Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders.

Takahashi, Hiroyuki; Hattori, Akira; Shibata, Akira

doi:10.1620/tjem.138.71

Cited by 13 publications

(6 citation statements)

References 31 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Takahashi et a1 [38] showed that RCoF was decreased in only one patient out of 36 cases with CML, but in most cases the ratio of vWF:Ag/RCoF was high. This finding suggested that RCoF was decreased absolutely or relatively compared with vWF:Ag in CML.…”

Section: Discussionmentioning

confidence: 96%

“…Concerning the level of factor VIII in patients with chronic myeloproliferative disorders, Fabris et al [37] reported that RCoF was decreased with loss of large multimers of vWF:Ag in 57% of patients with polycythemia Vera or essential thrombocythemia. Takahashi et a1 [38] showed that RCoF was decreased in only one patient out of 36 cases with CML, but in most cases the ratio of vWF:Ag/RCoF was high. This finding suggested that RCoF was decreased absolutely or relatively compared with vWF:Ag in CML.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Acquired von Willebrand disease and storage pool disease in chronic myelocytic leukemia

Mohri

1986

American J Hematol

View full text Add to dashboard Cite

Platelet function was evaluated in 20 patients with chronic myelocytic leukemia (CML), all Ph positive. Seven showed abnormal epinephrine-induced aggregation, while four had impaired both ADP- and collagen-induced aggregation. The platelets of all patients aggregated with arachidonic acid, thus ruling out cyclooxygenase or lipoxygenase deficiency. The intracellular concentrations of ATP and ADP were significantly below normal, and the ratio of ATP/ADP was greater than normal in all 12 patients. ATP released from platelets by Lumi-aggregometer was reduced. In four patients with abnormal ristocetin-induced aggregation, vWF:Ag, RCoF, and FVIII:C were all reduced. No significant inactivation of factor VIII was induced in normal plasma by incubation with patient's plasma. The crossed immunoelectrophoretic analysis revealed that vWF:Ag in these patients was mainly composed of more anodic component as compared with that of normal plasma. The ratio of vWF:Ag/RCoF was significantly greater than normal. A marked increase of factor VIII and a rapid return of vWF:Ag and RCoF to the baseline after the 1-deamino-8-arginine vasopressin (DDAVP) infusion were observed. Transient increase in vWF:Ag after the infusion of DDAVP appeared with less anodic forms and in the same relative proportion as that in normal plasma. The present study shows that in some patients with CML storage pool disease occurs with acquired von Willebrand disease.

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Acquired von Willebrand disease and storage pool disease in chronic myelocytic leukemia

Mohri

1986

American J Hematol

View full text Add to dashboard Cite

show abstract

“…However, causal relationships between these abnormalities and complications have not been clearly established. We have previously reported that, in many patients with CMPD, plasma ristocetin cofactor (RCof) level is decreased as compared with von Willebrand factor antigen (vWf:Ag) even when its absolute concentration is either normal or elevated (Takahashi, Hattori & Shibata 1982). Recently, the abnormalities of the multimeric composition of vWf have been shown in some patients with essential thrombocythaemia (ET) and polycythaemia vera (PV) (Fabris et at.…”

mentioning

confidence: 99%

Multimeric composition of plasma von Willebrand factor in chronic myeloproliferative disorders

Tatewaki

Takahashi

Shibata

1988

Clinical &Amp; Laboratory Haematology

View full text Add to dashboard Cite

In chronic myeloproliferative disorders (CMPD) thrombohaemorrhagic complications occur occasionally in association with thrombocytosis. We studied the multimeric composition of plasma von Willebrand factor (vWf) in 15 patients with polycythaemia vera (PV), 12 with essential thrombocythaemia (ET) and eight with primary myelofibrosis (PMF). The relative content of large (multimer band greater than or equal to 11) multimers calculated by densitometer scan following SDS-agarose gel electrophoresis was 18.5 +/- 4.4% (mean +/- SD) in normal controls, 8.3 +/- 7.9% in PV, 8.1 +/- 4.6% in ET and 19.6 +/- 6.7% in PMF. The patients with PV and ET but not PMF had a significantly lower percentage of large multimers than normal controls (P less than 0.001). The relative content of large multimers was negatively correlated with WBC and platelet count (P less than 0.02 each) in PV. It was negatively correlated with platelet count (P less than 0.005) and was positively correlated with a ratio of ristocetin cofactor/vWf antigen (RCof/vWf:Ag) (P less than 0.01) in ET. These results indicate that acquired defects of vWf are quite common in PV and ET but not in PMF. In addition, some CMPD patients with high platelet counts completely lacked large multimers. The negative correlation of the relative content of large multimers with platelet count suggests that large multimers may be preferentially consumed during thrombocytosis or degraded by protease(s) from increased blood cells.

show abstract

“…Although evidence is scarce, one other study has also shown that levels of plasmin inhibitor were significantly decreased in patients with chronic MPD. 40 Our findings suggest that the levels of TAFI and plasmin inhibitor were, in part, influenced by the presence of an underlying MPD.…”

Section: Discussionmentioning

confidence: 58%

Impaired fibrinolysis as a risk factor for Budd-Chiari syndrome

Hoekstra

Guimarães

Leebeek

et al. 2010

Blood

View full text Add to dashboard Cite

In Budd-Chiari syndrome (BCS), thrombosis develops in the hepatic veins or inferior vena cava. To study the relationship between hypofibrinolysis and BCS, we measured plasma levels of fibrinolysis proteins in 101 BCS patients and 101 healthy controls and performed a plasmabased clot lysis assay. In BCS patients, plasminogen activator inhibitor 1 (PAI-1) levels were significantly higher than in controls (median, 6.3 vs 1.4 IU/mL, P < .001). Thrombin-activatable fibrinolysis inhibitor and plasmin inhibitor levels were lower than in controls (13.8 vs 16.9 g/mL and 0.91 vs 1.02 U/L, both P < .001). Median plasma clot lysis time (CLT) was 73.9 minutes in cases and 73.0 minutes in controls (P ‫؍‬ .329). A subgroup of cases displayed clearly elevated CLTs. A CLT above the 90th or 95th percentile of controls was associated with an increased risk of BCS, with odds ratios of 2.4 (95% confidence interval, 1.1-5.5) and 3.4 (95% confidence interval, 1.2-9.7), respectively. In controls, only PAI-1 activity was significantly associated with CLT. Analysis of single nucleotide polymorphisms of fibrinolysis proteins revealed no significant differences between cases and controls. This case-control study provides the first evidence that an impaired fibrinolytic potential, at least partially caused by elevated PAI-1 levels, is related to the presence of BCS. (Blood. 2010;115: 388-395)

show abstract

Profile of blood coagulation and fibrinolysis in chronic myeloproliferative disorders.

Cited by 13 publications

References 31 publications

Acquired von Willebrand disease and storage pool disease in chronic myelocytic leukemia

Acquired von Willebrand disease and storage pool disease in chronic myelocytic leukemia

Multimeric composition of plasma von Willebrand factor in chronic myeloproliferative disorders

Impaired fibrinolysis as a risk factor for Budd-Chiari syndrome

Contact Info

Product

Resources

About