Depressed fibrinolysis in patients with acute leukaemia

Guarini, Anna; Mussoni, L.; Gugliotta, Luigi; Chetti, L.; Niewiarowski, Tomasz J.; Catani, Lucia; Macchi, Silvia; Donati, Maria Benedetta; Tura, S

doi:10.1111/j.1365-2141.1987.tb06918.x

Cited by 16 publications

(5 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although AML patients have an increased bleeding tendency (Estey et al , 1982; Guarini et al , 1987), there was no evidence of elevated sP‐selectin/platelet in plasma as an indication of recent platelet degranulation in 80% of the patients. In 10 patients sP‐selectin/platelet was increased.…”

Section: Discussionmentioning

confidence: 99%

Multiple platelet defects identified by flow cytometry at diagnosis in acute myeloid leukaemia

et al. 2004

View full text Add to dashboard Cite

SummaryPrevious findings of megakaryocytic hypogranulation and dysmegakaryocytopoietic features in acute myeloid leukaemia (AML) strongly indicate defects in platelet production. The bleeding tendency of these patients may result from dysregulated platelet production, resulting in thrombocytopenia as well as qualitative platelet defects. The present study examined platelet function at diagnosis in 50 AML patients by whole blood flow cytometry. Following in vitro platelet agonist stimulation, platelet activation markers were analysed and compared with 20 healthy individuals. To detect recent in vivo platelet activation, plasma soluble P-selectin (sP-selectin) was measured. Flow cytometric analysis of platelet activation markers demonstrated reduced CD62P [35AE6 vs. 118AE5 · 10 3 molecules of equivalent soluble fluorochrome (MESF); P < 0AE0001], CD63 (11AE3 vs. 50AE7 · 10 3 MESF; P < 0AE0001), and PAC-1 (41AE5 vs. 90AE5%; P ¼ 0AE0001) while reductions in CD42b were abnormal (45AE6 vs. 70%; P < 0AE0001). sP-selectin levels were similar in patients and healthy controls (0AE04 vs. 0AE27 fg/platelet; P ¼ 0AE84). The presented data indicate that AML pathogenesis may result in multiple platelet defects, involving adhesion, aggregation, and secretion and demonstrate that flow cytometry is a feasible method for platelet function analysis in patients with thrombocytopenia.

show abstract

Section: Discussionmentioning

confidence: 99%

Multiple platelet defects identified by flow cytometry at diagnosis in acute myeloid leukaemia

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Plasma levels of t-PA antigen were determined by a double antibody sandwich ELISA using anti t-PA goat IgO (Bio Pool, Umea, Sweden) as a coat, a home-made anti t-PA rabbit antiserum as a second antibody and peroxidase-labelled anti-rabbit goat IgO (Bio Rad Labs. Richmond, CA, USA) (10).…”

Section: Samplingmentioning

confidence: 99%

Defective Fibrinolytic Response in Atherosclerotic Patients – Effect of lloprost and Its Possible Mechanism of Action

Bertelé

Mussoni

et al. 1988

Thromb Haemost

View full text Add to dashboard Cite

SummaryPlasma fibrinolytic activity and tissue-type plasminogen activator (t-PA) were defective in response to venous stasis in five out of ten patients with peripheral occlusive artery disease. Discontinuous infusions of iloprost, a stable synthetic analogue of prostacyclin, restored a normal fibrinolytic response in all five patients but did not induce a parallel increase of plasma t-PA. These findings suggest that in addition to the possible benefits due to its vasodilatory and antiplatelet activity, iloprost may improve the fibrinolytic activity in patients with atherosclerotic disease, providing them with further antithrombotic protection. The profibrinolytic effect of iloprost seems not to depend on its ability to induce vascular t-PA release. Rather, it might be related to its inhibitory effect on PAI release from platelets, endothelial cells and/or hepatocytes. Venous occlusion test represents an easy diagnostic approach to fibrinolytic defects, even if related to arterial disease, and may help select patients who need therapeutic intervention.

show abstract

“…In one study [76] of patients with prostate carcinoma, increased fibrinogen levels at the time of diagnosis were associated with high death rates during the first year. Decreased fibrinolysis has also been described in patients with untreated acute leukemia, and this finding shared a significant correlation with the pressence of DIC [77].…”

Section: Procoagulant Activity (Present In Plasma Membrane Vesiclmentioning

confidence: 65%

Hemostasis in malignancy

Nand

Messmore

1990

American J Hematol

View full text Add to dashboard Cite

Hemostatic abnormalities are present in a majority of patients with metastatic cancer. These abnormalities can be categorized as 1) increased platelet aggregation and activation, 2) abnormal activation of coagulation cascade, 3) release of plasminogen activator, and 4) decreased hepatic synthesis of anticoagulant proteins like Protein C and antithrombin III. The abnormal activation of coagulation cascade is mediated through release of Tissue Factor, Factor X activators, and other miscellaneous procoagulants from the plasma membrane vesicles of tumor cells. Macrophages of a tumor-bearing host also produce increased amounts of Tissue Factor. Production of Factor X activators and macrophage Tissue Factor is decreased by warfarin. The ability of the tumor cells to produce platelet-aggregating activity and plasminogen activator parallels their metastatic potential in animal and experimental systems. These studies also show that antiplatelet agents and antibodies against plasminogen activator can suppress the metastatic process. One or more laboratory abnormalities of hemostasis can be shown in up to 95% of patients with metastatic cancer. These abnormalities, however, are unable to predict subsequent development of thromboembolic or hemorrhagic complications. Clinical complications occur in 9-15% of the patients in the form of thrombotic or hemorrhagic disorders. The therapy of tumor-related coagulopathy should be guided by its clinical expression. Subclinical DIC should not be treated. Coumadin is generally ineffective for therapy of thrombosis in cancer patients. There is no consensus regarding the use of heparin in acute promyelocytic leukemia (APL). The defibrination in APL may be from disseminated intravascular coagulation as well as systemic fibrinolysis, as shown by decreased alpha 2 antiplasmin levels. In such cases, epsilon aminocaproic acid plus heparin therapy may be of benefit.

show abstract

Depressed fibrinolysis in patients with acute leukaemia

Cited by 16 publications

References 21 publications

Multiple platelet defects identified by flow cytometry at diagnosis in acute myeloid leukaemia

Multiple platelet defects identified by flow cytometry at diagnosis in acute myeloid leukaemia

Defective Fibrinolytic Response in Atherosclerotic Patients – Effect of lloprost and Its Possible Mechanism of Action

Hemostasis in malignancy

Contact Info

Product

Resources

About