By Anne McLeod, MD

2009-12-07

Why exactly do sick patients get thrombocytopenia? As consultants, asked over and over again to answer these types of questions, we often simply write “multifactorial.” And sometimes in our day-to-day rush to get through the long list of things to be done, we forget to wonder about why exactly it happens (at least until the medical student asks us). For hemostasis and thrombosis consultants, the Special Symposium on the Basic Science of Hemostasis and Thrombosis is a chance to stop and wonder why again. This special interest session is scheduled for Tuesday morning from 7:30 to 9:00 in the Conference Auditorium AB of the Ernest N. Morial Convention Center.

Last year we learned about the fascinating interaction of neutrophils and platelets in severe sepsis and watched as platelets became ensnared in neutrophil extracellular traps. This year we will learn that platelets are not just passive victims of acute malarial infections but actually are involved in killing malarial parasites within red cells, valiantly giving their lives in the fight against the malaria infection with no bleeding in sight. Dr. Simon Foote from the University of Tasmania will present evidence from a mouse model in which murine-infected red cells preferentially bind platelets, and platelets are directly involved in killing malarial parasites within the red cells. In further experiments with P.falciparum grown in culture with human red cells, they were able to demonstrate similar findings for human platelets. This once again reminds us that the role of platelets extends far beyond just protection from bleeding, but also plays a significant role in our innate immunity.

Other highlights of the symposium include the identification of a new protein on the block, Kindlin-3. Dr. Tatiana Byzova of the Cleveland Clinic Foundation will describe how the study of two siblings with evidence of combined symptoms of recurrent bleeding and severe infections led to the discovery of Kindlin-3, which was missing in these siblings, and she will identify Kindlin-3 as a main regulator of integrin activation. Dr. Denisa Wagner of Harvard Medical School will shed light on the role of platelets in the maintenance of vascular integrity within tumors and propose that platelets may represent a target for the specific destabilization of tumor vessels. The last presentation, by Rudy Fuentes from the University of Pennsylvania, will demonstrate that infusion of cultured megakaryocytes in mice can lead to production of a clinically relevant level of functional platelets in thrombocytopenic mice. Could this be a treatment for thrombocytopenia in humans one day?

The symposium was established four years ago to highlight basic science breakthroughs in hemostasis and thrombosis by bringing them together in a special forum. Dr. David Lillicrap, co-chair of the symposium, said “The aim of this session is to provide an opportunity for ASH attendees to hear the latest advances in hemostasis and to see how they influence biological processes both within and outside the normal sphere of coagulation.” Tuesday morning, often a time reserved for packing suitcases, would be well spent by basic scientists and community hematologists alike attending this symposium. For although basic science will be the way the answers are unlocked, clinicians will be left to write the consult notes and answer the medical student, and the Special Symposium on the Basic Science of Hemostasis and Thrombosis will help us all answer why.

Dr. McLeod indicated no relevant conflicts of interest.

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