Greco A V, Altomonte L, Ghirlanda G, Rebuzzi A G, Manna R, Bertoli A
Acta Hepatogastroenterol (Stuttg). 1979 Jun;26(3):190-4.
Fasting gastrinemia in cirrhotics (48.35 +/- 2.77 pg/ml) was higher than in normal controls (32.93 +/- 0.75 pg/ml; P less than 0.001). After insulin-induced hypoglycemia, the mean increase of gastrin above basal level was 42.29 +/- 1.92 pg/ml in controls and 10.85 +/- 5.05 pg/ml in cirrhosis (P less than 0.001). BAO was 2.53 +/- 0.36 mEq/h in controls and 0.42 +/- 0.004 mEq/h in cirrhotics (P less than 0.001). After i.v. insulin, TAO was 8.42 +/- 0.72 mEq/h in controls and 3.06 +/- 0.26 mEq/h in cirrhotics (P less than 0.001). The authors suggest that the lack of an adequate gastrin and acid response to the hypoglycemic stimulus in cirrhotics might be accounted for by a decreased insulin sensitivity.
肝硬化患者的空腹胃泌素血症（48.35±2.77 pg/ml）高于正常对照组（32.93±0.75 pg/ml；P＜0.001）。胰岛素诱导低血糖后，对照组胃泌素较基础水平的平均增加值为42.29±1.92 pg/ml，肝硬化组为10.85±5.05 pg/ml（P＜0.001）。基础胃酸分泌量（BAO）在对照组为2.53±0.36 mEq/h，在肝硬化患者中为0.42±0.004 mEq/h（P＜0.001）。静脉注射胰岛素后，最大胃酸分泌量（TAO）在对照组为8.42±0.72 mEq/h，在肝硬化患者中为3.06±0.26 mEq/h（P＜0.001）。作者认为，肝硬化患者对低血糖刺激缺乏足够的胃泌素和胃酸反应可能是由于胰岛素敏感性降低所致。
