Hội chứng giảm tiểu cầu do heparin: Cơ chế bệnh sinh, chẩn đoán và điều trị

Heparin-induced thrombocytopenia (HIT) is a serious and potentially life-threatening complication that can occur in patients receiving heparin therapy. It is characterized by a decrease in platelet count and an increased risk of thrombosis. HIT is a complex condition with a multifaceted pathogenesis, involving both immune and non-immune mechanisms. Understanding the underlying mechanisms, diagnostic approaches, and treatment strategies is crucial for effective management and prevention of this adverse drug reaction.

<h2 style="font-weight: bold; margin: 12px 0;">Pathogenesis of HIT</h2>

The pathogenesis of HIT is centered around the formation of antibodies against heparin-platelet factor 4 (PF4) complexes. Heparin, a commonly used anticoagulant, binds to PF4, a protein released from platelets. This complex then triggers the production of antibodies in susceptible individuals. These antibodies, known as HIT antibodies, bind to the heparin-PF4 complex on the surface of platelets, leading to platelet activation and aggregation. This process results in a decrease in platelet count, known as thrombocytopenia.

<h2 style="font-weight: bold; margin: 12px 0;">Diagnosis of HIT</h2>

Diagnosing HIT requires a combination of clinical suspicion, laboratory testing, and risk assessment. The clinical presentation of HIT can be variable, ranging from mild thrombocytopenia to severe thrombosis. Laboratory testing plays a crucial role in confirming the diagnosis. The most reliable test is the platelet factor 4 (PF4) antibody assay, which detects the presence of HIT antibodies in the blood. Other laboratory tests, such as the serotonin release assay, can also be helpful in supporting the diagnosis.

<h2 style="font-weight: bold; margin: 12px 0;">Treatment of HIT</h2>

The mainstay of treatment for HIT is the immediate discontinuation of heparin and the initiation of alternative anticoagulants. Direct thrombin inhibitors, such as argatroban and fondaparinux, are commonly used as they do not interact with PF4 and are not affected by HIT antibodies. In severe cases, plasmapheresis may be considered to remove the HIT antibodies from the circulation. Supportive care, including monitoring for thrombosis and bleeding, is essential.

<h2 style="font-weight: bold; margin: 12px 0;">Conclusion</h2>

Heparin-induced thrombocytopenia is a serious complication of heparin therapy that requires prompt recognition and management. Understanding the pathogenesis, diagnostic approaches, and treatment strategies is crucial for effective patient care. Early diagnosis and appropriate treatment can significantly reduce the risk of thrombosis and improve patient outcomes.