Template Bleeding Time and Clinical Hemorrhage in Myeloproliferative Disease

Murphy, Scott; Davis, Joan L.; Walsh, Peter N.; Gardner, Frank H.

doi:10.1001/archinte.1978.03630330051014

Cited by 40 publications

(16 citation statements)

References 19 publications

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“…In agreement with previous reports, platelets of patients with PT had a decreased response to agonists [3,4]. In spite of this fact, other reports have found that activated platelets of patients with PT produce increased amount of thromboxane B2 [15,16].…”

Section: Discussionsupporting

confidence: 92%

“…Different studies have found an impairment of the platelet aggregation [3,4], while others have reported the presence of platelet aggregates either in platelet-rich plasma [5] or in citrated whole blood [6], suggesting that platelets of patients with PT could also be hyperactive. It has been described that phospholipase activity in thrombin-activated platelets of patients with PT is increased even though most of these patients had abnormal platelet aggregation studies [7].…”

Section: Introductionmentioning

confidence: 98%

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Phospholipase A2 activity in platelets of patients with primary thrombocythemia

Vecino

Cesar

2006

Platelets

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Patients with primary thrombocythemia (PT) have both, bleeding and thrombotic events. Although platelet aggregation tests are usually abnormal, synthesis of thromboxane B2 (TxB2) by platelets is increased. This feature could be the consequence of an increased phospholipase activity or a facilitated metabolism of arachidonate by prostaglandin synthetase pathway. We studied the activity of phospholipase A2 as well the arachidonate metabolism in platelets of patients suffering from PT. Eleven patients and 11 controls were included. Platelets were labelled with [14C]arachidonic acid ([14C]AA). Lost of radioactivity from phospholipids and new radioactive prostanoids were evaluated in calcium ionophore A23187 activated platelets, to explore phospholipase A2 activity. This assay was also carried out in aspirin-incubated platelets. We also studied the formation of prostanoids in platelets activated by radioactive free arachidonic acid. Platelet aggregation studies of patients were abnormal. [14C]AA incorporation in platelet phospholipids was normal. Ionophore activated platelets from patients and controls lost 26.1 +/- 8.3% and 24.1 +/- 10.5% of radioactivity, respectively, mainly from phosphatidylcholine. The main arachidonate metabolite was 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE), which comprised 14.1 +/- 5.1% of the radioactivity released from phospholipids in patients, and a similar amount in the controls (14.4 +/- 7.5%). Formation of TxB2 was also similar in patients (5.5 +/- 1.2%) and controls (4.9 +/- 2.9%). Formation of 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT) was also normal. Ionophore A23187 activation of aspirinized platelets of patients released 19.5 +/- 7.4% of radioactivity from phospholipids, which was completely metabolized to HETE. Formation of prostanoids HETE, HHT and TxB2 by arachidonic acid activated platelets of patients was normal. Phospholipase A2 activity as well both cyclooxygenase and lipoxygenase activities in platelets of patients with PT were found to be normal.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 98%

Phospholipase A2 activity in platelets of patients with primary thrombocythemia

Vecino

Cesar

2006

Platelets

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“…As previously noted [20,21,28] the low percentage of template bleeding time alteration demonstrate that this parameter is not correlated with the degree of functional platelet defects in MPD and cannot be considered as a reliable marker for these diseases. The occurrence of thrombohemorrhagic complications in our study group was in agreement with other studies [25-27, 30, 33].…”

Section: Discussionmentioning

confidence: 85%

“…The bleeding and thrombosis occur in varied patterns. The template bleeding time is usually normal; when prolonged, it does not corellate with an increased risk of hemorrhage or with aggregation abnormalities [20,21].…”

mentioning

confidence: 99%

Abnormalities of platelet aggregation in chronic myeloproliferative disorders

Avram

Lupu

Angelescu

et al. 2001

J Cellular Molecular Medi

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A large variety of platelet dysfunctions has been described in chronic myeloproliferative disorders. These abnormalities may be due to deficiency of platelet granules, arahidonic acid metabolism defects or platelet membrane glycoproteins abnormalities. In this study we intend to detect the incidence of platelet function defects in 76 patients with various types of chronic myeloproliferative disorders. The platelet activity was studied in vitro by measuring platelet aggregation in response to ADP, epinephrine, collagen, arachidonic acid and ristocetin. These results were subsequently correlated with bleeding time and clinical aspects (bleeding or thrombosis). We found complex changes in platelet response with all agonists, in varied proportions. These abnormalities include absent, decreased or abnormal platelet aggregation response. In a few cases we found a markedly decreased, almost absent platelet response to all agonists while in some patients a normal platelet aggregation was noted. The correlation between these results and template bleeding time, thrombotic or hemorrhagic events and the type of diseases was difficult to establish and sometimes conflictual. Despite this fact, we consider that investigating platelet aggregation may be useful not only for the assesment of the hemostatic balance in chronic myeloproliferative disorders but also for a better insight into cell abnormalities occuring in these pathologic conditions.

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“…In CMPD patients, bleeding and arterial (mostly microvascular) or venous thrombosis are common complications (1)(2)(3)(4)(5)(6)(7)(8) where mechanisms are still unclear. Qualitative functional platelet abnormalities frequently observed in CMPD patients (1,(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) have been correlated with these complications (8,13,19). Such abnormalities encompass decreased platelet aggregation (PA) to adenosine diphosphate (ADP), collagen and particularly epinephrine (14,15,18) and acquired storage pool disease (16) as well as platelet hyperfunction indicated by enhanced PA (4,13), increased levels of plasma P-throm-boglobulin (PTG) (15,17) and shortened platelet survival time (1 5).…”

Section: Introductionmentioning

confidence: 99%

An abnormal pattern of multiple platelet function abnormalities and increased thromboxane generation in patients with primary thrombocytosis and thrombotic complications

Zahavi¹,

Zahavi²,

Firsteter³

et al. 1991

European J of Haematology

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Platelet aggregation (PA) induced by ADP, collagen and epinephrine, plasma levels of β‐thromboglobulin (βTG) and thromboxane B2 (TXB2) and serum TXB2 generation were studied in 11 patients with primary thrombocytosis (7 with essential thrombocythaemia and 4 with polycythaemia vera) and compared with 16 healthy subjects. 5 patients suffered from peripheral vascular ischaemia and another 3 had venous thrombosis, but none had bleeding complications. The patients showed an abnormal pattern of platelet function and of thromboxane generation distinct from the healthy subjects in three aspects, a) Shape change was 5–26 times greater, the lag‐time of collagen PA was 2.3‐2.9 times longer and the extent of epinephrine PA was nil or very low. ADP‐or collagen‐induced PA was also reduced (p<0.02). b) Plasma TXB2 generation (corrected to a normal platelet concentration) stimulated by the three PA inducers was within the range of the healthy subjects in spite of the reduced extent of PA. c) Plasma βTG level and serum TXB2 generation (both corrected to a normal platelet concentration) were 2.9‐7.1 times higher (p < 0.001) indicating enhanced in vivo platelet activation and possibly increased thrombin generation. These abnormalities were not detected in another 4 patients with secondary thrombocytosis. The abnormal pattern of platelet function and thromboxane generation can be a useful laboratory method in the evaluation of patients with primary thrombocytosis. It might also explain the thrombotic complications which occurred in 8 of the patients in a manner such that increased or normal TXB2 generation overcomes the reduced extent of PA. In this respect, the pronounced serum TXB2 synthesis might be a marker of intravascular thrombosis.

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Template Bleeding Time and Clinical Hemorrhage in Myeloproliferative Disease

Cited by 40 publications

References 19 publications

Phospholipase A2 activity in platelets of patients with primary thrombocythemia

Phospholipase A2 activity in platelets of patients with primary thrombocythemia

Abnormalities of platelet aggregation in chronic myeloproliferative disorders

An abnormal pattern of multiple platelet function abnormalities and increased thromboxane generation in patients with primary thrombocytosis and thrombotic complications

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