Download PDF
Thromb Haemost 1982; 48(01): 072-075
DOI: 10.1055/s-0038-1657219
Original Article
Schattauer GmbH Stuttgart

Aspirin Ingestion in Primary Thrombocythemia

Akira Hattori
The 1st Department of Internal Medicine, Niigata University, Niigata, Japan
,
Masayoshi Sanada
The 1st Department of Internal Medicine, Niigata University, Niigata, Japan
,
Reizo Nagayama
The 1st Department of Internal Medicine, Niigata University, Niigata, Japan
,
Akira Shibata
The 1st Department of Internal Medicine, Niigata University, Niigata, Japan
,
Minoru Okuma
*   1st Department of Internal Medicine, Kyoto University, Kyoto, Japan
› Author Affiliations
Further Information

Publication History

Received 07 September 1981

Accepted 02 June 1982

Publication Date:
13 July 2018 (online)

  PDF Download  Permissions and Reprints

Summary

Recently Massotti et al. (14) and Patrono et al. (23) have proposed for antithrombotic therapy the use of small single dose of aspirin (ASA) every three or four days in order to inhibit thromboxane A2 production in the platelets but not to inhibit PGI2 production in the endothelium. Their data are theoretical and based on a small number of normal humans. We have examined the effect of a single ingestion of ASA (10 mg/kg) on spontaneous platelet aggregation (SPA) and collagen-induced aggregation (CA) in 11 patients with primary thrombocythemia using the original platelet-rich plasma. SPA and CA were positive in 8 out of 10 and in 11 out of 11 patients respectively before ASA ingestion. ASA abolished both types of aggregation in all patients at 12 h after the ingestion. But the recovery occurred in 1/11 in CA at 24 hr, in about half (3/8 SPA or 7/11 CA) of the patients at 48 hr, in 5/8 (SPA) and 10/11 (CA) at 72 hr and in 7/ 8 (SPA) and 11/11 (CA) at 96 hr. Since SPA and sometimes CA have been considered to be the parameters of the effect of ASA on hyperreactivity of the platelets in vivo, resulting in arterial thrombosis or insufficiency in these patients, our results suggest that daily or at least once per two days ingestion of ASA may be necessary in these patients. These results were discussed in relation to the platelet survivals (6.5–10 days) and the platelet cyclo-oxygenase or lipoxygenase activities (deficient in 3 patients for the former and in 2 for the latter) in our patients.

Keywords

Aspirin - Spontaneous platelet aggregation - Primary thrombocythemia - Antithrombotic drugs
 

  • References

  • 1 Amezcua JL, O'Grady J, Salmon JA, Moneada S. Prolonged paracoxical effect of aspirin on platelet behaviour and bleeding time in man. Thromb Res 1979; 16: 69-79
    CrossrefPubMedGoogle Scholar
  • 2 Bolin RB, Okimura T, Jamieson GA. Changes in distribution of platelet membrane glycoproteins in patients with myeloproliferative disorders. Am J Hematol 1977; 3: 63-71
    CrossrefPubMedGoogle Scholar
  • 3 Braunwald E, Friedewald WT, Furgerg CD. (Eds) Proceedings of the workshop on platelet-active drugs in the secondary prevention of cardiovascular events. Circulation Part II 1980; 62: 1-109
    PubMedGoogle Scholar
  • 4 Castalano PM, Smith JB, Murphy S. Platelet recovery from aspirin inhibition in vivo; differing patterns under various assay conditions. Blood 1981; 57: 99-105
    PubMedGoogle Scholar
  • 5 de Castellamau C, Cerletti C, Dejana E, Galletti F, Latini R, Livio M, de Gaetano G. Salicylate-aspirin interaction and thrombosis prevention trials. Thromb Haemostas 1981; 45: 294
    PubMedGoogle Scholar
  • 6 Dejana E, Barbieri B, Cerletti C, Livio M, de Gaetano G. Impaired thromboxane production by newly formed platelets after aspirin administration to thrombocytopenic rats. Br J Haematol 1980; 46: 465-469
    CrossrefPubMedGoogle Scholar
  • 7 Gerrard JM, Stoddard SF, Sbapiro RS, Coocia PF, Ramsay NK, Nesbit ME, Rao GH, Krivit W, White JG. Platelet storage pool deficiency and prostaglandin synthesis in chronic granulocytic leukemia. Br J Haematol 1978; 40: 597-607
    CrossrefPubMedGoogle Scholar
  • 8 Hattori A, Ito S, Koike K, Matsuoka M. Static and functional morphology of the pathological platelets in primary meylofibrosis and myeloproliferative syndrome. Ser Haematol 1975; 9: 126-150
    PubMedGoogle Scholar
  • 9 Hattori A, Sanada M, Fuse I, Koike T, Okuma M. Prostaglandin and platelets. Cyclo-oxygenase, lipoxygenase, aspirin and PGI2 (in Japanese). Niigata Igakukaishi 1981; 95: 80-87
    PubMedGoogle Scholar
  • 10 Hoagland HC, Silverstein MN. Primary thrombocythemia in the young patient. Mayo Clin Proc 1978; 53: 578-580
    PubMedGoogle Scholar
  • 11 Kaywin P, McDonough M, Alnsel P, Shattil SJ. Platelet function in essential thrombocythemia. Decreased epinephrine responsiveness associated with a deficiency of platelet α-adrenergic receptors. N Engl J Med 1978; 299: 505-509
    CrossrefPubMedGoogle Scholar
  • 12 Kelton JG, Hirsh J, Canter CJ, Buchanan MR. Thrombogenic effect of high-dose aspirin in rabbits. Relationship to inhibition of vessel wall synthesis of prostaglandin-I2-like activity. J Clin Invest 1978; 62: 892-895
    CrossrefPubMedGoogle Scholar
  • 13 Lecker D, Kumar A. Effect of 6-p-(4-phenylacetylpiperazin-1-yl)-phenyl-4,5-Dihydro-3(H)-pyridazinone (CCI-17810) and aspirin on experimental arterial thrombosis in rats. Thromb Haemostas 1980; 44: 9-11
    PubMedGoogle Scholar
  • 14 Massotti G, Galanti G, Poggesi L, Abbate R, Semeri GGN. Differential inhibition of prostacyclin production and platelet aggregation by aspirin. Lancet 1979; 2: 1213-1216
    PubMedGoogle Scholar
  • 15 Mielke CH, Britten AFH. Aspirin as an antithrombotic agent: Template bleeding time-test of antithrombotic effect (Abstr.). Blood 1970; 36: 855
    PubMedGoogle Scholar
  • 16 Nadell J, Bruno J, Varady J, Segre EJ. Effect of naproxen and of aspirin on bleeding time and platelet aggregation. J Clin Pharmacol 1974; 14: 176-182
    CrossrefPubMedGoogle Scholar
  • 17 O'Brien JR. Aspirin and platelet aggregation. Lancet 1968; 1: 779-783
    PubMedGoogle Scholar
  • 18 O'Brien JR. Effects of salicylates on human platelets. Lancet 1968; 1: 779-783
    PubMedGoogle Scholar
  • 19 O'Grady J, Moneada S. Aspirin: a paradoxical effect on bleeding time. Lancet 1978; 2: 789
    PubMedGoogle Scholar
  • 20 Okuma M, Uchino H. Platelet lipoxygenase deficiency. New Engl J Med 1977; 297: 1351-1352
    PubMedGoogle Scholar
  • 21 Okuma M, Uchino H. Altered arachidonate metabolism by platelets in patients with myeloproliferative disorders. Blood 1979; 54: 1258-1271
    PubMedGoogle Scholar
  • 22 Okuma M, Takayama H, Uchino H, Kondo N, Kawasaki A, Inagawa S. Effect of administration of thromboxane synthetase inhibitor on platelet aggregation and arachidonate metabolism. (Abstr. in Japanese). Proc 4th Congr Jap Soc Thromb Hemostas; Osaka: 1981: 84
    Google Scholar
  • 23 Patrono C, Ciabattoni G, Pinca E, Pugliese F, Castrucci G, De Salve A, Satta MA, Peskar BA. Low dose aspirin and inhibition of thromboxane B2 production in healthy subjects. Thromb Res 1980; 17: 317-327
    CrossrefPubMedGoogle Scholar
  • 24 Preston FE, Emmanuel IG, Winfield DA, Malia RG. Essential thrombocythemia and peripheral gangrene. Br Med J 1974; 3: 548-552
    CrossrefPubMedGoogle Scholar
  • 25 Preston FE, Whipps S, Jackson CA, French AJ, Wyld PJ, Stoddard CJ. Inhibition of prostacyclin and platelet thromboxane A2 after low-dose aspirin. New Engl J Med 1981; 304: 76-79
    CrossrefPubMedGoogle Scholar
  • 26 Singh AK, Wetherley-Mein G. Microvascular occlusive lesions in primary thrombocythaemia. Br J Haematol 1977; 36: 553-571
    CrossrefPubMedGoogle Scholar
  • 27 Taft E, Babcock RB, Scharfman WB, Tartaglia AYP. Platelet-pheresis in the management of thrombocytosis. Blood 1977; 50: 927-933
    PubMedGoogle Scholar
  • 28 Vreeken J, Van Aken WG. Spontaneous aggregation of blood platelets as a cause of idiopathic thrombosis and recurrent painful toes and fingers. Lancet 1971; 2: 1394-1397
    PubMedGoogle Scholar
  • 29 Wu KK. Platelet hyperaggregability and thrombosis in patients with thrombocythemia. Ann Intern Med 1978; 88: 7-11
    CrossrefPubMedGoogle Scholar