Bleeding, Platelets, and Macroglobulinemia

Pachter, M. Richard; Johnson, Shirley A.; Neblett, Thomas R.; Truant, Joseph P.

doi:10.1093/ajcp/31.6.467

Cited by 99 publications

(24 citation statements)

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“…PF3 availability is most consistently affected in IgG, and to a lesser extent in IgA myeloma. The bleeding time abnormalities have been recognized ear lier [1,3,4,[6][7][8]14]. Pachter et al [2] were the first to find decreased PF3 availability in patients with macroglobulinaemia, which was later confirmed by Penny et al [9].…”

Section: Discussionmentioning

confidence: 99%

“…Incubation of normal platelets with immunoglobulins enhanced the kaolin-in duced PF3 availability. It is suggested that in vivo platelet activation may bring about the PF3 release which subsequently manifests as poor PF3 availability and re duction in its total contents.The role of altered platelet functions in dysproteinaemia has been the subject of some recent studies [1][2][3][4][5][6][7][8][9]. In an earlier communication from this laboratory, it was reported that in macroglobulinaemia, platelet adhe sion, aggregation, platelet factor 3 (PF3) release and its total contents are all affected [10].…”

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confidence: 99%

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Platelet Functions in Dysproteinaemia

Kasturi¹,

Saraya²

1978

Acta Haematol

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Platelet functions were studied in 16 patients with multiple myeloma (MM) and 4 with primary macroglobulinemia (PM). The fall in immunoglobulins on therapy was correlated with the status of platelet function. Effect of incubation of normal platelets with immunoglobulins derived from these patients on kaolin-induced platelet factor 3 (PF3) release was studied to elucidate the mechanism of platelet function defect. Results show increased bleeding time, absence or poor platelet adhesion and aggregation, poor PF3 availability and reduced total PF3 in platelets more consistently in PM but to a lesser extent in MM. Normalisation or partial reduction in globulins on therapy was associated with improvement in platelet functions. Incubation of normal platelets with immunoglobulins enhanced the kaolin-induced PF3 availability. It is suggested that in vivo platelet activation may bring about the PF3 release which subsequently manifests as poor PF3 availability and reduction in its total contents.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Platelet Functions in Dysproteinaemia

Kasturi¹,

Saraya²

1978

Acta Haematol

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“…thrombocytopenia [24], infiltration of small vessels of the vascular tree by abnormal proteins [25], capillary damage from impaired blood flow due to the often greatly increased blood viscosity [25], various types of qualitative platelet defects [7,9], interference with fibrinogen to fibrin conversion [26][27][28][29], inhibition of various clotting factors [30,31], fibri nolysis [32], coating of platelets by macroglobulins [10] and absorption of clotting factors by abnormal proteins [33]. The exact mechanism underlying defective haemostasis in these dis orders is unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Tn particular various types of qualitative platelet de fects have been described [7][8][9], The presence of abnormal platelet fac tor 3 (PF3) release has been shown to be due to coating of the platelets by abnormal globulins [10]. P erkins [8], however, did not find the de creased PFS release.…”

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confidence: 99%

A Study of Haemostasis in Macroglobulinaemia

1972

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In 3 patients with dysproteinaemia the defects in haemostasis were investigated: Waldenström’s macroglobulinaemia, macroglobulinaemia associated with undifferentiated malignancy in the marrow, diffuse hypergammaglobulinaemia associated with drug sensitive purpura. Platelet factor 3 release, reduction of its total contents and poor platelet adhesion were found in all 3 patients. Platelet aggregation was absent in 2 patients who had macroglobulinaemia with monoclonal spike. It is suggested that the platelet factor 3 assay may be of value in the investigation of these changes in relation to dysproteinaemias.

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“…Failure of platelet aggregation have been considered as the possi ble cause of poor PF3 release [13]. However, poor PF3 release with normal aggregation have been noted in congenital [29] and acquired functional thrombopathies [31]. Studies of Horowitz and Papayoanou [14] also suggest that platelet aggregation and PF3 release are two inde pendent reactions.…”

Section: Discussionmentioning

confidence: 99%

Platelet Factor 3 in Glanzmann’s Thrombasthenia

Saraya¹,

Kasturi²,

Kishan³

1972

Acta Haematol

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The present paper describes 3 cases of classical thrombasthenia and 3 cases of combined platelet factor 3 defi- 3 ciency and absence of platelet aggregation. The bleeding time and the clot retraction in the latter 3 patients were They, however, did not differ in clinical presentation of classical thrombasthenia. These cases have been designated as thrombopathic thrombasthenia. The possibility of an in vivo platelet activation leading to variable amounts of platelet factor 3 release in thrombasthenia has been raised. Mechanism of PF3 release in vivo in thrombasthenia, however, is not known and needs further study.

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Bleeding, Platelets, and Macroglobulinemia

Cited by 99 publications

References 0 publications

Platelet Functions in Dysproteinaemia

Platelet Functions in Dysproteinaemia

A Study of Haemostasis in Macroglobulinaemia

Platelet Factor 3 in Glanzmann’s Thrombasthenia

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