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In recent decades, the understanding, diagnosis, and treatment of haemorrhagic diseases have made great progress. This progress has improved patient care and a greater emphasis on evidence-based medicine. This book provides an in-depth review of primary hemostasis disorders. Each condition is described by including its background, pathophysiology, diagnosis, and treatment. Relevant references are provided for readers seeking more information. Tables are used to aid the presentation of knowledge. This book is for students in medicine, pharmacy, dentistry, and biology. They will find all the essential knowledge required for primary hemostasis disorders. It is also for all physicians from various specialities such as hematology, surgery, internal medicine, obstetrics, nephrology, cardiology, rheumatology, gastroenterology, etc, who manage patients with bleeding due to primary hemostasis disorder.
The presence of multiple limitations for bleeding time has led to the development of automated assays assessing primary hemostasis. Platelet closure time measured with the Platelet Function Analyzer (PFA) is an innovative approach that explores primary hemostasis. Closure time has largely replaced bleeding time in the hospital setting due to its greater applicability. From a technical point of view, the test is equivalent in vitro to the traditional in vivo bleeding time. Thus, closure time is also known as in vitro bleeding time. This book is a review of the literature on platelet closure time. It is a detailed presentation of the PFA test and an update of the current knowledge of the use of this test in exploring primary hemostasis and monitoring the antiplatelet agents (APA) treatment. Finally, the manuscript gives a comparative performance analysis of this test and the classical tests studying primary hemostasis.
Primary hemostasis represents all phenomena that lead to the initial closure of a ruptured blood vessel by the formation of a clot consisting essentially of platelets. The vascular endothelium is a thromboresistance surface. Vascular endothelium lesion will lead to vasoconstriction. Thus, platelets will come in contact with subendothelial thrombogenic components. Currently, knowledge of this process at the biochemical, pharmacological, and even molecular levels is very accurate. It aids in the diagnosis of diseases due to the impairment of one or more stages of primary hemostasis. Therefore, the support is more appropriate. However, a certain number of disorders still elude a precise diagnosis, justifying the continuation of the studies at a physiological or pathophysiological level. Hence, the analysis of such abnormalities may lead to major advances in understanding platelet pathology.
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