Table 2.
Representative studies on the effect of Diclofenac on platelets.
| NSAID Drug (s) | Study Design | Effects on Platelets | Ref |
|---|---|---|---|
| Diclofenac and Dexibuprofen | In vivo in 21 participants (11 patients treated with orthopedic injuries and 10 healthy individuals as control group). Dose: Diclofenac 75 mg or Dexibuprofen 400 mg Diclofenac was administrated twice a day for 3.2 ± 2.1 days. |
Diclofenac significantly reduced AA-induced platelet aggregation in hPRP from patients undergoing elective orthopedic surgery while receiving such a NSAID(IC50 for ACP was 2.7 ± 3.7, while for control group was 563 ± 61) There were no notable variances observed in platelet aggregation responses to collagen, ADP, or TRAP-6 stimulation when contrasted with the control participants. PRP generated from individuals who have taken such NSAID exhibit notable deficiencies in platelet function. Should such an NSAID administration be necessary, it should be carried out subsequent to blood collection for autologous PRP preparation to avoid potential diminishment of therapeutic efficacy. |
[61] |
| Diclofenac and Aspirin | In vivo (Clinical Trial) in 12 healthy volunteers. Εach participant was randomly classified in 1 of 5 cases of medicines administration, with a cleanse period between treatments. Dose of each category: (a) aspirin 325 mg and after 2 h 50-mg of oral diclofenac potassium, (b) topical diclofenac epolamine 1.3%, (c) diclofenac patch (twice a day) followed by aspirin 325 mg after 21 h, (d) oral diclofenac potassium 50 mg, and (e) aspirin 325 mg. Blood samples were taken every 0, 2, 4, 6, 8, 12, 24, 48, and 96 for each case. |
Diclofenac patch in healthy subjects did not hinder the antiplatelet effects of aspirin in both collagen and AA agonists (collagen agonist 95% CI –284.609 to 79.942; AA agonist 95% CI –117.479 to 310.395). Oral diclofenac exhibited varying effects on aspirin-induced inhibition of platelet aggregation (for collagen 95% CI 302.568 to 971.765 while for AA P = 0.973 95% CI –173.506 to 546.756). |
[77] |
| Diclofenac sodium and Aspirin | In vivo (Clinical Trial) in 18 healthy people (segregated into 3 groups). Dose: 150 mg of aspirin once a day and 50 mg of diclofenac sodium 3 times a day for 6 days without the consumption of any other pharmaceutical. |
When administering aspirin in conjunction with three daily doses of diclofenac sodium in healthy subjects, the antiplatelet efficacy and thus the thromboprophylactic effect of aspirin remained intact, against both ADP and collagen induced platelet aggregation (minor inhibition of 22.10% and 38,87%, respectively) and in relation to the decrease in the mean TxB2 levels (reduced to 702.99 ± 101.59 pg/mL from 971.11 ± 128.91 pg/mL) | [76] |
| Diclofenac or Indomethacin | In vivo study (Clinical Trial). 20 patients for cataract surgery participated in a simultaneous randomized trial. Dose: 1 mg/mL Diclofenac or 1 mg/mL Indomethacin for 3 days 4 times a day. |
Administration of diclofenac eye-drops in patients preparing for cataract surgery did not result in a significant reduction in AA-induced TxB2 generation and platelet aggregation, as well as in circulating platelet P-selectin expression. | [62] |
| Diclofenac sodium and etoricoxib | In vivo study (Animal model). 41 male rats were exposed to –18 °C for 2 h Dose: 7 mg/kg to diclofenac sodium alleviate the effects of hypothermia |
Diclofenac sodium exhibited a notable decrease in D-dimer (from 2454.0 ± 250.3 to 1660.0 ± 293.6) and serum fibrinogen levels (from 306.8 ± 34.4 to 237.1 ± 29.2), accompanied by the restoration of thrombin time to normal levels [75]. |
Abbreviations: NSAID(s) = non-steroidal anti-inflammatory drug(s); AA = arachidonic acid; ADP = adenosine 5′ diphosphate;TRAP-6 = peptide fragment that is a selective agonist of the protease activating receptor 1 (PAR1); PRP = platelet-rich plasma; TxB2 = thromboxane B2.