Effect of dipyridamole and aspirin in thrombotic microangiopathy.

Giromini, M; Bouvier, C A; Dami, R; Denizot, Mélanie; Jeannet, M

doi:10.1136/bmj.1.5799.545

Cited by 62 publications

(19 citation statements)

References 6 publications

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“…ASA also potentiates the anti-thrombotic effect of dipyridamole (Giromini et al, 1972;Harker & Slichter, 1972;Moncada & Korbut, 1978). In our study, 2.6 or 5.7 mg/kg of ASA in combination with dipyridamole almost completely inhibited the platelet cyclo-oxygenase without changing the PGI2 formation.…”

Section: Discussion 5o0supporting

confidence: 59%

“…It is also known that platelet aggregation can be inhibited by acetylsalicylic acid (ASA) (Weiss & Aledort, 1967;Smith & Willis, 1971;Weiss, 1976;Burch & Majerus, 1979) and that dipyridamole exerts an anti-aggregating effect in vivo (Emmons, Harrison, Honour & Mitchell, 1965;Arfors, Hint & Dhall, 1968;Didisheim, 1968;Sullivan, Harken & Gorlin, 1968;Harker & Slichter, 1970). Furthermore, it has been shown that ASA and dipyridamole have a synergistic anti-thrombotic effect in vivo (Harker & Slichter, 1970;Giromini. Bouvier, Dami, Denizot & Jeannet, 1972;Weiss, 1976) which effect, however, depends critically on the dose of ASA used (Moncada & Korbut, 1978 PGI2 and TxA2 production were studied indirectly by measuring the stable metabolites of these prostanoids, namely 6-keto-prostaglandin Fl2 (6-keto-PGF,,) and thromboxane B2 (TxB2), respectively (Hamberg et al, 1975;Johnson, Morton, Kinner, Gorman, McGuire, Sun, Whiltaker, Bunting, Salmon, Moncada & Vane, 1976).…”

Section: Introductionmentioning

confidence: 99%

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Effect of Various Doses of Acetylsalicylic Acid in Combination With Dipyridamole on the Balance Between Prostacyclin and Thromboxane in Human Serum

Viinikka

Ylikorkala

1981

British J Pharmacology

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I Thirty-six healthy human subjects were randomly divided into six groups which were treated with a single dose of 75 mg (1.3 mg/kg) of dipyridamole alone, or 75 mg of dipyridamole in combination with 30 mg (0.5 mg/kg), 50 mg (0.8 mg/kg), 160 mg (2.6 mg/kg) and 330 mg (5.7 mg/kg) of acetylsalicylic acid (ASA), or with placebo. 2 The concentrations of prostacyclin (PGI2) and thromboxane A2 (TxA2) metabolites, 6-keto-prostaglandin Fl, ) and TxB2 respectively, were measured in serum with specific radioimmunoassays before and 1 and 3 h after the ingestion of the test dose.3 The basal concentrations of 6-keto-PGF1, and TxB2 correlated significantly (r = 0.588, P < 0.001). 4 Dipyridamole alone did not change PGI2 or TxA2 production. 5 Dipyridamole-ASA combinations with ASA doses between 0.5 and 0.8 mg/kg inhibited TxB2 production by 48 to 74%, and with the ASA doses between 2.6 and 5.7 mg/kg by about 90%. None of these combinations changed PGI2 production. 6 The ratio of 6-keto-PGF1, to TxB2 increased 3.5 to 6 times with ASA doses of 0.5 to 0.8 mg/kg and 21 to 29 times with doses between 2.6 to 5.7 mg/kg. 7 These results suggest that the anti-thrombotic effect of dipyridamole in vivo is not mediated through direct changes in PGI2 and/or TxA2 production.

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Section: Discussion 5o0supporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Effect of Various Doses of Acetylsalicylic Acid in Combination With Dipyridamole on the Balance Between Prostacyclin and Thromboxane in Human Serum

Viinikka

Ylikorkala

1981

British J Pharmacology

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“…One of our patients undoubtedly had leptospirosis, confirmed by repeated titre for leptospirae (Leptospira icterohaemorrhagiae 1:1.000) with minimal liver lesion, but with a marked platelet depletion, microangiopathic anemia, CNS and renal lesions. Different treatment strategies have been attempted in TTP, ranging from an- tiplatelet therapy with dipyridamole and aspirin, to chemotherapy with vincristine, prostacyclin, and plasma transfusion [9,10,11,12]. It appears that plasma exchange is of greatest benefit, with replacement of the removed volume with fresh frozen plasma [13,14,18].…”

Section: Discussionmentioning

confidence: 99%

Possibilities and limits of treatment in patients with thrombotic thrombocytopenic purpura

et al. 2000

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Results of treatment of 18 patients fulfilling the criteria for TTP are presented. Thrombocytopenia was present in all patients (100%). Sixteen of the 18 patients (88.8%) had mental status changes, and seven of the 18 patients (38.8%) had renal impairment. One patient had a secondary type of TTP, caused by non-Hodgkin's lymphoma of the large intestine (that was diagnosed later) and was excluded from the study. Immunosuppresive therapy with steroids, plasma exchange and replacement of removed volume with fresh frozen plasma in a dosage of 25 ml/kg body weight resulted in a statistically significant increase of platelet count (P = 0.00222), and a significant improvement in consciousness defined by increased GCS after 2 weeks (P = 0.00222). In two patients renal function recovered, and in one of them hemodialysis was no longer needed. This improvement in a small group of patients had no statistical significance. TTP recurred in seven patients. High doses of steroids caused serious side effects in two patients: in one patient, steroid diabetes, and in the other one, intestinal perforation.

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“…Aspirin in one study (43) decreased the incidence of venous thrombosis after hip arthroplasty but failed in another (19) ment with aspirin or sulfinpyrazone in combination with an inhibitor of ADP-induced platelet aggregation would be more effective than treatment with a platelet release inhibitor alone. The combination of aspirin and dipyridamole has been reported to be useful in the treatment of thrombotic thrombocytopenic purpura (TTP) (44,45). However, dipyridamole is only a weak inhibitor of ADP-induced platelet aggregation (46), and it is uncertain whether its beneficial effects in patients with TTP (44,45) and patients with prosthetic heart valves (47,48) can be attributed to inhibition of this particular platelet function.…”

Section: Introductionmentioning

confidence: 99%

“…The combination of aspirin and dipyridamole has been reported to be useful in the treatment of thrombotic thrombocytopenic purpura (TTP) (44,45). However, dipyridamole is only a weak inhibitor of ADP-induced platelet aggregation (46), and it is uncertain whether its beneficial effects in patients with TTP (44,45) and patients with prosthetic heart valves (47,48) can be attributed to inhibition of this particular platelet function.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Primary ADP-Induced Platelet Aggregation in Normal Subjects after Administration of Nitrofurantoin (Furadantin)

Rossi¹,

Levin²

1973

J. Clin. Invest.

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A B S T R A C 'r The evidence indicating that platelets may play a role in the occurrence of certain thromboembolic phenomena has stimulated a search for inhibitors of platelet function. This report presents data to indicate that nitrofurantoin is a potent inhibitor of primary ADP-induced platelet aggregation. The addition of 10 SKI nitrofurantoin to citrated platelet-rich plasma obtained from 12 normal subjects produced a p9946% (2 SD) inhibition of the velocity of platelet aggregation induced by 2 IAIM ADP. The inhibitorv effect of nitrofurantoin demonstrated competitive kinetics in respect to ADP. The intravenous (180 mg) or oral (200 mg) administration of nitrofurantoin produced a serum nitrofurantoin concentration ranging from 2.7 to 23 MM in 28 normal subjects. Platelet-rich plasma obtained from these subjects demonstrated inhibition of the velocity of ADP-induced platelet aggregation that correlated with the log of the serum nitrofurantoin concentration (P < 0.001). Collagen-induced platelet aggregation was also inhibited in a doserelated manner, and the bleeding time was significantly prolonged in the two subjects with the highest serum nitrofurantoin concentration. These studies indicate that nitrofurantoin in vivo inhibits platelet function to a degree that is proportional to the serum nitrofurantoin concentration.

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Effect of dipyridamole and aspirin in thrombotic microangiopathy.

Cited by 62 publications

References 6 publications

Effect of Various Doses of Acetylsalicylic Acid in Combination With Dipyridamole on the Balance Between Prostacyclin and Thromboxane in Human Serum

Effect of Various Doses of Acetylsalicylic Acid in Combination With Dipyridamole on the Balance Between Prostacyclin and Thromboxane in Human Serum

Possibilities and limits of treatment in patients with thrombotic thrombocytopenic purpura

Inhibition of Primary ADP-Induced Platelet Aggregation in Normal Subjects after Administration of Nitrofurantoin (Furadantin)

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