Blood Platelet Disorders

About: Blood Platelet Disorders is a research topic. Over the lifetime, 578 publications have been published within this topic receiving 18993 citations.

A critical reappraisal of the bleeding time.

Abstract: Since its initial invention by the French worker Milian in 1901, the bleeding time has been put forward as a clinically useful test in three contexts: diagnosis (particularly of platelet disorders), prediction of clinically important bleeding, and assessment of the adequacy of various forms of therapy. Attempting a complete review of the published experience with this test, we assessed 862 articles. Original bleeding time data appeared in 664 of these articles, from which we tabulated 1083 distinct studies in humans. ROC analysis, which characterizes the sensitivity and specificity of the test, was applied in every instance in which published data were adequate (34 studies). ROCs from 27 studies of the bleeding time in association with aspirin ingestion reveal high variability in the ability of the bleeding time to detect aspirin intake, and provide evidence against claims that recently devised bleeding time methods have improved discriminatory ability based on improved reproducibility. Two ROCs from surgical studies, in which the bleeding time was used to try to predict abnormal bleeding, were statistically indistinguishable from that of a completely noninformative test. In ROCs from five studies of abnormal bleeding in uremia, the test performed approximately the same as the platelet count or hematocrit (taken singly); in one of these studies, prothrombin consumption was determined and was a better predictor of bleeding than bleeding time, hematocrit, or platelet count. In the settings of renal biopsy (one study) and massive transfusion (one study), data allowed estimation of predictive value: in no instance was there evidence that the bleeding time significantly altered a priori estimates (based on prevalence) of the risk of bleeding. Linear regression analysis was applied to data from 23 studies relating platelet count to bleeding time, to assess published claims that the bleeding time and platelet count follow a predictively useful linear relationship. In 22 of 23 instances, the inverse relationship between bleeding time and platelet count was associated with broad statistical scatter, making it impossible to predict precisely one variable given the other. The pathophysiology of an abnormal bleeding time remains poorly understood. The bleeding time is affected by a large number of diseases, drugs, physiologic factors, test conditions, and therapeutic actions, not all of them platelet-related. The test is likely to remain widely used for the diagnosis of inherited disorders of platelet function, such as von Willebrand's syndrome, despite the lack of clear criteria for its use in this context.(ABSTRACT TRUNCATED AT 400 WORDS)

Platelet dysfunction in renal failure.

Abstract: Patients with end-stage renal disease suffer from complex hemostatic disorders. Uremic patients show a bleeding diathesis that is mainly due to abnormalities of primary hemostasis; in particular, platelet dysfunction and impaired platelet-vessel wall interaction. However, despite decreased platelet function, these patients have a high prevalence of cardiovascular and thrombotic complications. Platelet dysfunction in uremic patients is partially due to uremic toxins present in circulating blood. Dialysis improves platelet abnormalities and reduces, but does not eliminate, the risk of hemorrhage. Hemodialysis can even contribute to the bleeding through the continuous platelet activation induced by the interaction between blood and artificial surfaces. Thrombocytopenia, glomerular thrombosis, and thrombi in small arteries and glomerular capillaries are common pathological features in many renal diseases. Platelets are also involved directly in the pathogenesis of glomerular diseases through a variety of mechanisms, including release of active molecules, by enhancing immune complex deposition, and by altering glomerular permeability.

Platelet dysfunction and end-stage renal disease.

Abstract: Patients with end-stage renal disease (ESRD) develop hemostatic disorders mainly in the form of bleeding diatheses Hemorrhage can occur at cutaneous, mucosal, or serosal sites Retroperitoneal or intracranial hemorrhages also occur Platelet dysfunction is the main factor responsible for hemorrhagic tendencies in advanced kidney disease Anemia, dialysis, the accumulation of medications due to poor clearance, and anticoagulation used during dialysis have some role in causing impaired hemostasis in ESRD patients Platelet dysfunction occurs both as a result of intrinsic platelet abnormalities and impaired platelet-vessel wall interaction The normal platelet response to vessel wall injury with platelet activation, recruitment, adhesion, and aggregation is defective in advanced renal failure Dialysis may partially correct these defects, but cannot totally eliminate them The hemodialysis process itself may in fact contribute to bleeding Hemodialysis is also associated with thrombosis as a result of chronic platelet activation due to contact with artificial surfaces during dialysis Desmopressin acetate and conjugated estrogen are treatment modalities that can be used for uremic bleeding Achieving a hematocrit of 30% improves bleeding time in ESRD patients

Secretable storage pools in platelets.

Abstract: Knowledge gained during the past two decades has greatly increased our understanding of the roles of platelets in hemostasis, thrombosis, and other biological processes (1-3). However, much remains to be learned. The present review summarizes our current knowledge about granule-bound platelet substances that are released extracellularly after platelet stimula­ tion. We briefly review the in vitro responses of platelets to various agonists, emphasizing the granule-bound substances and the mechanism(s) involved in their storage and release. These substances (some of which are also present in plasma, adsorbed on platelets, or present in nonsecretable platelet pools) comprise the secretable storage pool substances of the platelet. Where information is available, we discuss the physiological significance of the secreted substances and their stability following release into the blood. Finally we review congenital and acquired disorders of hemostasis in which the deficiencies of storage pool substances have been described.