We read with great interest the article by Vaz et al. who investigated markers of oxidative stress in 70 thrombotic primary antiphospholipid patients (PAPS) and in 74 controls [1]: the authors were surprised not to fnd elevated plasma levels of such markers, amongst which 8-isoprostanes, in their PAPS population; this seem contrary to what was found in a recent meta-analysis, where pooled data from PAPS patients showed higher urinary/plasma concentrations of 8-isoprostanes compared to systemic lupus erythematosus with APS and to systemic lupus without APS [2]. There are potential explanations for the discrepancy noted by Vaz et al. in terms of methodology of 8-isoprostane measurement, patient population, comorbidities, treatment and expression of antiphospholipid antibody results. With regards to the frst issue, plain immunoassays for 8-isoprostane, not preceded by a purifcation step, are poorly reliable in plasma and less so in urine owing to the cross-reactivity between several prostaglandins and to the binding of the antibody that may be hampered by impurities, therefore underestimating true values [3]. In addition, total antioxidant capacity is a non-specifc method to assess oxidative imbalance; a more specifc assay evaluating specifc antioxidant pathways, such as the blood hydrogen peroxide break-down activity may provide more precise and reliable results.
REPLY to “Association Between Plasmatic Oxidative Stress and Thrombosis in Primary Antiphospholipid Syndrome” / Bucci, T.; Pastori, D.; Ames, P. R. J.. - In: JOURNAL OF THROMBOSIS AND THROMBOLYSIS. - ISSN 0929-5305. - (2022). [10.1007/s11239-021-02625-x]
REPLY to “Association Between Plasmatic Oxidative Stress and Thrombosis in Primary Antiphospholipid Syndrome”
Bucci T.;Pastori D.;
2022
Abstract
We read with great interest the article by Vaz et al. who investigated markers of oxidative stress in 70 thrombotic primary antiphospholipid patients (PAPS) and in 74 controls [1]: the authors were surprised not to fnd elevated plasma levels of such markers, amongst which 8-isoprostanes, in their PAPS population; this seem contrary to what was found in a recent meta-analysis, where pooled data from PAPS patients showed higher urinary/plasma concentrations of 8-isoprostanes compared to systemic lupus erythematosus with APS and to systemic lupus without APS [2]. There are potential explanations for the discrepancy noted by Vaz et al. in terms of methodology of 8-isoprostane measurement, patient population, comorbidities, treatment and expression of antiphospholipid antibody results. With regards to the frst issue, plain immunoassays for 8-isoprostane, not preceded by a purifcation step, are poorly reliable in plasma and less so in urine owing to the cross-reactivity between several prostaglandins and to the binding of the antibody that may be hampered by impurities, therefore underestimating true values [3]. In addition, total antioxidant capacity is a non-specifc method to assess oxidative imbalance; a more specifc assay evaluating specifc antioxidant pathways, such as the blood hydrogen peroxide break-down activity may provide more precise and reliable results.File | Dimensione | Formato | |
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