A bleeding diathesis characterized by in-vitro platelet dysfunction and prolongation of the template bleeding time (TBT) has been reported in patients receiving latamoxef ('moxalactam'), but not cefotaxime or cefoperazone. Hypoprothrombinaemia has been associated with the use of both latamoxef and cefoperazone in seriously ill and malnourished patients. We administered either latamoxef, cefotaxime or cefoperazone intravenously, at dosages within the range recommended by each manufacturer, to 14 normal volunteers. Latamoxef caused a dose and time dependent defect in platelet function characterized in vitro by abnormalities in aggregation to adenosine diphosphate and in vivo by prolongation of the template bleeding time. In two out of two subjects, a single 4 g dose of latamoxef caused neither prolongation of template bleeding times nor aggregation abnormalities. Two out of two subjects receiving latamoxef 6 g/day for six days had progressive prolongation of bleeding times to 12 and 15 min. Two additional subjects receiving latamoxef 12 g/day for four days had prolongation of template bleeding times to greater than 20 min. Of four subjects receiving cefotaxime 12 g/day for seven days, none had prolongation of template bleeding times or abnormalities in platelet aggregations. Of four subjects receiving cefoperazone 6 g/day, none had significant prolongation of template bleeding times and one had abnormalities in aggregation attributed to inadvertent salicylate ingestion. Prolongation of the prothrombin time or activated partial thromboplastin time did not occur in any of the 14 volunteers. Latamoxef is more likely to interfere with platelet function than either cefotaxime or cefoperazone.