Platelet-Factor-3 Availability in a Patient With Glanzmann's Disease

Inceman, S; Tangün, Y

doi:10.1016/s0140-6736(68)90639-9

Cited by 7 publications

(4 citation statements)

References 3 publications

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“…6 for the platelet resuspensions prepared in physiologic saline and 13.9 ± 1.6 for those prepared iri distilled water. The way the Stypven-calcium solution used in all three tests was prepared has b een described in our previous reports ( 11).…”

Section: Methodsmentioning

confidence: 99%

Platelet Aggregation and Platelet Factor 3 Activity in Myeloproliferative Disorders

Tangün¹

1971

Thromb Haemost

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Summary33 patients with myeloproliferative disorder were studied and in 28 (84%) various anomalies of platelet function were observed. Single, or more commonly, multiple platelet aggregation defects and impaired release of platelet ADP and platelet factor 3 activity were the chief anomalies noted, whether thrombocytosis was present or not. The effect of myelosuppressive therapy upon the defects demonstrated varied from patient to patient, and from one anomaly to another. Reducing the high platelet count to normal levels does not seem to be sufficient to eradicate qualitative platelet defects.

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Section: Methodsmentioning

confidence: 99%

Platelet Aggregation and Platelet Factor 3 Activity in Myeloproliferative Disorders

Tangün¹

1971

Thromb Haemost

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“…Usage of this term had earlier been done in GT associated with poor PF3 release but with no reduction in its total amount in platelets [26]. However, poor PF3 re lease in GT noted by various workers [2,3,[9][10][11][12] has been recognised as a constituent defect of the disorder [27]. Congenital [27][28][29] and he reditary [30] PF3 deficiency (deficit thrombopathy) associated with se vere bleeding have been described and are considered as rare platelet disorders.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, Papayannis and Israels [7] and Karaca and N ilsson [8] have conclud ed that clot retraction is an important finding and may be the only means of diagnosing a heterozygous form of thrombasthenia. Platelet factor 3 (PF3) release is abnormal in GT [2,3,[9][10][11][12]. However, these reports do not comment on its total content in platelets.…”

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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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“…Platelet factor 3 availability is abnormal in thrombasthenia [38,46,108,136,137,174,239,268,304]. (PF 3 is not a true factor.…”

Section: Characteristic Laboratory Findingsmentioning

confidence: 99%