Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin

Rodica M. Van Solingen, Elliot Rosenstein, Gabriel Mihailescu, Michele L. Drejka, Amita Kalia, Alice J. Cohen, Neil Kramer

Research output: Contribution to journalArticle

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Abstract

PURPOSE: Although aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert inhibitory effects on platelets in vitro and in vivo, there are insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet function. SUBJECTS AND METHODS: We enrolled 25 healthy adult volunteers who were administered ketoprofen (extended-release capsules, 200 mg daily) for 1 week, followed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprofen (200 mg daily) alone during the second week. Platelet aggregation, stimulated by epinephrine and arachidonic acid, and cyclooxygenase activity, measured by thromboxane B 2 , were measured at baseline, on day 8, and on day 15. RESULTS: On day 8, all subjects demonstrated abnormal platelet aggregation ( > 50% inhibition), which persisted at day 15 in both the aspirin and no aspirin groups. One week of keto-profen treatment reduced thromboxane B 2 levels by 84% in the aspirin group and by 85% in the no aspirin group (P = 0.8), without any further inhibition measured on day 15. CONCLUSION: Extended-release ketoprofen significantly inhibited platelet aggregation and thromboxane B 2 production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patients who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy.

Original languageEnglish (US)
Pages (from-to)285-289
Number of pages5
JournalAmerican Journal of Medicine
Volume111
Issue number4
DOIs
StatePublished - Oct 2 2001
Externally publishedYes

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Ketoprofen
Aspirin
Blood Platelets
Anti-Inflammatory Agents
Thromboxanes
Platelet Aggregation
Healthy Volunteers
Pharmaceutical Preparations
Platelet Aggregation Inhibitors
Prostaglandin-Endoperoxide Synthases
Combination Drug Therapy
Epinephrine
Capsules

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Van Solingen, Rodica M. ; Rosenstein, Elliot ; Mihailescu, Gabriel ; Drejka, Michele L. ; Kalia, Amita ; Cohen, Alice J. ; Kramer, Neil. / Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin. In: American Journal of Medicine. 2001 ; Vol. 111, No. 4. pp. 285-289.
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abstract = "PURPOSE: Although aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert inhibitory effects on platelets in vitro and in vivo, there are insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet function. SUBJECTS AND METHODS: We enrolled 25 healthy adult volunteers who were administered ketoprofen (extended-release capsules, 200 mg daily) for 1 week, followed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprofen (200 mg daily) alone during the second week. Platelet aggregation, stimulated by epinephrine and arachidonic acid, and cyclooxygenase activity, measured by thromboxane B 2 , were measured at baseline, on day 8, and on day 15. RESULTS: On day 8, all subjects demonstrated abnormal platelet aggregation ( > 50{\%} inhibition), which persisted at day 15 in both the aspirin and no aspirin groups. One week of keto-profen treatment reduced thromboxane B 2 levels by 84{\%} in the aspirin group and by 85{\%} in the no aspirin group (P = 0.8), without any further inhibition measured on day 15. CONCLUSION: Extended-release ketoprofen significantly inhibited platelet aggregation and thromboxane B 2 production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patients who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy.",
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Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin. / Van Solingen, Rodica M.; Rosenstein, Elliot; Mihailescu, Gabriel; Drejka, Michele L.; Kalia, Amita; Cohen, Alice J.; Kramer, Neil.

In: American Journal of Medicine, Vol. 111, No. 4, 02.10.2001, p. 285-289.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Comparison of the effects of ketoprofen on platelet function in the presence and absence of aspirin

AU - Van Solingen, Rodica M.

AU - Rosenstein, Elliot

AU - Mihailescu, Gabriel

AU - Drejka, Michele L.

AU - Kalia, Amita

AU - Cohen, Alice J.

AU - Kramer, Neil

PY - 2001/10/2

Y1 - 2001/10/2

N2 - PURPOSE: Although aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert inhibitory effects on platelets in vitro and in vivo, there are insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet function. SUBJECTS AND METHODS: We enrolled 25 healthy adult volunteers who were administered ketoprofen (extended-release capsules, 200 mg daily) for 1 week, followed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprofen (200 mg daily) alone during the second week. Platelet aggregation, stimulated by epinephrine and arachidonic acid, and cyclooxygenase activity, measured by thromboxane B 2 , were measured at baseline, on day 8, and on day 15. RESULTS: On day 8, all subjects demonstrated abnormal platelet aggregation ( > 50% inhibition), which persisted at day 15 in both the aspirin and no aspirin groups. One week of keto-profen treatment reduced thromboxane B 2 levels by 84% in the aspirin group and by 85% in the no aspirin group (P = 0.8), without any further inhibition measured on day 15. CONCLUSION: Extended-release ketoprofen significantly inhibited platelet aggregation and thromboxane B 2 production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patients who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy.

AB - PURPOSE: Although aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) exert inhibitory effects on platelets in vitro and in vivo, there are insufficient data to substantiate the use of NSAIDs alone as antiplatelet drugs in patients already taking aspirin. We therefore sought to determine whether aspirin, added to NSAID therapy, further suppresses platelet function. SUBJECTS AND METHODS: We enrolled 25 healthy adult volunteers who were administered ketoprofen (extended-release capsules, 200 mg daily) for 1 week, followed by ketoprofen (200 mg daily) and aspirin (325 mg daily) or ketoprofen (200 mg daily) alone during the second week. Platelet aggregation, stimulated by epinephrine and arachidonic acid, and cyclooxygenase activity, measured by thromboxane B 2 , were measured at baseline, on day 8, and on day 15. RESULTS: On day 8, all subjects demonstrated abnormal platelet aggregation ( > 50% inhibition), which persisted at day 15 in both the aspirin and no aspirin groups. One week of keto-profen treatment reduced thromboxane B 2 levels by 84% in the aspirin group and by 85% in the no aspirin group (P = 0.8), without any further inhibition measured on day 15. CONCLUSION: Extended-release ketoprofen significantly inhibited platelet aggregation and thromboxane B 2 production in healthy volunteers. Addition of aspirin had no additional effect. Trials are warranted to determine whether these in vitro effects result in clinical antiplatelet activity in patients who require chronic treatment with NSAIDs, thereby avoiding the toxicity of NSAID/aspirin combination therapy.

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