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Low dose of acetylsalicylic acid and oxidative stress-mediated endothelial dysfunction in diabetes: a short-term evaluation.

Tassone EJ, Perticone M, Sciacqua A, Mafrici SF, Settino C, Malara N, Mollace V, Sesti G, Perticone F - Acta Diabetol (2014)

Bottom Line: As expected, after 4 weeks of treatment, ASA induced a significant reduction of plasma thromboxane-A2, as a consequence of cyclooxygenase-1 inhibition.By contrast, ASA significantly increased the plasma and urine 8-iso-PGF2α, a well-known prothrombotic molecule, parallel to an increase of plasma NOX2 levels.The enhancement of this oxidative pathway is associated with a significant impairment of endothelial vasodilation, assessed by reactive hyperemia index (RHI).

View Article: PubMed Central - PubMed

Affiliation: Department of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, Campus Universitario di Germaneto, V.le Europa, 88100, Catanzaro, Italy, eli.jo@alice.it.

ABSTRACT
Current guidelines suggest the use of low doses of acetylsalicylic acid (ASA) for patients with diabetes mellitus (DM) in primary prevention. However, the evidences demonstrating the beneficial effect of ASA in primary prevention are conflicting. In this pilot study, we evaluated in a group of diabetic patients, in primary prevention, the impact of ASA treatment on oxidative stress and vascular function. We enrolled 22 newly diagnosed diabetic patients, without any previous clinical evidence of cardiovascular disease, to receive, in primary prevention, ASA (100 mg/daily). We tested, in basal condition, after 4 weeks of ASA administration and after 4 weeks of pharmacological washout, the impact of ASA treatment on endothelial function, assessed by a semipletysmographic method, measuring the main oxidative stress parameters related to it. As expected, after 4 weeks of treatment, ASA induced a significant reduction of plasma thromboxane-A2, as a consequence of cyclooxygenase-1 inhibition. By contrast, ASA significantly increased the plasma and urine 8-iso-PGF2α, a well-known prothrombotic molecule, parallel to an increase of plasma NOX2 levels. The enhancement of this oxidative pathway is associated with a significant impairment of endothelial vasodilation, assessed by reactive hyperemia index (RHI). The pharmacological washout reverted all parameters to basal condition. Our findings suggest that ASA utilization for primary prevention in diabetic patients causes a significant increase of oxidative stress burden impairing the vascular function. Present data, if confirmed on a larger population, could permanently discourage the use of the ASA for the primary prevention in patients with DM.

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Effects of ASA on NOX2 plasma levels in diabetic patients. ASA treatment was able to induce a significant increase of NOX2 levels, which returned to basal values after 4 weeks of pharmacological washout. * = P < 0.05 by ANOVA for repeated measures
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Fig3: Effects of ASA on NOX2 plasma levels in diabetic patients. ASA treatment was able to induce a significant increase of NOX2 levels, which returned to basal values after 4 weeks of pharmacological washout. * = P < 0.05 by ANOVA for repeated measures

Mentions: Four weeks administration of ASA was able to induce a NOX2 overexpression. In particular, NOX2 levels increased in plasma samples, from 7.93 ± 0.57 to 8.75 ± 1.38 ng/ml (P = 0.010). Interestingly, after the washout period, NOX2 levels decreased, returning nearly to basal levels (Fig. 3).Fig. 3


Low dose of acetylsalicylic acid and oxidative stress-mediated endothelial dysfunction in diabetes: a short-term evaluation.

Tassone EJ, Perticone M, Sciacqua A, Mafrici SF, Settino C, Malara N, Mollace V, Sesti G, Perticone F - Acta Diabetol (2014)

Effects of ASA on NOX2 plasma levels in diabetic patients. ASA treatment was able to induce a significant increase of NOX2 levels, which returned to basal values after 4 weeks of pharmacological washout. * = P < 0.05 by ANOVA for repeated measures
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4374120&req=5

Fig3: Effects of ASA on NOX2 plasma levels in diabetic patients. ASA treatment was able to induce a significant increase of NOX2 levels, which returned to basal values after 4 weeks of pharmacological washout. * = P < 0.05 by ANOVA for repeated measures
Mentions: Four weeks administration of ASA was able to induce a NOX2 overexpression. In particular, NOX2 levels increased in plasma samples, from 7.93 ± 0.57 to 8.75 ± 1.38 ng/ml (P = 0.010). Interestingly, after the washout period, NOX2 levels decreased, returning nearly to basal levels (Fig. 3).Fig. 3

Bottom Line: As expected, after 4 weeks of treatment, ASA induced a significant reduction of plasma thromboxane-A2, as a consequence of cyclooxygenase-1 inhibition.By contrast, ASA significantly increased the plasma and urine 8-iso-PGF2α, a well-known prothrombotic molecule, parallel to an increase of plasma NOX2 levels.The enhancement of this oxidative pathway is associated with a significant impairment of endothelial vasodilation, assessed by reactive hyperemia index (RHI).

View Article: PubMed Central - PubMed

Affiliation: Department of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, Campus Universitario di Germaneto, V.le Europa, 88100, Catanzaro, Italy, eli.jo@alice.it.

ABSTRACT
Current guidelines suggest the use of low doses of acetylsalicylic acid (ASA) for patients with diabetes mellitus (DM) in primary prevention. However, the evidences demonstrating the beneficial effect of ASA in primary prevention are conflicting. In this pilot study, we evaluated in a group of diabetic patients, in primary prevention, the impact of ASA treatment on oxidative stress and vascular function. We enrolled 22 newly diagnosed diabetic patients, without any previous clinical evidence of cardiovascular disease, to receive, in primary prevention, ASA (100 mg/daily). We tested, in basal condition, after 4 weeks of ASA administration and after 4 weeks of pharmacological washout, the impact of ASA treatment on endothelial function, assessed by a semipletysmographic method, measuring the main oxidative stress parameters related to it. As expected, after 4 weeks of treatment, ASA induced a significant reduction of plasma thromboxane-A2, as a consequence of cyclooxygenase-1 inhibition. By contrast, ASA significantly increased the plasma and urine 8-iso-PGF2α, a well-known prothrombotic molecule, parallel to an increase of plasma NOX2 levels. The enhancement of this oxidative pathway is associated with a significant impairment of endothelial vasodilation, assessed by reactive hyperemia index (RHI). The pharmacological washout reverted all parameters to basal condition. Our findings suggest that ASA utilization for primary prevention in diabetic patients causes a significant increase of oxidative stress burden impairing the vascular function. Present data, if confirmed on a larger population, could permanently discourage the use of the ASA for the primary prevention in patients with DM.

Show MeSH
Related in: MedlinePlus