What is the most appropriate therapy for the following patient at this time?
A 68-year-old man presents to the emergency department with headache and shortness of breath. The patients oxygen saturation on room air is 90%, and he is tachycardic (110 beats/min) and tachypneic (26 breaths/min). On examination, the patients lungs are clear. The neurologic examination is completely normal. On laboratory testing, the patients platelet count is 1,600 ( 109/L. A chest CT scan is remarkable for bilateral pulmonary thromboemboli. The patients coagulation parameters and the rest of his blood counts are within normal limits.
A. Aspirin B. Clopidogrel C. Hydroxyurea plus aspirin D. Interferon alfa
Hydroxyurea plus aspirin-indications for therapy in essential thrombocytosis are based on the risk of thrombohemorrhagic complications. risk factors include age older than 60 years, a history of a thrombotic or bleeding event, and a platelet count above 1,500 ( 109/l. the risk of thrombosis can be safely and effectively reduced with the combination of low-dose aspirin and cytoreductive therapy. a 2005 study compared the efficacy of aspirin in combination with either hydroxyurea or anagrelide in 809 patients with et who were at high risk for vascular events. long-term control of the platelet count was achieved in both groups. however, anagrelide-treated patients were significantly more likely than patients in the hydroxyurea group to experience arterial thrombosis, serious hemorrhage, and transformation to myelofibrosis. on the other hand, the rate of venous thromboembolism was lower with anagrelide. these researchers concluded that hydroxyurea plus low-dose aspirin is superior to anagrelide. interferon alfa has demonstrated activity in reducing the platelet count in et, but the toxicity of this agent has been responsible for a high rate of early discontinuance. on the other hand, a high number of durable responses and improved compliance have been reported in a study of treatment using pegylated interferon. observations that interferon-based therapy preferentially targets jak2-v617f mutated clones await further confirmation.