Rebound acid hypersecretion after long-term inhibition of gastric acid secretion

被引:79
作者
Fossmark, R
Johnsen, G
Johanessen, E
Waldum, HL
机构
[1] Norwegian Univ Sci & Technol, Fac Med, Dept Canc Res & Mol Med, N-7489 Trondheim, Norway
[2] St Olavs Hosp, Dept Surg, Trondheim, Norway
[3] St Olavs Hosp, Dept Internal Med, Gastroenterol Sect, Trondheim, Norway
关键词
D O I
10.1111/j.1365-2036.2004.02271.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Rebound acid hypersecretion develops after the use of acid inhibitors. Aim: To estimate the duration of hypersecretion and to elucidate the role of the enterochromaffin-like (ECL) cell in rebound acid hypersecretion. Methods: Patients waiting for anti-reflux surgery who had used a proton pump inhibitor daily > 1 year were included. All patients discontinued taking acid inhibiting drugs after the operation. Basal and pentagastrin stimulated acid output was measured at 4, 8, 16 and 26 weeks postoperatively. Oxyntic mucosal biopsies were collected before and 26 weeks after the operation for counting of histidine decarboxylase (HDC) immunoreactive cells. Serum chromogranin A (CgA) and gastrin were measured before and at 4, 8, 16 and 26 weeks after the operation. Results: Pentagastrin stimulated acid secretion was higher at 4 and 8 weeks than at 26 weeks after the operation. Gastrin and CgA were significantly reduced at 4 and 8 weeks, respectively. The number of HDC immunoreactive cells was reduced by 60% at 26 weeks postoperative. Discussion: Rebound acid hypersecretion lasts more than 8 weeks, but less than 26 weeks after long-term proton pump inhibition. Conclusion: The findings indicate that not only the parietal cell mass, but also ECL cell mass and activity are involved in the mechanism of acid hypersecretion.
引用
收藏
页码:149 / 154
页数:6
相关论文
共 36 条
[1]  
Bakke I, 2000, ACTA PHYSIOL SCAND, V169, P29
[2]  
BILCHIK AJ, 1989, SURGERY, V106, P1119
[3]   TROPHIC EFFECT OF GASTRIN ON THE ENTEROCHROMAFFIN LIKE CELLS OF THE RAT STOMACH - ESTABLISHMENT OF A DOSE-RESPONSE RELATIONSHIP [J].
BRENNA, E ;
WALDUM, HL .
GUT, 1992, 33 (10) :1303-1306
[4]   Gastric mucosa during treatment with lansoprazole: Helicobacter pylori is a risk factor for argyrophil cell hyperplasia [J].
Eissele, R ;
Brunner, G ;
Simon, B ;
Solcia, E ;
Arnold, R .
GASTROENTEROLOGY, 1997, 112 (03) :707-717
[5]   TOXICOLOGICAL STUDIES ON OMEPRAZOLE [J].
EKMAN, L ;
HANSSON, E ;
HAVU, N ;
CARLSSON, E ;
LUNDBERG, C .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1985, 20 :53-&
[6]   AUGMENTED POSTPRANDIAL GASTRIC-ACID SECRETION DUE TO EXPOSURE TO RANITIDINE IN HEALTHY-SUBJECTS [J].
FRISLID, K ;
AADLAND, E ;
BERSTAD, A .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1986, 21 (01) :119-122
[7]   REBOUND NOCTURNAL HYPERSECRETION AFTER 4 WEEKS TREATMENT WITH AN H-2-RECEPTOR ANTAGONIST [J].
FULLARTON, GM ;
MCLAUCHLAN, G ;
MACDONALD, A ;
CREAN, GP ;
MCCOLL, KEL .
GUT, 1989, 30 (04) :449-454
[8]   Helicobacter pylori eradication releases prolonged increased acid secretion following omeprazole treatment [J].
Gillen, D ;
Wirz, AA ;
McColl, KEL .
GASTROENTEROLOGY, 2004, 126 (04) :980-988
[9]   Problems related to acid rebound and tachyphylaxis [J].
Gillen, D ;
McColl, KEL .
BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY, 2001, 15 (03) :487-495
[10]   Rebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status [J].
Gillen, D ;
Wirz, AA ;
Ardill, JE ;
McColl, KEL .
GASTROENTEROLOGY, 1999, 116 (02) :239-247