Abstract
I read with interest the article ‘The diagnosis and treatment of acute pulmonary thromboembolism’ (TN Martin, AJB Brady. J R Coll Physicians Edinb 2009; 39: 107–12) and would like to give some comments.
Firstly, the authors did not mention important hereditary and acquired thrombophilic conditions such as antiphospholipid antibody syndrome, factor V Leiden and prothrombin gene mutations, protein C, protein S, antithrombin III deficiencies as risk factors for venous thromboembolism. In my opinion, they are worth mentioning.
Secondly, with increasing prophylactic and therapeutic use of heparin, I would like to point out that development of heparin-induced thrombocytopenia (HIT) and thrombosis (HITT) is not rare. The incidence for HIT ranges from 0.1% to 5% depending on the type of heparin used and the risk group of patients. Approximately 40% of patients with HIT subsequently develop thrombosis. Of note, 26% of patients are noted to have concurrent thrombocytopenia and thrombosis.1
The condition is usually typical in that thrombocytopenia (either below 150,000/mm3 or 50% decline in baseline platelet count) develops within 5–10 days of heparin use in patients who have had no heparin exposure or who have had remote history of exposure (more than 100 days). Rarely, precipitous fall in platelet count can occur within hours if there is recent exposure to heparin.1
The management of acute pulmonary embolism due to HITT is entirely different. In those patients, heparin must be avoided. Anticoagulation is commenced with direct thrombin inhibitors such as lepirudin or argatroban. Warfarin therapy should be postponed until there has been substantial resolution of thrombocytopenia as warfarin therapy is associated with a severe reduction in the natural anticoagulant protein C, making the hypercoaguable state worse during the acute phase of HITT.2
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