Abnormalities of Epinephrine-Induced Platelet Aggregation and Adenine Nucleotides in Myeloproliferative Disorders

Koichiro Yamamoto; Eisuke Sekiguchi; Osamu Takatani

doi:10.1055/s-0038-1661198

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1984; 52(03): 292-296
DOI: 10.1055/s-0038-1661198

Original Article

Schattauer GmbH Stuttgart

Abnormalities of Epinephrine-Induced Platelet Aggregation and Adenine Nucleotides in Myeloproliferative Disorders

Authors

Koichiro Yamamoto

¹The 3rd Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan
Eisuke Sekiguchi

²The Division of Case History, National Defense Medical College, Tokorozawa, Saitama, Japan
Osamu Takatani

¹The 3rd Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan

Abstract

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Summary

Platelet aggregation was studied in 18 patients with myeloproliferative disorders, including 14 patients with chronic myelogenous leukemia, 2 with polycythemia vera, 1 with myelofibrosis and 1 with thrombocythemia. Fourteen patients (78%) were abnormal in epinephrine-induced platelet aggregation, while 3 (17%) and 4 (22%) cases showed impaired ADP or collagen induced platelet aggregation, respectively. A significant decrease of total ADP content in resting unstimulated platelets and of the amount released to the medium after aggregation was found in all six patients who were evaluated. ATP and AMP in resting platelets tended to be slightly higher in patients compared with the control group. Released ATP was also significantly less, and the percentage release of ADP and ATP was significantly decreased in patients. A storage pool deficiency of adenine nucleotides was considered to be responsible for abnormal platelet function in patients with myeloproliferative disorders.

Key words

Myeloproliferative disorders - Platelet aggregation - Adenine nucleotides - Storage pool deficiency

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Referenzen

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