The Plasma Protamine Paracoagulation Test: Clinical and Laboratory Evaluation

Kidder, Wayne R.; Logan, L. J.; Rapaport, Samuel I.; Patch, Mary Jane

doi:10.1093/ajcp/58.6.675

Cited by 58 publications

(17 citation statements)

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“…The observation that a plasma concentration of 24% did not yield a two fold greater increase in turbidity than a plasma concentration of 12% might be due to the fact that not only soluble fibrin is diluted but all plasma proteins,· and albumin för example is said to have an inhibitory effect on protamine sulphate. A plasma fraction of 0.20 in the test provided better results than concentrations of 50 to 90% äs required for visual estimations by other authors (11,12,(24)(25)(26)). …”

Section: Kineticsmentioning

confidence: 62%

“…The initial turbidity of the plasma sample does not affect the results during kinetic measurements. Earlier studies used endpoint measurements after 5 -10 minutes or visual estimations 15 -30 minutes after addition of protamine sulphate (11,12,(24)(25)(26). In some studies additional controls were performed after 24 hours, in order to avoid false positive results through precipitation of fibrinogen (11,13).…”

Section: Kineticsmentioning

confidence: 99%

“…pH-value, protamine sulphate concentrations and plasma fractions were varied in order to establish optimal test conditions, äs in earlier studies of this kind (12,13,19,21,24,27).…”

Section: Kineticsmentioning

confidence: 99%

“…Several other authors have used protamine sulphate concentrations up to 2 g/l (14,25), and the effect of such concentrations on fibrinogen precipitation has been discussed controversially (10,11,15,24,29). Gurewich also used final protamine sulphate concentrations of 0.2 g/l or less in order to avoid fibrinogen precipitation (11).…”

Section: Kineticsmentioning

confidence: 99%

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Determination of Soluble Fibrin by Turbidimetry of its Protamine Sulphate-Induced Paracoagulation

Wieding¹,

Eisinger²,

Köstering³

1989

Clinical Chemistry and Laboratory Medicine

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Summary: Protamine sulphate-induced aggregation of soluble fibrin causes an increase of turbidity in the plasma sample, which can be measured by means of kinetic turbidimetry.A method was developed which is sufficiently sensitive for the determination of soluble fibrin in plasma without iüterfering with the sensitivity for fibrinogen. The performance of the assay was studied by analysing plasma samples with high concentrations of fibrinogen and soluble fibrin at different pH values, at different concentrations of plasma and protamine sulphate, and using different wavelengths and analysis times. Measurement of thrombin-induced fibrinogen-fibrin-transformation by the developed turbidimetric method, gave results that correlated well with the release of fibrinopeptide A.The new protamine sulphate method for turbidimetric dclcrmination of soluble fibrin is charactcrizcd by its practicability, rapid availability of reproducible, quantitative results, and ils economy ofreagenls and time in single and serial analysis. Therefore it seems well-suited for the routine diagnosis of hypercoagulability with increased fibrinogen turnover.

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Section: Kineticsmentioning

confidence: 62%

Section: Kineticsmentioning

confidence: 99%

“…pH-value, protamine sulphate concentrations and plasma fractions were varied in order to establish optimal test conditions, äs in earlier studies of this kind (12,13,19,21,24,27).…”

Section: Kineticsmentioning

confidence: 99%

Section: Kineticsmentioning

confidence: 99%

See 2 more Smart Citations

Determination of Soluble Fibrin by Turbidimetry of its Protamine Sulphate-Induced Paracoagulation

Wieding¹,

Eisinger²,

Köstering³

1989

Clinical Chemistry and Laboratory Medicine

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“…The protamine sulfate test, as described by Kidder et. al [128], is the most sensitive and clinically applicable test for detecting circulating soluble fibrin. A quantitative assay for fibrin monomer, the FM-test (KABI) has been shown to be a sensitive marker in the management of chronic DIC in cancer patients [129].…”

Section: Global Coagulation Tests In Dicmentioning

confidence: 99%

Disseminated Intravascular Coagulation

Bick¹,

Arun²

1999

Pathophysiol Haemos Thromb

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Disseminated intravascular coagulation (DIC) is a complex disorder, with pathophysiology being variable and highly dependent upon the triggering event(s), host response(s) and comorbid conditions. As a result of these complicated interactions, the clinical expression and laboratory findings are varied, thereby affecting the specifics of diagnosis and therapeutic approaches. The highly complex and variable pathophysiology of DIC often results in a lack of uniformity in clinical manifestations, a lack of consensus in the specific appropriate laboratory criteria of diagnosis, and a lack of specific therapeutic modalities. Indeed, recommendations for therapy are often difficult because the morbidity and survival is more dependent on the specific cause of DIC and because the generally used specific therapeutic approaches, which include for example heparin, low-molecular-weight-heparin antithrombin concentrate and protein C concentrate, have never been subjected to objective prospective randomized trials, except antithrombin concentrates. An analysis of the complex and varied pathophysiological events in DIC provide objective guidelines and criteria for the clinical diagnosis, the laboratory diagnosis, and the definition of severity. These data compounded by an understanding of complex and varied pathophysiology can be used for objective evaluation of therapeutic responses and results. DIC is an intermediary mechanism of disease usually seen in association with well-defined clinical disorders. The pathophysiology of DIC serves as an intermediary mechanism in many disease processes, which sometimes remain organ specific. This catastrophic syndrome spans all areas of medicine and presents a broad clinical spectrum that is confusing to many. Most physicians consider DIC to be a systemic hemorrhagic syndrome; however, this is only because hemorrhage is evident and often impressive. Less commonly appreciated is the profound microvascular thrombosis and sometimes, large vessel thrombosis. The hemorrhage is often simple to contend with in patients with fulminant DIC, but it is the small- and large-vessel thrombosis, with impairment in blood flow, ischemia, and associated end-organ damage that usually leads to irreversible morbidity and mortality. In conclusion, the pathophysiological mechanisms, clinical, and laboratory manifestations of DIC are complex in part due to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents, and agents which can block, blunt or modify cytokine activity and the activity of vasoactive substances appear to be of value. The complexity and variable degree of clinical expression suggests that therapy should be individualized depending o...

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Prothrombin Complex Concentrate

DeWitt¹

1977

Arch Intern Med

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The Plasma Protamine Paracoagulation Test: Clinical and Laboratory Evaluation

Cited by 58 publications

References 0 publications

Determination of Soluble Fibrin by Turbidimetry of its Protamine Sulphate-Induced Paracoagulation

Determination of Soluble Fibrin by Turbidimetry of its Protamine Sulphate-Induced Paracoagulation

Disseminated Intravascular Coagulation

Prothrombin Complex Concentrate

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