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Effect of cobaltous chloride on aggregation of platelets from normal and afibrinogenaemic human blood
The aggregation of normal human platelets in vitro induced by ADP was severely inhibited after preincubation of platelet-rich plasma (PRP) with CoCl2. Platelets from a patient with congenital afibrinogenaemia did not aggregate until fibrinogen was added. This recovered response was also inhibited by CoCl2. The impairment of aggregation seemed to be due to the action of cobalt on surrounding fibrinogen and not to a direct action on the platelets themselves. These results illustrate another aspect of the potential toxicity resulting from the use of cobaltous salts in treating the anaemia of renal failure, in which bleeding disorders have been reported.
The aggregation of normal human platelets in vitro induced by ADP was severely inhibited after preincubation of platelet-rich plasma (PRP) with CoCl2. Platelets from a patient with congenital afibrinogenaemia did not aggregate until fibrinogen was added. This recovered response was also inhibited by CoCl2. The impairment of aggregation seemed to be due to the action of cobalt on surrounding fibrinogen and not to a direct action on the platelets themselves. These results illustrate another aspect of the potential toxicity resulting from the use of cobaltous salts in treating the anaemia of renal failure, in which bleeding disorders have been reported.