Lanas A, Miguel G, Escolar F, Sainz R, Abos D
Hospital Reina Sofía, Tudela, Navarra.
Rev Esp Enferm Dig. 1990 Jun;77(6):397-402.
At present the mechanisms by which the use of tobacco produces a damaging effect on duodenal ulcerous disease are not clearly understood. This paper reports the results of a study of basal and postprandial gastrin and pepsinogen I (PG I) levels of 74 duodenal ulcer (DU) patients and 18 controls in relation to their smoking habits. There was no difference between the UD group and the control group as far as basal gastrin levels were concerned, but there was in the PG I levels (107 +/- 54 ng/ml in UD vs. 69 +/- 30 ng/ml in control) (p less than 0.05). The postprandial gastrin and PG I responses in 34 UD subjects only differed in relation to smoker/non-smoker status; there was no correlation with age less than greater than 35, positive family history or duration of illness. Patients who had had UD less than 10 years showed higher postprandial PG I levels; however, this group included the 83.3% smokers with UD. It was concluded that chronic smoking is clearly related to the existence of hyperpepsinogenemia I, and probably also to postprandial hypergastrinemia in UD sufferers.
目前，烟草的使用对十二指肠溃疡病产生损害作用的机制尚不清楚。本文报告了一项针对74例十二指肠溃疡（DU）患者和18例对照者的基础和餐后胃泌素及胃蛋白酶原I（PG I）水平与其吸烟习惯关系的研究结果。就基础胃泌素水平而言，DU组和对照组之间没有差异，但PG I水平存在差异（DU组为107±54 ng/ml，对照组为69±30 ng/ml）（p<0.05）。仅34例DU受试者的餐后胃泌素和PG I反应因吸烟/不吸烟状态而有所不同；与年龄小于或大于35岁、阳性家族史或病程无关。患DU时间少于10年的患者餐后PG I水平较高；然而，该组包括83.3%的DU吸烟者。研究得出结论，长期吸烟显然与I型高胃蛋白酶原血症的存在有关，可能也与DU患者的餐后高胃泌素血症有关。
