SUMMARYBackground: The majority of gastro-oesophageal reflux disease (GERD) seems to be non-erosive reflux disease. Nonerosive reflux disease includes minimal change oesophagitis (whitish or reddish, oedematous change and erosion that is not regarded as mucosal break) and no endoscopic abnormalities. Aim: To investigate the accurate proportion of those with minimal change oesophagitis and to clarify its characteristics. In addition, we evaluated the effect of famotidine (40 mg/ day) in those with minimal change. Methods: Prospective endoscopic assessment was performed for consecutive 606 out-patients. Of the 582 patients suitable for analysis, 347 were non-treated. The latter were divided into those with erosive GERD or
A 63-year-old male complainined of right upper abdominal pain and jaundice. Laboratory data on admission showed hyperbilirubinemia, elevation of biliary enzymes and an extra ordinarily high value of serum CA19-9 (60,000 U/ml). Diagnostic imaging modalities including abdominal ultrasonogram, abdominal CT and PTC suggested a stone impaction of the common bile duct. Jaundice subsided after PTC-drainage in association with decreasing serum CA19-9 value, which returned to the normal level six weeks later. Spontaneous delivery of the stone via the fistula was confirmed by cholangiography through the drainage tube. Though there are few reports of such a high serum CA19-9 level, the possibility of benign biliary tract disease should be considered in patients showing an extraordinarily high serum CA19-9 value.
Background:
Polaprezinc has been shown to exert an anti‐oxidant property in a tube experiment, protect gastric mucosa from experimental ulcerations in vivo, and accelerate the healing of gastric ulcer in humans.
Aim:
To examine a possible protective effect of polaprezinc on oxidant‐mediated injury in primary monolayer cultures of rat gastric fundic mucosa.
Methods:
Cytotoxicity was quantified by measuring 51Cr release. Whether or not polaprezinc exerts an antioxidant property was investigated by determining the effect of this agent on hydrogen peroxide (H2O2)‐induced injury. The effects of polaprezinc on superoxide (O2–·) generation as well as on ethanol (EtOH)‐induced injury were also examined. Generation of O2–· was assessed by the reduction in cytochrome c.
Results:
H2O2 caused a time‐ and dose‐dependent increase in 51Cr release. The dose‐response curve of 51Cr release by H2O2 shifted to the right in the presence of polaprezinc. Polaprezinc, at submillimolar concentrations, prevented H2O2‐induced 51Cr release. EtOH also caused a dose‐dependent increase in 51Cr release, which was prevented by the addition of polaprezinc. The incubation of cells with EtOH caused an increase in cytochrome c reduction, as the concentrations of EtOH increased. Polaprezinc inhibited EtOH‐induced cytochrome c reduction. Protection by polaprezinc was microscopically associated with the prevention of monolayer disruption.
Conclusions:
Polaprezinc is antioxidative and directly protects gastric mucosal cells from noxious agents through its antioxidant properties in vitro. This finding may provide the theoretical basis for the usage of an antiulcer drug with antioxidant properties for the treatment of gastric inflammation, such as that induced by ethanol.
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