Reactive thrombocytosis usually is mediated by increased release of a number of cytokines in response to infections, inflammation, vasculitis, tissue trauma, and other factors. Thrombopoietin (TPO), the primary cytokine for platelet production and maturation, and interleukin (IL)-6, are usually initially elevated in response to the primary events mentioned earlier, and they stimulate an increase in platelet production. However, serum or plasma levels of these cytokines do not seem to be correlated with degree of thrombocytosis. Other cytokines may participate in the stimulation of platelet production. They include IL-3, IL-11, granulocyte-macrophage colony-stimulating factor (GM-CSF), and erythropoietin. These cytokines are released directly or indirectly during the primary events. When the original stimulation stops, the platelet count then returns to the reference range.
In severe infections, such as bacterial meningitis, one of the causes may be a rebound phenomenon after initial thrombocytopenia due to rapid consumption of platelets. This most commonly occurs in neonates and infants, indicating the labile nature of platelet count control in these subjects. The rebound thrombocytosis also is observed in the recovery phase of chemotherapy-induced thrombocytopenia and during the recovery phase of immune thrombocytopenic purpura (ITP).
In some instances, such as chronic hemolytic anemia, the stimulus (hypoxia) to produce cytokines persists, causing long-term elevation of platelet counts.
Although thrombocytosis in association with iron deficiency anemia is well documented, the mechanism remains unclear. A recent study showed that an elevation of erythropoietin, although observed in thrombocytosis patients with iron deficiency anemia, had no correlation with platelet count. Other cytokines potentially responsible for thrombocytosis, such as IL-6 and TPO, were not elevated.
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