There is ample evidence that indeed, erythropoietin regulates platelets. It also regulates megakaryocytes which produce platelets. Endothelial cells, blood clotting, and calcium (Ca++) which regulates blood pressure are also regulated. A number of diseases and clinical conditions may be favorably treated by erythropoietin therapy as listed below. Uremia, aplastic anemia, refractory anemia, myelodysplastic syndrome, bone marrow transplants, post-hepatitic aplastic anemia, extremely low birth weight infants, uremic thromboembolism, hemodialysis and thrombocytopenia patients are benefited from erythropoietin therapy. Erythropoietin does not support platelet production during antiviral therapy. The response to erythropoietin is dose dependent both in men and in mice and rats. If high dose of recombinant human erythropoietin is used, it will stimulate platelet production, which is a transient effect. Expanded erythropoiesis exerts a negative impact on platelet production. Secondary thrombocytopenia was not related to splenic pooling, and its very slow correction after cessation of erythropoietin therapy was not compatible with changes in platelet survival. Rather, it is consistent with stem cell competition between erythroid and megakaryocytic development. Low dose erythropoietin administration improved platelet adhesion/aggregation and ameliorated prolongation of bleeding time in chronic renal failure rats. Long-term erythropoietin (150 U/kg, twice weekly for 6 weeks) administration led to Ca++ levels normalization. Detailed studies revealed that improved Ca++ signaling with erythropoietin is associated with increased Ca++ uptake and expanded Ca++ stores in platelets.
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