Thrombocytosis medical therapy

Often, no treatment is required or necessary for reactive thrombocytosis.

However, in primary thrombocytosis, if platelet counts are over 750,000 or 1,000,000, and especially if there are other risk factors for thrombosis. Aspirin at low doses is thought to be protective, and extreme levels are treated with hydroxyurea (a cytoreducing agent). The new agent anagrelide (Agrylin®) has recently been introduced for the treatment of essential thrombocytosis. However, recent studies show that anegrilide is not significantly more effective than traditionally used hydroxyurea (Harrison et al 2005).

Treatment should exclude spurious thrombocytosis secondary to mixed cryoglobulinemia, or cytoplasmic fragments from lymphoma, leukemia, hemolysis and burns. Look for splenomegaly (seen in CML, polycythemia.vera, AMM and myodysplastic syndrome). Consider measurement of ferritin, CRP (C-reactive protein), fibrinogen and ESR (erythrocyte sedimentation rate) as well as DIC (disseminated intravascular coagulation) parameters. Thrombopoeitin levels have not been shown to be helpful yet. Review smear with special attention to the presence/absence of schistocytes (DIC), teardrops/nucleated red blood cells (agnogenic myeloid metaplasia), Howell-Jolly bodies/target cells (post splenectomy), toxic granulations/Dohle bodies/neutrophillia/bands (infection). Essential thrombocytopenia is a diagnosis of exclusion. In these cases, giant clusters of platelets or megakaryocyte clusters may be seen. Less than 5% will have, cytogenetic abnormalities.

Bleeding should prompt discontinuation of platelet poisons. The patient should also be worked up for DIC. Acquired Factor V deficiency or von Willebrand disease can be seen in association with extreme thrombocytosis and is managed with factor replacement, fresh frozen plasma and/or platelet apheresis coupled with a platelet lowering agent (Hydrea or anagrelide)^[1]. Rarely, thrombocytosis is associated with thrombosis. For this reason, routine antiplatelet therapy is not necessary (exception post- coronary artery bypass graft-CABG) and has not shown to be effective in preventing thrombosis. Budd-Chiari, portal and splenic vein thrombosis occur and suggest an autonomous cause. Immediate platelet apheresis and a platelet lowering agent are advised for those with counts >800K. Work-up for hypercoagulable state is suggested (Protein C,S, ATIII, anticardiolipin, homocysteine, Factor V and prothrombin gene mutation).

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