Key result
High concentrations of cephalothin or penicillin G inhibited multiple platelet functions in vitro, including aggregation and release, likely by coating the platelet surface.
Why the study?
Do high concentrations of cephalothin or penicillin G inhibit platelet function in vitro?
Do high concentrations of cephalothin or penicillin G inhibit platelet function in vitro?
High concentrations of cephalothin and penicillin G inhibit platelet function in vitro, providing a mechanistic explanation for excessive bleeding in patients receiving high doses of these antibiotics.
May increase bleeding risk at high doses; leaves open clinical relevance without in vivo data.
High concentrations of cephalothin or penicillin G inhibit a number of the functions of human or rabbit platelets in citrated platelet-rich plasma (PRP) and in suspensions of washed platelets. The reactions shown to be inhibited are: ADP-induced shape change and the primary and secondary phases of aggregation and release induced by ADP or adrenaline in human cirtated PRP; release and aggregation of washed human platelets exposed to collagen, thrombin, vasopressin, or the ionophore A 23,187; aggregation of washed human platelets exposed to phytohaemagglutinin from Phaseolus vulgaris (PHA) or polylysine; release induced by concanavalin A or PHA in suspensions of washed platelets from rabbits; platelet adherence to a collagen-coated surface or to the damaged intimal surface of the rabbit aorta; platelet factor 3 availability; lysis of rabbit platelets by an antiserum directed against them; and clot retraction. Neither antibiotic affected serotonin-induced aggregation; a high concentration of cephalothin slightly inhibited the initial rate of serotonin uptake. Penicilloic acid showed about half the inhibitory effect of penicillin G on ADP-induced aggregation. In citrated human platelet-rich plasma, ampicillin and oxacillin inhibited ADP-induced aggregation to the same extent as similar concentrations of penicillin G; in suspensions of washed platelets, however, ampicillin was less inhibitory than penicillin G or oxacillin. Platelet ultrastructure, assessed by transmission electron microscopy, was not visibly altered. Evidence that the antibiotics become bound to platelets is the finding that platelets incubated with the antibiotics ans resuspended in fresh media showed less response to aggregating agents compared with control platelets. Penicillin G and related antibiotics may be inhibitory because they coat the platelet surface. Their effects on platelet functions are probably responsible for excessive bleeding and increased bleeding times observed in patients and volunteers receiving high doses of these antibiotics.
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Cazenave et al. (1977) studied this question. Cephalothin and Penicillin G vs. Control platelets was evaluated on Platelet function (aggregation, release, adherence, and clot retraction). High concentrations of cephalothin or penicillin G inhibited multiple platelet functions in vitro, including aggregation and release, likely by coating the platelet surface.
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