Hematologic Complications Associated with β-Lactam Antibiotics

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Abstract
Antibiotics of the β-lactam class can adversely affect the function of blood components in a variety of ways. Through immune mechanisms these antibiotics can cause destruction of erythrocytes, leukocytes, and platelets. These events are rare and usually reversible upon withdrawal of the drug. In rare instances β-lactam agents can inhibit blood coagulation through incompletely understood immune mechanisms. β-lactam agents may also interfere with normal hemostasis either through suppression of the biosynthesis of vitamin K-dependent procoagulants or through suppression of normal platelet function. In vitro studies demonstrated that the β-lactam antibiotics cefamandole and moxalactam had no direct inhibitory effects on vitamin K-dependent clotting factors; in vivo studies excluded any warfarin-like effect of these antibiotics. Thus, the complication of hypoprothrombinemic hemorrhage seen with broad-spectrum antibiotics may result from eradication of vitamin K-producing intestinal microorganisms. Moxalactam inhibited adenosine diphosphate (ADP)-induced platelet aggregation in vivo and at high concentrations in vitro, probably as a result of perturbation of the platelet membrane with masking of ADP receptors. Similar results were found with 27 of 33 β-lactam agents examined to date.

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