Malesci A, Basilico M, Bersani M, Bonato C, Ballarin E, Ronchi G
Institute of Internal Medicine, University of Milan, Italy.
Scand J Gastroenterol. 1988 Jun;23(5):602-6. doi: 10.3109/00365528809093919.
We measured serum pepsinogen I (sPG-I) in 269 patients undergoing upper GI endoscopy and then classified by endoscopic diagnosis, gastric mucosal histology, and smoking habit. Both ulcer-free and duodenal ulcer smokers had significantly higher sPG-I levels than their non-smoking controls. In contrast, sPG-I values were not different in smokers and non-smokers with gastric ulcer. In ulcer-free smokers the overall increase in sPG-I simply reflected the high prevalence of patients with superficial gastritis and elevated sPG-I levels. Conversely, in duodenal ulcer smokers the increase in sPG-I, which was related to the number of cigarettes smoked daily, was not an epiphenomenon of concomitant gastritis. The smoking-induced increase in sPG-I in duodenal ulcer is proposed to reflect an augmented pepsin secretory capacity, which can be of aetiologic significance in the association between cigarette smoking and duodenal ulcer.
我们对269例接受上消化道内镜检查的患者测定了血清胃蛋白酶原I(sPG-I),然后根据内镜诊断、胃黏膜组织学和吸烟习惯进行分类。无溃疡和十二指肠溃疡的吸烟者的sPG-I水平均显著高于其不吸烟的对照者。相比之下,胃溃疡患者中吸烟者和不吸烟者的sPG-I值并无差异。在无溃疡的吸烟者中,sPG-I的总体升高仅仅反映了浅表性胃炎患者的高患病率以及sPG-I水平的升高。相反,在十二指肠溃疡吸烟者中,sPG-I的升高与每日吸烟量有关,并非伴随胃炎的附带现象。十二指肠溃疡患者中吸烟导致的sPG-I升高被认为反映了胃蛋白酶分泌能力增强,这在吸烟与十二指肠溃疡的关联中可能具有病因学意义。