beta-thromboglobulin and platelet factor 4 levels in retinal vein occlusion.

SummaryTo determine whether platelets play a role in the pathogenesis of retinal vein occlusion (RVO), platelets and coagulation were evaluated in 28 patients with RVO. Platelet coagulant activities concerned with the initiation and early stages of intrinsic coagulation were 2–4 fold increased in 9 patients with acute primary RVO but not in patients with acute secondary (10 patients) or chronic (9 patients) RVO. Platelet factor 3 activity, platelet aggregation, serotonin release by platelets and plasma coagulation were normal in all patients. Platelets may provide a trigger mechanism for venous thrombosis in the eye when local conditions permit.

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Half-Life of Platelet Factor 4 (PF-4) in Plasma and Platelets from Macaca Mulatta

Thrombosis and Haemostasis ◽

10.1055/s-0038-1649203 ◽

1977 ◽

Vol 37 (01) ◽

pp. 073-080 ◽

Cited By ~ 5

Author(s):

Knut Gjesdal ◽

Duncan S. Pepper

Keyword(s):

Macaca Mulatta ◽

Half Life ◽

Human Platelet ◽

Gel Filtration ◽

Platelet Factor 4 ◽

Active Protein ◽

Platelet Factor ◽

Membrane Bound

SummaryHuman platelet factor 4 (PF-4) showed a reaction of complete identity with PF-4 from Macaca mulatta when tested against rabbit anti-human-PF-4. Such immunoglobulin was used for quantitative precipitation of in vivo labelled PF-4 in monkey serum. The results suggest that the active protein had an intra-platelet half-life of about 21 hours. In vitro 125I-labelled human PF-4 was injected intravenously into two monkeys and isolated by immuno-precipita-tion from platelet-poor plasma and from platelets disrupted after gel-filtration. Plasma PF-4 was found to have a half-life of 7 to 11 hours. Some of the labelled PF-4 was associated with platelets and this fraction had a rapid initial disappearance rate and a subsequent half-life close to that of plasma PF-4. The results are compatible with the hypothesis that granular PF-4 belongs to a separate compartment, whereas membrane-bound PF-4 and plasma PF-4 may interchange.

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Beta-Thromboglobulin (βtg) and Platelet Factor 4 (PF4) in Patients with Myeloproliferative Diseases

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648896 ◽

1994 ◽

Vol 72 (03) ◽

pp. 484-485

Author(s):

Fabrizio Fabris ◽

Guido Luzzatto ◽

Maria Luigia Randi ◽

Giuseppe Cella

Keyword(s):

Platelet Factor 4 ◽

Platelet Factor ◽

Myeloproliferative Diseases

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Release of Platelet Factor 4 in Vivo during Intravascular Coagulation and in Thrombotic States

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651237 ◽

1968 ◽

Vol 19 (03/04) ◽

pp. 578-583 ◽

Cited By ~ 11

Author(s):

R Farbiszewski ◽

S Niewiarowski ◽

K Worowski ◽

B Lipiński

Keyword(s):

Coronary Thrombosis ◽

Laboratory Diagnosis ◽

Tolerance Test ◽

Platelet Factor 4 ◽

Thrombin Time ◽

Significant Elevation ◽

Platelet Factor ◽

Thrombotic Diseases ◽

Disseminated Intravascular Clotting

SummaryPlatelet factor 4 released from platelets into the circulating blood was determined using both the heparin thrombin time and paracoagulation methods. It has been found that thrombin injected intravenously into rabbits releases large amounts of this factor. Infusion of plasmin does not release this factor and this finding may be of importance for the differential diagnosis between disseminated intravascular clotting and primary fibrinolysis. PF4 is not released during the hyper coagulable condition induced by HgCl2 intoxication. Only small amounts of this factor are released after contact factor infusion.A significant elevation of extraplatelet PF4 was found in 23 patients with fresh coronary thrombosis and in 9 patients with thrombophlebitis and thromboembolic complications.The significance of the above findings for the pathogenesis, treatment and laboratory diagnosis of thrombotic diseases with particular reference to heparin tolerance test is discussed.

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Comparison between Platelet Factor 4/Heparin Complexes ELISA and Platelet Aggregation Test in Heparin-induced Thrombocytopenia

Thrombosis and Haemostasis ◽

10.1055/s-0038-1649823 ◽

1995 ◽

Vol 74 (02) ◽

pp. 804-805 ◽

Cited By ~ 8

Author(s):

Philippe Nguyên ◽

Chantal Droullé ◽

Gérard Potron

Keyword(s):

Platelet Aggregation ◽

Platelet Factor 4 ◽

Platelet Factor ◽

Heparin Induced Thrombocytopenia ◽

Heparin Complexes

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Hypercoagulability and High Lipoprotein(a) Levels in Patients with Central Retinal Vein Occlusion

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648808 ◽

1994 ◽

Vol 72 (01) ◽

pp. 039-043 ◽

Cited By ~ 46

Author(s):

Francesco Bandello ◽

Silvana Vigano’ D’Angelo ◽

Mariella Parlavecchia ◽

Alessandra Tavola ◽

Patrizia Della Valle ◽

...

Keyword(s):

Retinal Vein Occlusion ◽

Central Retinal Vein Occlusion ◽

Specific Treatment ◽

Fibrin Deposition ◽

Heparin Cofactor Ii ◽

Lipoprotein A ◽

Vein Occlusion ◽

Acute Event ◽

D Dimer ◽

Central Retinal Vein

SummaryA series of coagulation parameters and lipoprotein(a) (Lp(a)) were explored in plasma from 40 patients with central retinal vein occlusion (CRVO, non-ischemic type n = 12; ischemic type n = 28) free of local and systemic predisposing factors, 1 to 12 months after the acute event. Forty age- and sex-matched patients with cataract served as controls. Prothrombin fragment 1.2 (FI.2), D-dimer, FVII:C - but not FVII: Ag - were higher and fibrinogen was lower in CRVO patients than in controls. Patients with non-ischemic CRVO had higher FI .2 and FVII:C and lower heparin cofactor II than patients with ischemic CRVO. Lp(a) levels greater than 300 mg/1 were observed in 12 patients with CRVO and in 4 controls (30% vs 10%, p <0.025). Patients with high Lp(a) - consistently associated with the S2 phenotype - had higher FVII:C, FVII:C/Ag ratio, and fibrinogen than the remaining CRVO patients. Plasma FI.2 and D-dimer correlated fairly in controls (r = 0.41) and patients with normal Lp(a) levels (r = 0.55), but they did not in the group of patients with high Lp(a) (r = 0.19), where the latter parameter was negatively related to D-dimer (r = −0.55). There was no dependence of the abnormalities observed on the time elapsed from vein occlusion. The findings of activated FVII and high FI.2, D-dimer, and Lp(a) are not uncommon in patients with CRVO. Increased thrombin formation with fibrin deposition and impaired fibrinolysis may play a role in the pathophysiology of CRVO and require specific treatment

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Neutralization of Antithrombin VI (Fibrinogen Breakdown Products) with Platelet Antiheparin Factor (Platelet Factor 4)*

Thrombosis and Haemostasis ◽

10.1055/s-0038-1654885 ◽

1965 ◽

Vol 14 (03/04) ◽

pp. 490-499 ◽

Cited By ~ 4

Author(s):

S Niewiarowski ◽

R Farbiszewski ◽

A Popławski

Keyword(s):

Zinc Acetate ◽

Antithrombin Iii ◽

Platelet Factor 4 ◽

Breakdown Product ◽

Platelet Factor ◽

Chromatography Column ◽

Antiheparin Activity

SummaryIt has been found that fibrinogen breakdown product – antithrombin VI – is neutralized by the purified preparation of platelet factor 4, obtained by means of zinc acetate precipitation and DEAE chromatography column. It has been suggested that antiheparin activity of platelet factor 4 and its ability to neutralize antithrombin VI may be related to the same protein.The purified preparation of platelet factor 4 does not influence the fibrinogen – fibrin conversion by thrombin. This means that platelet factor 2 and platelet factor 4 are not the same substance.Crude platelet extracts neutralize antithrombin III and V. However, the purified product did not interferes with the action of these antithrombins.

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Coagulation Disorders in Thrombocythaemia, a Study of Seven Cases

Thrombosis and Haemostasis ◽

10.1055/s-0038-1655460 ◽

1962 ◽

Vol 07 (01) ◽

pp. 114-128 ◽

Cited By ~ 2

Author(s):

Stefan Niewiarowski ◽

Halina Zywicka ◽

Zbigniew Latałło

Keyword(s):

Liver Parenchyma ◽

Platelet Factor 4 ◽

Coagulation System ◽

Severe Bleeding ◽

Clotting Factors ◽

Platelet Factor ◽

Antiheparin Activity ◽

Thromboplastic Activity ◽

Bleeding Episodes ◽

Routine Coagulation

SummaryThe blood coagulation system has been studied in 7 patients with thrombocythaemia. 4 of these patients had thrombocythaemia after splenectomy, 2 of them had thrombocythaemia associated with myeloid leukemia, and 1 thrombocythaemia associated with polycythaemia. Severe bleeding episodes were noted in 5 cases, 2 patients had only mild bleeding symptoms.Each patient was examined several times. The period of observations varied from 2 months to 3 years. Platelet count varied from 350 000 to 3 800 000 per mm3.Bleeding time and tourniquet test were normal in all cases. Routine coagulation and fibrinolysis studies did not reveale characteristic abnormalities in plasma clotting factors. A decrease of prothrombin complex components was observed in 4 cases. This disturbance was due to the coexisting injury of liver parenchyma or myeloid changes but not to an increase of platelets or to the abnormalities in the platelet system.An increase of antiheparin activity was found in the plasma of 4 patients. This activity is probably due to the escape of platelet factor 4 from destroyed or qualitatively changed platelets into plasma.Platelet clotting factors were investigated in isolated platelet suspensions, A significant decrease of platelet factor 1 was observed in all patients and a decrease of platelet factor 4 in 5 patients. In 2 cases platelet factor 4 increased. Platelet thromboplastic activity showed a great variety of disturbances in conformity with other workers observations.Recent views on the pathogenesis of bleedings in thrombocythaemia are discussed. On the basis of their own investigations the authors suggest that the significant disturbances of platelet function may contribute to the development of bleeding, and that the increase of antiheparin activity in plasma may produce hypercoagulability and favorize the formation of thrombi.

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