AIM: To study basal pepsinogen I levels in patients with duodenal ulcer and in subjects with normal endoscopy, depending on Helicobacter pylori status. METHODS: One-hundred and one patients with duodenal ulcer and 74 controls with normal endoscopy were studied. Mean age and gender distribution were: 46 vs 42 years, and 74% vs 43% males, respectively. At endoscopy biopsies from the gastric antrum and body were obtained for histologic (H&E) and microbiologic (Gram and culture) study. Basal levels of serum pepsinogen I were measured (RIA). RESULTS: Among the subjects with a normal endoscopy, those with H. pylori infection had higher pepsinogen I levels (m +/- SD) than non-infected patients (77 +/- 27 vs 62 +/- 28 ng/ml; p < 0.05). Basal levels in duodenal ulcer patients were 107 +/- 38 ng/ml, higher (p < 0.001) than in the group with normal endoscopy (both with and without H. pylori). In multivariate analysis pepsinogen I levels were correlated with H. pylori infection (regression coef.= 17; SE= 8.1), duodenal ulcer (regr. coef.= 22; SE= 5.8) and smoking habit (regr. coef.= 24; SE= 5.2). CONCLUSION: Basal pepsinogen I levels were significantly higher in duodenal ulcer patients than in H. pylori infected subjects with normal endoscopy. The lowest levels corresponded to non-infected patients. Therefore, an additional factor other than H. pylori infection is likely involved in the hyperpepsinogenemia classically reported in duodenal ulcer patients.
AIM: To study basal pepsinogen I levels in patients with duodenal ulcer and in subjects with normal endoscopy, depending on Helicobacter pylori status. METHODS: One-hundred and one patients with duodenal ulcer and 74 controls with normal endoscopy were studied. Mean age and gender distribution were: 46 vs 42 years, and 74% vs 43% males, respectively. At endoscopy biopsies from the gastric antrum and body were obtained for histologic (H&E) and microbiologic (Gram and culture) study. Basal levels of serum pepsinogen I were measured (RIA). RESULTS: Among the subjects with a normal endoscopy, those with H. pylori infection had higher pepsinogen I levels (m +/- SD) than non-infectedpatients (77 +/- 27 vs 62 +/- 28 ng/ml; p < 0.05). Basal levels in duodenal ulcerpatients were 107 +/- 38 ng/ml, higher (p < 0.001) than in the group with normal endoscopy (both with and without H. pylori). In multivariate analysis pepsinogen I levels were correlated with H. pylori infection (regression coef.= 17; SE= 8.1), duodenal ulcer (regr. coef.= 22; SE= 5.8) and smoking habit (regr. coef.= 24; SE= 5.2). CONCLUSION: Basal pepsinogen I levels were significantly higher in duodenal ulcerpatients than in H. pylori infected subjects with normal endoscopy. The lowest levels corresponded to non-infectedpatients. Therefore, an additional factor other than H. pylori infection is likely involved in the hyperpepsinogenemia classically reported in duodenal ulcerpatients.
Authors: J P Gisbert; M Blanco; J M Mateos; L Fernández-Salazar; M Fernández-Bermejo; J Cantero; J M Pajares Journal: Dig Dis Sci Date: 1999-11 Impact factor: 3.199