Impact of Automation on the Quantitation of Low Molecular Weight Markers of Hemostatic Defects

Fareed, Jawed; Walenga, Jeanine M.; Bick, Rodger L.; Bermes, Edward W.; Messmore, Harry L.

doi:10.1055/s-2007-1005036

Cited by 16 publications

(9 citation statements)

References 87 publications

(107 reference statements)

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“…Noting decreases in PF4 levels or BTG levels after the institution of antiplatelet therapy may also be indicative of clinical efficacy for stopping or blunting increased fibrin deposition. [234][235][236] Some investigations, however, have failed to show decreases in PF4 or BTG levels in patients with arterial occlusive disease being treated with antiplatelet drugs. 237 Newer methods available to assess platelet hyperactivity and "consumption," most of which are amenable to full automation, are summarized in Table 16 and consist of MPV and molecular markers of platelet reactivity.…”

Section: Hyperactive Prethrombotic Plateletsmentioning

confidence: 99%

Platelet Function Defects: A Clinical Review

Bick¹

1992

Semin Thromb Hemost

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Platelet dysfunction, especially acquired forms, are common causes of hemorrhage, especially in association with trauma and surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients developing easy and spontaneous bruising, mild to moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the presence of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable and platelet aggregation or lumi-aggregation should be done in appropriate clinical situations. The mainstay of therapy for essentially all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects, of course, should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should promptly be discontinued.

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Section: Hyperactive Prethrombotic Plateletsmentioning

confidence: 99%

Platelet Function Defects: A Clinical Review

Bick¹

1992

Semin Thromb Hemost

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“…Although this is rather high, hopefully batch processing of specimens in the future will reduce the cost factor. 11 The significance of Bβ RP testing in the clinical laboratory is obvious and direct application to diagnostic, prog nostic, and therapeutic evaluation can be readily adapted.…”

Section: Assay Limitations and Precautionsmentioning

confidence: 99%

Diagnostic Efficacy of a Simple Radioimmunoassay Test for Fibrinogen/Fibrin Fragments Containing the Bβ 15-42 Sequence

Walenga¹,

Fareed²,

Mariani³

et al. 1984

Semin Thromb Hemost

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A simple RIA method for B beta 15-42 RPs has been evaluated in our laboratory to investigate experimental and clinical fibrinolytic states. The assay utilizes bentonite precipitation to remove cross-reacting fibrinogen. Due to the heterogeneity in molecular weights of the B beta RPs, the results are expressed as nanograms per milliliter. The linear range of the assay is 2 to 40 ng/ml, with a capability of detecting up to 200 ng/ml. A special anticoagulant mixture (heparin or EDTA/aprotinin) is required for sample collection. Certain precautions in the care and handling of specimens are also necessary. Increased levels of B beta RPs were observed in the following conditions: malignancy (associated with increased release of tissue plasminogen activators), pancreatitis, liver diseases, pregnancy, and postexercise testing (associated with increased release of tissue plasminogen activators). Increased levels of B beta RPs were also found during thrombolytic therapy, anabolic steroid treatment, prothrombin complex concentrate therapy, blood component therapy, and low molecular weight heparin subcutaneous therapy (associated with an increase in tissue plasminogen activator release). Our studies suggest that B beta RPs are sensitive molecular markers of the endogenous activation of fibrinolytic system and may provide useful diagnostic information on a pathologic process that often remains undetectable by routine laboratory methods.

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“…Products of activated macrophages, such as platelet activating factor, 21 and the generation of thrombin through the production of tissue factor result in platelet activation. Exercise, emotional stress, tobacco, and epinephrine infusion have been shown to increase the levels of platelet markers in the blood.…”

Section: Platelet Release In Pathologic States Mechanismsmentioning

confidence: 99%

“…38 Thromboxane A 2 has a very short half-life, but it can be quantitated by measuring its stable degradation product, thromboxane B 2 (TXB 2 ), a substance readily assayed by radioimmunoassay (RIA) methods. 21,35,80,83 The majority of clinical studies use RIA methods and the plasma levels of PF4, BTG, and TxB 2 to assess the role of platelets in the pathologic processes in question. It is recognized that the platelet may be an innocent bystander rather than an active participant in some processes, and that the resultant platelet release products arise as a result of platelets being destroyed in the reaction even though they did not participate in the primary pathologic process.…”

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confidence: 99%