Helicobacter pylori eradication releases prolonged increased acid secretion following omeprazole treatment

被引:47
作者
Gillen, D
Wirz, AA
McColl, KEL [1 ]
机构
[1] Univ Glasgow, Dept Med & Therapeut, Glasgow, Lanark, Scotland
[2] Aberdeen Royal Infirm, GI Unit, Aberdeen, Scotland
关键词
D O I
10.1053/j.gastro.2004.01.004
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Rebound increased acid secretion has been observed at 2 weeks after discontinuing omeprazole treatment in Helicobacter pylori-negative, but not H. pylori-positive, subjects. It is unknown whether this is a prolonged phenomenon or whether a similar phenomenon appears later in H. pylori positives or is released by eradication therapy. The aims of this study were to answer these 3 questions. Methods: Twelve H. pylori-negative and 20 H. pylori-positive subjects were studied. Each had a basal, submaximal, and maximal pentagastrin-stimulated acid secretion study before, during, and at 7, 14, 28, 42, and 56 days after a 56-day course of omeprazole 40 mg/day. Ten of the H. pylori-positive subjects had their infection eradicated during the last week of treatment. Results: In the H. pylorinegative subjects, there was rebound secretion of submaximal (P < 0.003) and maximal (P < 0.003) acid output, which persisted until at least 56 days after discontinuing omeprazole. The H. pylori-uneradicated subjects had no rebound increased secretion other than in maximal acid output at 28 (P < 0.01) and at 42 days after treatment (P < 0.02). In those eradicated of H. pylori close to the end of omeprazole, there was rebound increased secretion of submaximal acid output (P < 0.04) lasting until 56 days and of maximal acid output (P < 0.01) lasting until 28 days after treatment. Conclusions: Rebound increased acid secretion following orneprazole is a prolonged phenomenon in H. pylorinegative subjects. There is little evidence of it in H. pylori-infected subjects, but eradicating the infection releases the phenomenon. The accentuated H. pylorirelated oxyntic gastritis induced by orneprazole is likely to protect against the rebound phenomenon.
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页码:980 / 988
页数:9
相关论文
共 45 条
[31]   EFFECTS OF 8 WEEKS CONTINUOUS TREATMENT WITH ORAL RANITIDINE AND CIMETIDINE ON GASTRIC-ACID SECRETION, PEPSIN-SECRETION, AND FASTING SERUM GASTRIN [J].
MOHAMMED, R ;
HOLDEN, RJ ;
HEARNS, JB ;
MCKIBBEN, BM ;
BUCHANAN, KD ;
CREAN, GP .
GUT, 1983, 24 (01) :61-66
[32]  
Mowat C, 1998, AM J GASTROENTEROL, V93, P20, DOI 10.1111/j.1572-0241.1998.020_c.x
[33]   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
[34]   GASTRIN RECEPTOR ANTAGONIST YM022 PREVENTS HYPERSECRETION AFTER LONG-TERM ACID SUPPRESSION [J].
NISHIDA, A ;
KOBAYASHIUCHIDA, A ;
AKUZAWA, S ;
TAKINAMI, Y ;
SHISHIDO, T ;
KAMATO, T ;
ITO, H ;
YAMANO, M ;
YUKI, H ;
NAGAKURA, Y ;
HONDA, K ;
MIYATA, K .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1995, 269 (05) :G699-G705
[35]   HISTAMINE-SECRETION FROM RAT ENTEROCHROMAFFIN-LIKE CELLS [J].
PRINZ, C ;
KAJIMURA, M ;
SCOTT, DR ;
MERCIER, F ;
HELANDER, HF ;
SACHS, G .
GASTROENTEROLOGY, 1993, 105 (02) :449-461
[36]   INTERLEUKIN-1 IS CYTOPROTECTIVE, ANTISECRETORY, STIMULATES PGE2 SYNTHESIS BY THE STOMACH, AND RETARDS GASTRIC-EMPTYING [J].
ROBERT, A ;
OLAFSSON, AS ;
LANCASTER, C ;
ZHANG, WR .
LIFE SCIENCES, 1991, 48 (02) :123-134
[37]   OMEPRAZOLE AND RANITIDINE, ANTISECRETAGOGUES WITH DIFFERENT MODES OF ACTION, ARE EQUALLY EFFECTIVE IN CAUSING HYPERPLASIA OF ENTEROCHROMAFFIN-LIKE CELLS IN RAT STOMACH [J].
RYBERG, B ;
BISHOP, AE ;
BLOOM, SR ;
CARLSSON, E ;
HAKANSON, R ;
LARSSON, H ;
MATTSSON, H ;
POLAK, JM ;
SUNDLER, F .
REGULATORY PEPTIDES, 1989, 25 (02) :235-246
[38]   Reflux esophagitis: A complication of Helicobacter pylori eradication therapy? [J].
Sacca, N ;
DeMedici, A ;
Rodino, S ;
DeSiena, M ;
Giglio, A .
ENDOSCOPY, 1997, 29 (03) :224-224
[39]   Neural and paracrine regulation of gastrin and gastric acid secretion [J].
Schubert, ML ;
Makhlouf, GM .
GASTROENTEROLOGY, 1996, 111 (03) :837-838
[40]  
SUNDLER F, 1989, SCAND J GASTROENTE S, V118, P39