Plasma .BETA.-thromboglobulin and platelet factor 4 in patients with chronic renal failure and effect of hemodialysis.

Endo, Yasuyuki; Mamiya, S; Satoh, Maki; Takahashi, Keiko; Harada, Tadashi

doi:10.1620/tjem.135.349

Cited by 14 publications

(12 citation statements)

References 12 publications

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“…Platelet aggregation was mea sured with Bryston's aggregometer (Canada) accord ing to Born [4], and platelet adhesiveness was mea sured with a glass bead filter using a modification of one of the authors [8]. Platelet factor 3 (PF3) was measured by the kaolin-clotting methods [ 15] and the kaolin-Russel viper venom method [26], Cyclic AMP in platelets was measured by the RIA method (Hoechst, FRG) [25] and platelet malondialdehyde (MDA) production was measured by the thiobarbituric acid turbidity method [10], /5-Thromboglobulin (Amersham Corp., England) and platelet factor 4 (PF4) (Abbott Laboratory, USA) were measured by the RIA method [13]. Factor XIII and fibrinogen in platelets were determined by single radial immuno diffusion using antisera against the individual pro teins (Behringwerke, FRG), and the level of fibrinog en in the platelets was determined by an FDP kit (Wellcome, USA) [9].…”

Section: Methodsmentioning

confidence: 99%

Factor XIII Deficiency Associated with Klippel-Weber Disease, Platelet Dysfunction and Cryofibrinogenemia

et al. 1983

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A 23-year-old woman with factor XIII deficiency was presented. The patient had no consanguinity, but familial traits were present. A bleeding tendency and poor wound healing had been noted in the patient since birth. She had hemangiomas in the leg and vulva (Klippel-Weber disease). Hematologic studies revealed platelet dysfunction, cryofibrinogenemia and mild chronic disseminated intravascular coagulation with prolonged PT and PTT, hypofibrinogenemia, a high turnover rate of ¹²⁵I-fibrinogen and mild elevation of fibrinogen-fibrin degradation products, β-thromboglobulin and platelet factor 4. A decrease in clot retraction and a marked reduction in maximal amplitude of thrombelastogram were also found. The assay of the factor XIII level was 10% by the antiserum inhibition method, and the assay of subunits A and S were 16 and 29%, respectively, by the electroimmunoassay method. Transamidase activity of factor XIII was 26%. The level of factor XIII of her sister was low, similar to that of the patient. The concentration of cold-insoluble globulin in EDTA-plasma was 36.5 mg/dl.

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Section: Methodsmentioning

confidence: 99%

Factor XIII Deficiency Associated with Klippel-Weber Disease, Platelet Dysfunction and Cryofibrinogenemia

et al. 1983

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“…Also, the inflammatory milieu in the setting of bacterial infections has been shown to enhance anti-PF4/heparin antibody formation and HIT [35, 36]. PF4/heparin antibody formation may also be facilitated in other conditions characterized by elevated plasmatic PF4 levels such as diabetes [73], atherosclerosis [74], and cardiovascular [75] and renal disease [76]. A study on diabetic patients with increased vascular risk found anti-PF4/heparin antibodies more frequently than in nondiabetic patients [77].…”

Section: Discussionmentioning

confidence: 99%

Anti-Platelet Factor 4/Heparin Antibody Formation Occurs Endogenously and at Unexpected High Frequency in Polycythemia Vera

Meyer

Steinmann

Lehmann

et al. 2017

BioMed Research International

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Background Myeloproliferative neoplasms (MPN) encounter thromboses due to multiple known risk factors. Heparin-induced thrombocytopenia (HIT) is a thrombotic syndrome mediated by anti-platelet factor 4 (PF4)/heparin antibodies with undetermined significance for thrombosis in MPN. We hypothesized that anti-PF4/heparin Ab might occur in MPN and promote thrombosis. Methods Anti-PF4/heparin antibodies were analyzed in 127 MPN patients including 76 PV and 51 ET. Screening, validation testing, and isotype testing of anti-PF4/heparin Ab were correlated with disease characteristics. Results Anti-PF4/heparin antibodies were detected in 21% of PV and 12% of ET versus 0.3–3% in heparin-exposed patients. Validation testing confirmed anti-PF4/heparin immunoglobulins in 15% of PV and 10% of ET. Isotype testing detected 9.2% IgG and 5.3% IgM in PV and exclusively IgM in ET. IgG-positive PV patients encountered thromboses in 57.1% suggesting anti-PF4/heparin IgG may contribute to higher risk for thrombosis in MPN. Overall, 45% of PV patients experienced thromboses with 11.8% positive for anti-PF4/heparin IgG versus 7.1% in PV without thrombosis. Conclusion Anti-PF4/heparin antibodies occur endogenously and more frequently in MPN than upon heparin exposure. Thrombotic risk increases in anti-PF4/heparin IgG-positive PV reflecting potential implications and calling for larger, confirmatory cohorts. Anti-PF4/heparin IgG should be assessed upon thrombosis in PV to facilitate avoidance of heparin in anti-PF4/heparin IgG-positive PV.

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“…Thromboxane B2 and 6-keto PGF1 a in plasma were measured by the RIA method (New England Nuclear, Boston, MA, USA) (Watanabe 1983). Q-Thromboglobulin (3-TG) (Amerssham, Buckinghamshire, England) and platelet factor 4 (PF4) (Abbott Laboratory, North Chicago, IL, USA) were ascertained by the RIA method (Endo et al 1981). …”

Section: Methodsmentioning

confidence: 99%

A new bleeding tendency due to hereditary hyper .ALPHA.2-macroglobulinemia.

Endo

Iwamoto

Mamiya

et al. 1988

Tohoku J. Exp. Med.

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Plasma .BETA.-thromboglobulin and platelet factor 4 in patients with chronic renal failure and effect of hemodialysis.

Cited by 14 publications

References 12 publications

Factor XIII Deficiency Associated with Klippel-Weber Disease, Platelet Dysfunction and Cryofibrinogenemia

Factor XIII Deficiency Associated with Klippel-Weber Disease, Platelet Dysfunction and Cryofibrinogenemia

Anti-Platelet Factor 4/Heparin Antibody Formation Occurs Endogenously and at Unexpected High Frequency in Polycythemia Vera

A new bleeding tendency due to hereditary hyper .ALPHA.2-macroglobulinemia.

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