Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 579

Drugs can cause thrombocytopenia by a variety of mechanisms, including direct bone marrow suppression – for example, cytotoxic drugs, alcohol, and chloramphenicol – or by inducing an immune response. Those most commonly implicated are aspirin, paracetamol, antibiotics, anticonvulsants, diuretics, and other miscellaneous drugs such as tolbutamide, quinine, and quinidine. Heparin causes a characteristic syndrome of heparin‐induced thrombocytopenia (HIT), which, unlike other drug‐induced causes of thrombocytopenia that cause bleeding, is associated not only with decreased platelet survival and thrombocytopenia due to immune destruction but also with platelet activation and hence arterial and venous thrombosis.

Consequently, this condition is associated with severe morbidity due to severe venous or arterial thrombosis and mortality of around 30% if not recognized and treated. It is more common with unfractionated heparin than with low‐molecular‐weight heparin but can occur with either. Patients receiving heparin for both therapeutic indications, particularly cardiac patients treated with UFH, should have their platelet counts regularly monitored to anticipate this serious complication. Treatment of suspected HIT involves immediate withdrawal of heparin and commencement of an alternative method of anticoagulation, such as argatroban by IV infusion for acute HIT or fondaparinux given by daily subcutaneous injection for subsequent treatment or prophylaxis. Warfarin can make acute HIT more severe and should be withdrawn or reversed with vitamin K, and an alternative anticoagulant started.⁵