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        An Overview of Thrombocytosis in Rheumatoid Arthritis

        Een DGReview van"Pathologic thrombopoiesis of rheumatoid arthritis"
        Rheumatology International

        10/30/2003
        By Jill Taylor


        Clarification of the pathobiologic basis of thrombopoiesis in rheumatoid arthritis (RA) can increase understanding of the exact pathogenesis of megakaryocytopoiesis and improve management of the patients with inflammatory thrombocytosis, according to Turkish experts.

        Thrombocytosis, a frequent complication of RA, usually occurs during the active clinical stages of the disease. Although recent investigations have provided information regarding the possible link between the ongoing inflammatory events of RA, thrombocytosis, and their mediators, the exact pathogenetic mechanisms remain undetermined.

        In a recently published summary of current literature regarding the dual relationships of pathologic thrombopoiesis and inflammation of RA, Ihsan Ertenli, MD, and colleagues of Hacettepe University School of Medicine, Ankara, also discuss the underlying cytokine network and their experience regarding the dual relationships of the pathologic thrombopoiesis of RA.

        Megakaryocytopoiesis, the development of megakaryocytes (MKs) from pluripotent stem cells, is a complex process of cell division, endoreplication, abortive mitosis, and maturation that results in the biogenesis of platelets shed by mature MKs. Excessive proliferation of MKs and/or their progenitors results in thrombocytosis, the overproduction of platelets.

        The proliferation and maturation steps of megakaryocytopoiesis are regulated by several lineage non-specific megakaryocytopoietic cytokines, including IL-6, and the lineage-specific cytokine, thrombopoietin (TPO).

        IL-6 appears to predominate for the induction of megakaryopoiesis, and may be responsible for increased TPO in inflammatory events.

        Furthermore, IL-6 and TPO may be play a role in the development of reactive thrombocytosis in conditions such as infections, postsurgical stress, iron deficiency, splenectomy, RA, and some autoimmune disorders.

        Rheumatol Int 2003 Mar;23:2:49-60. Epub 2003 Feb 11. "Pathologic thrombopoiesis of rheumatoid arthritis"

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