The frequency of Helicobacter pylori was histopathologically evaluated in biopsy specimens of the gastric mucosa from 112 patients which endoscopically diagnosed as erosion. The specimens, histopathologically diagnosed as chronic gastritis, were divided into eight groups according to age, sex and location. The Helicobacter pylori infection was revealed in 65% of all specimens observed, and the frequency in patients of their sixties was lower than that of the forties. The frequency in the elder was the lowest in the transitional zone of the gastric mucosa. These findings indicate that the decrease in the frequency of Helicobacter pylori begins in the transitional zone and subsequently in the antrum.
We investigated the effect of 4-weeks famotidine administration (15mg/kg/day) on gastrin cell (G-cell), somatostatin cell (D-cell) and prostaglandin E2 (PGE2) of gastric mucosa in pyloric stenosis rats. As a result, the increase of G-cell number and serum gastrin level in pyloric stenosis rats were potentiated by famotidine administration. However, the increase of D-cell number in pyloric stenosis was remarkably abolished by famotidine administration, and G/D cell ratio was increased accordingly. Moreover, famotidine administration decreased PGE2 concentration in fundic mucosa of the stomach without altering PGE2 concentration in pyloric mucosa. Our results suggested that famotidine administration in pyloric stenosis had a possibility to worsen the balance of endocrine cell kinetics in stomach, and PGE2 in fundic mucosa would play a roll on the proliferation of D-cell in pyloric stenosis.
Effect of ursodeoxycholic acid (600mg/day 12 weeks) on liver function tests and bile acid metabolism were investigated in 6 patients with compensatory liver cirrhosis (CLC) and 6 with chronic active hepatitis (CAH). Serial determination of serum GOT, GPT and γ-GTP after the initiation of UDCA revealed significant reduction in mean levels of these enzymes after 4 weeks, and further improvement was observed at the end of the 12-weeks treatment regimen (CLC: 79.3%, 81.1%, 51.5% of initial values, respectively, CAH: 61.2%, 59.3%, 42.8%). On the other hand, after UDCA administration, serum total bile acid increased and UDCA became the predominant bile acid in CLC and CAH patients. Other endogenous bile acids decreased in both groups, but reduction rate of serum chenodeoxycholic acid level in CLC was smaller than that in CAH group (CLC: 86.1% of initial values, respectively, CAH: 54.2%). During UDCA treatment, apparent side effect was not observed. We suggest that UDCA administration might constitute effective treatment for compensatory liver cirrhosis as well as chronic hepatitis.