Venom-Induced Recurrent Thrombocytopenia: A Model of Intervention-Driven Platelet Modulation

We present the case of a <i>Vipera ammodytes ammodytes</i> (<i>Vaa</i>, nose-horned viper)-bitten patient with recurrent thrombocytopenia. A 53-year-old patient envenomated by <i>Vaa</i> experienced three episodes of venom-dependent thrombocytopenia (4, 57 and 11 × 10⁹/L), all of which we managed with antivenom Fab fragments. Despite these three severe episodes of thrombocytopenia within 24 h, platelet function remained intact, as demonstrated by normal thromboelastometry and aggregometry (96, 126, and 150 U) results after antivenom was administered and the platelet count normalized. Furthermore, flow cytometry showed only 0.3-1.7% expression of P-selectin on platelets, indicating that platelets did not activate but remained functional during and after thrombocytopenia. We assessed platelet function using rotational thromboelastometry, which evaluates the overall kinetics of hemostasis, including clot formation and stability. We performed aggregometry, which also reflects platelet function, only when the platelet count was within the normal range. Flow cytometry quantified P-selectin expression as a key marker of platelet activation. This case demonstrates that a component of <i>Vaa</i> venom can repeatedly induce venom-dependent thrombocytopenia, which is reversible by intervention, while platelet function remains intact.