Pathophysiology and implications for treatment of acute respiratory distress syndrome.

Acute respiratory distress syndrome is a complex group of signs and symptoms caused by direct or indirect lung injury. In spite of decades of research, it is still associated with a high mortality rate. Pathogenesis of this disease is related to alveolar endothelial and epithelial cell injury and associated release and sequestration of inflammatory mediators and cells, including cytokines and neutrophils, respectively. Pharmacologic interventions have been largely unsuccessful, and ventilation strategies to support oxygenation while limiting ventilator associated lung injury have not demonstrated any significant reductions in the mortality rate. However, novel therapies are in development, based on the knowledge of the pathologic processes of acute respiratory distress syndrome. In this article an overview of the disease process and mediator involvement is presented, followed by a review of pharmacologic and ventilation treatments currently in use or under study.

Norfloxacin interaction with antacids and minerals.

The urinary excretion of norfloxacin was measured in eight healthy volunteers after its co-administration with a variety of over-the-counter preparations, each containing a different metal ion. Commonly used doses of ferrous sulphate, zinc sulphate, aluminium hydroxide and magnesium hydroxide reduced the 24 h urinary excretion of norfloxacin by 50 to 90%. Bismuth subsalicylate had no significant effect. In vitro experiments demonstrated the formation of complexes between norfloxacin and iron, zinc, aluminium, and magnesium ions, respectively. Many pharmaceuticals contain the same metal ions that caused significant interactions with norfloxacin. The efficacy of norfloxacin treatment may be compromised when it is taken concurrently with preparations containing these metal ions.