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Platelets are critical elements in the blood stream, supporting hemostasis (defense against bleeding), as well as performing even more complex tasks within networks of biological (immunity) and pathophysiological processes, such as cancer and ischemia/reperfusion injury. Changes in the number (and function) of platelets may have a substantial impact on any of these processes. The "simple" finding of a reduced platelet count (thrombocytopenia) has a history (origin) and a consequence (e.g., bleeding). This book brings together international experts to provide an up-to-date overview of the impact of thrombocytopenia from a clinical perspective.

Thrombocytopenia.

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Goal : Analyze the various randomized controlled trials and recent reviews based on platelet transfusion therapy in adult and pediatric patients with central thrombocytopenia secondary to chemotherapy or hematopoietic stem cell transplantation. Method: This is a retrospective study based on the research of the literature. The publications were journals, theses and articles by various authors. The materials were published in English from 2012 to 2015.The research was carried out on the basis of the computer data available on Pubmed. Results : It is recommended that prophylactic platelet transfusions be administered to adult non-hemorrhagic and pediatric patients with central thrombocytopenia using a platelet count threshold of 10.000/ ml. The transfusions of platelets at low or standard dose (1.1 x 10 11/m2 or 2.2 x 10 11/ m2, respectively) should be used in hospitalized patients. Pathogen-reduced platelets appear to be an acceptable alternative to standard platelets due to their reduced risk of infectious complications and their comparable efficacy to minimize clinically significant bleeding. Adjuvant treatments for prophylactic platelet transfusions, such as anti-fibrinolytics and rhTPO /TPO agonists, may have a beneficial effect in improving bleeding results in patients with central thrombocytopenia, particularly those with PTR. Future treatments may include laboratory-grown platelets and artificial platelet substitutes if they are found to be safe and effective in humans, and would be favorable to compensate for the know, disadvantages of standard platelet concentrates used in transfusions for patients suffering of thrombocytopenia.

Platelet transfusion --- Hematology --- Thrombocytopenia

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Heparin --- Thrombocytopenia --- Anticoagulants

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La thrombopénie auto immunitaire est une maladie sanguine qui peut-être sévère et, dans certains cas, même mortelle. C’est une maladie dans laquelle les plaquettes du patient sont détruites par son propre système immunitaire. La raison pur laquelle celui-ci détruit spécifiquement les plaquettes reste inconnue. Cependant, différents modèles animaux existent mais aucun n’est réellement adapté pour l’étude de cette maladie car ils ne sont pas limités à la thrombopénie auto immunitaire. Un nouveau modèle animal a donc été développé récemment dans notre laboratoire. Dans ce modèle, des souris sont immunisées par des injections hebdomadaires de plaquettes de rats. Ces souris développent une thrombopénie aigue et produisent des auto anticorps anti-plaquettes.
Dans ce travail, nous avons utilisé ce modèle animal pour produire des anticorps monoclonaux. Ces anticorps ont ensuite été soumis à une série de tests. Ces tests sont le Western blot, ELISA, la cytométrie et la rétraction du caillot. L’effet des anticorps ont notamment été testé in vivo. Nous avons ainsi confirmé que les souris soumises à cette immunisation produisent bel et bien des autos anticorps et que ces autos anticorps reconnaissent les plaquettes de rats et de souris. Nous avons aussi montré que ces anticorps, de classe IgM, reconnaissent CD42b et cd41 en Western blot.
Ensuite, nous avons montré que ces anticorps ont des effets pathogènes différent. Deux d’entre eux inhibaient la fonction plaquettaire in vitro tandis qu’ils étaient quatre à induire une thrombopénie in vivo. Finalement, nous avons constaté que ces anticorps reconnaissent mieux les plaquettes activées par la thrombine que les plaquettes non-activées .La raison n’en est, cependant, pas déterminée Autoimmune thrombocytopenic purpura is a bleeding disorder which can be severe and even life threatening. It is an autoimmune disease in which the patients own platelets are targeted and destroyed by his own immune system. The reason why the immune system targets self-platelets remains unknown. Different animal models of this disease, however, exist but none of these animal models are really suitable to study the disease because they are not restricted to immune thrombocytopenia. A new experimental model was therefore developed previously in our laboratory. In this model, mice are immunized with rat platelet by weekly injections. These mice develop a transient thrombocytopenia and anti-platelet auto antibodies are produced.
In the present work, we used this animal model to produce monoclonal anti bodies. These anti bodies were then submitted to a series of assays including western blot, ELISA, flow cytometry and clot retraction. Their thrombocytopenic effect was tested in vivo.
We first confirmed that the mice in this models do produce auto antibodies and that these anti bodies bind equally to rat and mouse platelets. We also showed that these auto bodies, which were all of the IgM isotype, possibly bind CD42b and CD41 in western blot.
We later showed that these anti bodies has different pathogenic effects both in vitro and in vivo. Two were found to inhibit platelet function in vitro and four lowered the platelet count in vivo. Finally, we showed that these anti bodies are more potent at binding activated platelets that resting platelets even though the reason for this is not clear

Autoantibodies --- Antibodies, Monoclonal --- Mice --- Thrombocytopenia --- Blood Platelets

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Blood --- Diseases. --- Clinical hematology --- Hematologic diseases --- Hematology --- Purpura, Thrombocytopenic, Idiopathic --- Thrombocytopenia --- Hematologic Diseases