Data on the natural course of gastrooesophageal reflux disease are sparse. One hundred and sixty six patients with typical reflux symptoms (heartburn and/or acid regurgitation) and pathologic pH monitoring (reflux time >8*2% upright and/or >3*0% supine) were studied.The patients were followed up by questionnaire and interview for a mean of 41 (seven to 86) months after diagnosis of reflux disease.

The staphylococcal enterotoxin serotype B (SEB)-induced enteric intoxication and the immediate-type reaction in the skin of unsensitized monkeys was used to define whether agents competing with SEB for target cell receptors may inhibit pathophysiological effects. For this purpose a duodenal provocation test was developed by use of a pediatric gastroscope, allowing the evaluation of the influence of antagonists on the intestinal disorder upon SEB challenge at the same duodenal site. First, carboxymethylation of histidine residues of SEB caused a complete loss of emetic and skinsensitizing activity without changing the immunological specificity. However, carboxymethylated SEB is a strong inhibitor of enteric intoxications and immediate-type skin reactions upon SEB challenge. Second, after immunization of BALB/c mice with monoclonal anti-SEB antibodies, monoclonal antiidiotypic antibodies (anti-Id) were obtained by the "hybridoma technique" and purification by idiotype-affinity chromatography. Anti-Id specifically inhibited the binding of horseradish peroxidase-labeled anti-SEB to the ligand, and SEB blocked as well the interaction of these two antibody species, indicating a high degree of binding-site selectivity. Anti-Id completely protected against emetic response and diarrhea upon duodenal provocation with SEB and inhibited immediate-type skin reactions as well. Further, anti-Id acted as an antagonist without triggering biologic functions themselves. This shows that anti-Id constitute a useful tool to protect against a bacterial toxininduced intestinal disorder.Staphylococcal enterotoxins (SE) are responsible for one of the most common types of food poisoning in humans (1). All SE produce emesis and diarrhea in humans and other primates as a result of oral administration, whereas the toxin appears to have little, if any, clinical effect in other laboratory animals (1). Although considerable efforts have been expended on attempts to define the pathogenesis, so far very little information has been available on the mode and cellular site of SE action in the gastrointestinal tract.Recently, however, evidence was provided that unsensitized monkeys develop an immediate-type reaction in the skin upon intradermal challenge with SE serotype B (SEB; ref.2). As shown by a series of experiments, SEB administered intradermally causes skin reactions by affecting mast cells (2). This type of nonimmunological mast cell stimulation by SEB offered a new approach, providing a model for investigating the mechanisms of SEB action. In addition, evidence was provided that carboxymethylation of SEB resulted in a loss of toxicity associated with the complete abrogation of skin-sensitizing activity without changing the immunological specificity of the toxin. It has been established that carboxymethylated SEB (CM-SEB) could compete with SEB for binding sites on the target-cell surface (2). To define whether SEB exerts its effect on mast cells by binding to specific celt-surface receptors or whether a less specific type of ligand-...

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Pantoprazole. a novel proton pump inhibitor. is a potent inhibitor of gastric acid secretion. In this review. data are presented from nine controlled. prospective. clinical pharmacodynamic investigations. The effects of oral and intravenous doses of pantoprazole (administered for 5-7 days) on continuously monitored 24-h intragastric pH and serum gastrin are discussed: oral pantoprazole 20 to 80 mg/day (given in the morning before breakfast) induced a dose-related increase in both the 24-h intra gastric pH and the serum gastrin profile. The effects of pantoprazole doses of 60 and 80 mg were not significantly different from those of the 40 mg dose. It was concluded that oral pantoprazole at 40 mg/day is the optimal antisecretory dose for the treatment of acid-related diseases. In two INTRODUCTION