We investigated the effect of H. pylori therapy on serum concentrations of pepsinogens on 87 patients of gastro-duodenal disease. In addition, we intended to see whether serum pepsinogen can serve as markers of response to H. pylori eradication. In 48 successfully eradicated cases, there was a significant decrease in gastritis score, and was a significant fall in serum pepsinogen II (PG II) level, and was a significant increase in pepsinogen I / II ratio (PG I / II ratio). In contrast, no change in gastritis score, PG II, and PG I / II ratio were observed in 39 unsuccessfully eradicated patients. No change in serum pepsinogen I (PG I) level was observed in both groups. In provisional successfully eradicated cases in PG II of decrease greater than 30% in after treatment, there was a sensitivity of 83.3% and a specificity of 89.7%. For the PG I / II ratio of increased greater than 30% in after treatment, the sensitivity was 95.8%, and the specificity was 94.9%. These findings suggest that PG II, PG I / II ratio can be useful for clinical evaluation of eradication therapy.
To evaluate the mechanism of gastric adaptive relaxation (GAR), we designed and established the experimental system for the measurement of GAR in isolated stomach from the guinea-pig by modifying the method of Desai. We also investigated the roles of non-adrenergic, non-cholinergic (NANC) nerves and endogenous nitric oxide (NO) in GAR by using this system. The rapid increase in the capacity of isolated stomach was observed over a certain pressure as GAR. GAR was abolished by tetrodotoxin (10-6M) in the presence of atropine (3×10-6M) and guanethidine (5×10-6M). NG-nitro L-arginine (LNNA) (10-4M), a NO synthesis inhibitor, also abolished GAR. L-arginine (10-3M), a precursor for NO synthesis, reversed LNNA-induced impairment of GAR. Sodium nitroprusside (10-6-10-4M), a NO-donor, induced the gastric relaxation. These results suggest that GAR is mediated by NANC nerves, possibly via endogenous NO.
Up to now, the diagnosis of H. pylori infection has been made by the breath test using 13C-urea. In this study, 13C-urea breath samples were tested in 34 patients (peptic ulcer scar 17, chronic gastritis 17 cases) with an automated breath 13C analyzer (ABCA. Europa Scientific, Crewe, UK) and compared with the results of endoscopical diagnosis for H. pylori infection. Endoscopic and 13C-urea breath test (13C-UBT) were performed before eradicative medication. We described a modified protocol for the growth grade of H. pylori colonies in microbiology (H. pylori score), and for the δ13C area under curve (AUC ; permil*hr) obtained from each sample of expired breath. There was a significant correlation between δ13C-AUC and the δ13C level of each sample, but the correlation coefficient obtained at 10min (R2=0.582) was lower than that obtained at the other four time points (20min ; 0.891, 30min ; 0.949, 40min ; 0.946, 50min ; 0.946, 60min ; 0.820). The δ13C-AUC well correlated with H. pylori score (p<0.01), none of 26 H. pylori positive patients detected by culture was 13C-UBT negative (δ13C-AUC<8.2 permil*hr in mean + 2SD of H. pylori negative group). In conclusion, 13C-UBT using ABCA has high sensitivity and specificity, and it provides a non-invasive method for the detection of H. pylori urease activity.
The diagnostic criteria of endoscopic ultrasonography (EUS) in the management of polypoid lesions of the gallbladder was established by a retrospective study using 57 cases with polypoid lesions of the gallbladder that were all resected and confirmed histologically. By this study, EUS findings of polypoid lesions of the gallbladder were classified into the following six groups ; Type I with a foamy high echogram, Type II with a globular high echogram, Type III with a papillary high echogram, Type IV with a papillary solid echogram, Type V with a nodular solid echogram and Type VI with a nodular solid echogram including multiple spotty an-echoic areas which suggested the presence of Rokitansky-Aschoff sinus. Comparing the types of EUS findings with histological diagnosis, Type I and II corresponded to cholesterol polyps. Type III and IV contained benign pseudo tumors such as cholesterol polyp or hyperplastic polyp as well as tumorous lesions such as adenocarcinoma or adenoma. Type III with over 10 mm in size and IV with over 5 mm in size had a possibility of tumorous lesions. Type V usually corresponded to adenocarcinoma, and Type VI to adenomyomatous hyperplasia. From these results, the following criteria was established ; (1) Polypoid lesions showing Type I, II, III with less than 10 mm in size, IV with less than 5 mm in size and VI should be followed-up as benign diseases. (2) Polypoid lesions of Type III with over 10 mm in size and IV with over 5 mm in size was considered to be relative indications for surgery as tumors. (3) Polypoid lesions of Type V was an absolute surgical indication as malignant. The reliability of this EUS criteria was followingly evaluated by a prospective study using 94 cases with polypoid lesions of the gallbladder ; 32 cases with open or laparoscopic cholecystectomy and 62 cases with over one year follow-up observations. The criteria corresponded well with the histological or follow-up findings in Type I, II, III with less than 10 mm in size, IV with less than 5 mm in size, V and VI. It had, however, a tendency of over indications to surgery in Type III with over 10 mm in size and IV with over 5 mm in size because these types were widely set not to overlook tumorous lesions such as adenoma and small adenocarcinoma. From these results, it is apparent that this diagnostic criteria of EUS is effective in the management of polypoid lesion of the gallbladder though there are still some points to revise or improve.