On the Influence of Normal and Leukemic Human Leukocytes on Blood Coagulation

Lisiewicz, J; Astaldi, G; Okulski, J; Merolla, R

doi:10.1159/000208701

Cited by 8 publications

(9 citation statements)

References 9 publications

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“…It is well established that procoagulant activity can be demonstrated in leukocytes (1)(2)(3)(4) and that this activity is related to the extrinsic (tissue factor) pathway of blood coagulation (4)(5)(6)(7)(8). In addition, it has been shown that the procoagulant activity present in leukocytes can be greatly enhanced by endotoxin.…”

Section: Introductionmentioning

confidence: 99%

The Stimulatory Effect of Platelets and Platelet Membranes on the Procoagulant Activity of Leukocytes

Niemetz¹,

Marcus²

1974

J. Clin. Invest.

119

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A B S T R A C T Leukocytes can generate procoagulant (tissue factor) activity when incubated with endotoxin. These studies were undertaken to determine whether platelets could influence the procoagulant activity generated by leukocytes. Intact or disrupted platelets (rabbit or human) enhanced the clot-promoting properties of rabbit leukocytes.The enhancing effect of human platelets on human leukocytes required the presence of human serum (devoid of factor VII and X activities). When platelets were incubated with endotoxin in the absence of leukocytes, no increase in their clot-promoting properties was discernible. However, a mixture of platelets, leukocytes, and endotoxin generated procoagulant activity which appeared rapidly and was fivefold greater than that produced by leukocytes incubated with endotoxin alone. The enhancement produced by platelets was even more pronounced if homogenates were used. The platelet effect was examined in more detail by the substitution of membranes, granules, and the "soluble" fraction for whole platelets in the test system. The stimulating activity was localized to the particulate fractions, i.e., membranes and granules. Prior treatment of platelet membranes with phospholipase C or gangliosides or by extraction of lipid resulted in loss of enhancing activity, whereas no inhibition was observed after exposure to neuraminidase or trypsin. It is proposed that platelets contribute a membrane lipoprotein surface which enhances the procoagulant activity generated by leukocytes in the presence of endotoxin. This mechanism may be involved in some of the clinical and pathologic manifestations of gram-negative sepsis with disseminated intravascular coagulation.

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Section: Introductionmentioning

confidence: 99%

The Stimulatory Effect of Platelets and Platelet Membranes on the Procoagulant Activity of Leukocytes

Niemetz¹,

Marcus²

1974

J. Clin. Invest.

119

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“…Extracts of these granulocytes shorten the re calcification times of normal plasma in vitro and can be used instead of platelets in the thromboplastin generation test. They also increase thrombin formation in the thrombin generation test [92,93]. The procoagulant activity of these granulocytes is, however, weaker than that of platelets.…”

Section: Chronic Granulocytic Leukemia Cells and Hemorrhagic Complicamentioning

confidence: 99%

“…It has been shown that these lymphocytes do not contain fibrinolytic activity [81,150]. Also, antithrombin activity is very low in these cells [93]. The possible role of the various proteolytic enzymes in the lymphocytes in inducing changes in hemostasis is not known.…”

Section: Lymphocytes Of Chronic Lymphocytic Leukemia and Hemorrhagic mentioning

confidence: 99%

Mechanisms of Hemorrhage in Leukemias

Lisiewicz¹

2008

Semin Thromb Hemost

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“…In the in vitro prothrombin consumption test leukemic myeloblasts show a little higher procoagulant activity than that of a normal leukocyte mass extract, but lower than that of a brain tissue extract. 57 ' 58 A myeloblast extract may be substituted for platelets in the thromboplastin generation test. The procoagulant activity of that extract is similar to that of platelets and markedly stronger than that of normal leukocyte mass extract.…”

Section: Leukemic Cells and Disseminated Intravascular Coagulationmentioning

confidence: 99%

Disseminated Intravascular Coagulation in Acute Leukemia

Lisiewicz¹

1988

Semin Thromb Hemost

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The mechanisms of hemorrhage in acute leukemias (AL) are related to the direct effect of leukemic cells infiltrating the vascular walls and affecting the blood coagulation, causing damage to the megakaryo cyte system, changes in liver function, and subsequent decrease in the synthesis of some blood coagulation factors, increase in blood fibrinolytic activity, and the disseminated intravascular coagulation 1-4 (DIC). The effects of antileukemic agents on the blood coagula tion system in patients with leukemia represent sepa rate problems. Hemorrhagic diathesis is one of the most severe complications of AL and is often the direct cause of death. The basic difference between the particular forms lies in the cytologic type of leu kocytes undergoing the leukemic proliferation. There are, moreover, some differences in the clinical evolu tion and the response to therapy between AL of the myeloblastic and the lymphoblastic types. The mor phologic classification of AL is still a subject of dis cussion and in that regard the French-AmericanBritish (FAB) and World Health Organization (WHO) classifications should be mentioned. The FAB classi fication divides AL into six types of acute nonlymphocytic leukemias, that is, acute myeloblastic leukemias (AML), designed as M 1 to M 6 , and three types of acute lymphoblastic leukemia (ALL) corresponding to L 1 to L 3 . 5 However, currently several other AL classifications have been proposed and difficulties of reproducing the morphologic classification at dif ferent centers and the uncertainty about the impor tance of such classifications for prognosis is still un resolved. 6

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On the Influence of Normal and Leukemic Human Leukocytes on Blood Coagulation

Cited by 8 publications

References 9 publications

The Stimulatory Effect of Platelets and Platelet Membranes on the Procoagulant Activity of Leukocytes

The Stimulatory Effect of Platelets and Platelet Membranes on the Procoagulant Activity of Leukocytes

Mechanisms of Hemorrhage in Leukemias

Disseminated Intravascular Coagulation in Acute Leukemia

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