THE RESULT OF A SELECTIVE INCREASE IN GASTRIN-17 [J].
MULHOLLAND, G ;
ARDILL, JES ;
FILLMORE, D ;
CHITTAJALLU, RS ;
FULLARTON, GM ;
MCCOLL, KEL .
GUT, 1993, 34 (06) :757-761
[45]   MUCOSAL TUMOR-NECROSIS-FACTOR-ALPHA, INTERLEUKIN-1-BETA, AND INTERLEUKIN-8 PRODUCTION IN PATIENTS WITH HELICOBACTER-PYLORI INFECTION [J].
NOACH, LA ;
BOSMA, NB ;
JANSEN, J ;
HOEK, FJ ;
VANDEVENTER, SJH ;
TYTGAT, GNJ .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1994, 29 (05) :425-429
[46]   ENTEROCHROMAFFIN-LIKE CELLS IN RAT STOMACH RESPOND TO SHORT-TERM INFUSION OF HIGH-DOSES OF CHOLECYSTOKININ BUT NOT TO LONG-TERM, SUSTAINED, MODERATE HYPERCCKEMIA CAUSED BY CONTINUOUS CHOLECYSTOKININ INFUSION OR PANCREATICOBILIARY DIVERSION [J].
NYLANDER, AG ;
CHEN, D ;
LILJA, I ;
AXELSON, J ;
IHSE, I ;
REHFELD, JF ;
SUNDLER, F ;
HAKANSON, R .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1993, 28 (01) :73-79
[47]  
ODERDA G, 1989, LANCET, V1, P690
[48]  
PETERS MN, 1983, GASTROENTEROLOGY, V85, P35
[49]   EFFECT OF HELICOBACTER-PYLORI ERADICATION ON ANTRAL GASTRIN-IMMUNOREACTIVE AND SOMATOSTATIN-IMMUNOREACTIVE CELL-DENSITY AND GASTRIN AND SOMATOSTATIN CONCENTRATIONS [J].
QUEIROZ, DMM ;
MENDES, EN ;
ROCHA, GA ;
MOURA, SB ;
RESENDE, LMH ;
BARBOSA, AJA ;
COELHO, LGV ;
PASSOS, MCE ;
CASTRO, LP ;
OLIVEIRA, CA ;
LIMA, GF .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1993, 28 (10) :858-864
[50]  
Qvigstad G, 1998, SCAND J GASTROENTERO, V33, P1244