高胃泌素血症：一种新机制。

Hypergastrinaemia: a new mechanism.

作者信息

Deprez P H, Ghosh P, Goodlad R A, Lacey S L, Millership S, Playford R J, Lee C Y, Calam J

机构信息

Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.

出版信息

Lancet. 1991 Aug 17;338(8764):410-1. doi: 10.1016/0140-6736(91)91034-r.

DOI:10.1016/0140-6736(91)91034-r

PMID:1678084

Abstract

The mechanism by which lack of gastric acid causes hypergastrinaemia was investigated in seven patients with pernicious anaemia. Perfusion of gastric juice from the fasting patients (adjusted to pH 7.0) into the stomachs of conscious rats caused a significant rise in plasma gastrin (median 14 [range 2-20] pmol/l to 27 [12-65] pmol/l; p less than 0.01), whereas perfusion of bicarbonate buffer (18 [13-23] pmol/l to 20 [9-25] pmol/l) or gastric juice from a duodenal ulcer patient (also pH 7.0; 13 [3-30] pmol/l to 17 [9-27] pmol/l) had no significant effect. During gastric lavage at pH 7.0 the median plasma gastrin concentration of the pernicious anaemia patients fell from 320 (63-1760) pmol/l to 125 (46-760) pmol/l (p less than 0.03).

摘要

对7名恶性贫血患者研究了胃酸缺乏导致高胃泌素血症的机制。将空腹患者的胃液（调至pH 7.0）灌注到清醒大鼠胃内，可使血浆胃泌素显著升高（中位数从14[范围2 - 20]pmol/L升至27[12 - 65]pmol/L；p<0.01），而灌注碳酸氢盐缓冲液（从18[13 - 23]pmol/L至20[9 - 25]pmol/L）或十二指肠溃疡患者的胃液（也是pH 7.0；从13[3 - 30]pmol/L至17[9 - 27]pmol/L）则无显著影响。在pH 7.0进行洗胃期间，恶性贫血患者的血浆胃泌素浓度中位数从320（63 - 1760）pmol/L降至125（46 - 760）pmol/L（p<0.03）。