Vol 20, No 2 (2013)
Original articles
Published online: 2013-04-05
Association of plasma concentrations of salicylic acid and high on ASA platelet reactivity in type 2 diabetes patients
DOI: 10.5603/CJ.2013.0030
Cardiol J 2013;20(2):170-177.
Abstract
Background: The objective of this study was to investigate the association between plasma
concentrations of salicylic acid (SA) and other minor acetylsalicylic acid (ASA) metabolites
and high on ASA platelet reactivity assessed with different methods in type 2 diabetic patients
(T2DM).
Methods: Study cohort consisted of 293 T2DM patients on chronic ASA therapy. Platelet
function inhibition was analyzed using measurements of serum thromboxane B2 (S-TxB2),
VerifyNow Aspirin and Platelet Function Analyzer (PFA)-100 assays. The concentration of ASA
metabolites in plasma was measured with a high-performance liquid chromatography (HPLC).
Results: In logistic regression analysis both ASA dose/kg of body weight and plasma SA
concentration were found to be predictive of S-TxB2 concentrations above 0.72 ng/mL cut-off
point (OR 16.9, 95% CI 2.29–125.8, p = 0.006 and OR 5.34, 95% CI 2.67–10.68, p < 0.001,
respectively). When using the VerifyNow Aspirin Assay, the concentrations of SA were signifi -
cantly lower (p = 0.007) in the group with high on ASA platelet reactivity when compared with
the group with normal on ASA platelet reactivity. In logistic regression analysis plasma SA
concentration was found to be predictive of VerifyNow Aspirin Reaction Units (ARU) ≥ 550
(OR 3.86, 95% CI 1.86–8.00, p < 0.001).
Conclusions: Our study suggests that disturbances of pharmacokinetic mechanisms might
contribute to lower plasma SA levels, and subsequently incomplete inhibition of thromboxane A2
synthesis as measured with S-TxB2 concentrations and increased platelet reactivity measured
with VerifyNow in T2DM patients.
concentrations of salicylic acid (SA) and other minor acetylsalicylic acid (ASA) metabolites
and high on ASA platelet reactivity assessed with different methods in type 2 diabetic patients
(T2DM).
Methods: Study cohort consisted of 293 T2DM patients on chronic ASA therapy. Platelet
function inhibition was analyzed using measurements of serum thromboxane B2 (S-TxB2),
VerifyNow Aspirin and Platelet Function Analyzer (PFA)-100 assays. The concentration of ASA
metabolites in plasma was measured with a high-performance liquid chromatography (HPLC).
Results: In logistic regression analysis both ASA dose/kg of body weight and plasma SA
concentration were found to be predictive of S-TxB2 concentrations above 0.72 ng/mL cut-off
point (OR 16.9, 95% CI 2.29–125.8, p = 0.006 and OR 5.34, 95% CI 2.67–10.68, p < 0.001,
respectively). When using the VerifyNow Aspirin Assay, the concentrations of SA were signifi -
cantly lower (p = 0.007) in the group with high on ASA platelet reactivity when compared with
the group with normal on ASA platelet reactivity. In logistic regression analysis plasma SA
concentration was found to be predictive of VerifyNow Aspirin Reaction Units (ARU) ≥ 550
(OR 3.86, 95% CI 1.86–8.00, p < 0.001).
Conclusions: Our study suggests that disturbances of pharmacokinetic mechanisms might
contribute to lower plasma SA levels, and subsequently incomplete inhibition of thromboxane A2
synthesis as measured with S-TxB2 concentrations and increased platelet reactivity measured
with VerifyNow in T2DM patients.
Keywords: aspirindiabetessalicylic acidplatelet reactivityplatelet function testing
