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Abstract Number: 7

Beneficial Effects of in Vivo Ubiquinol Supplementation on Athero-Thrombosis Prevention in Antiphospholipid Syndrome Patients

Chary Lopez-Pedrera1, Carlos Perez-Sanchez1, Ángeles Aguirre Zamorano1, Nuria Barbarroja1, Patricia Ruiz-Limon1, Yolanda Jiménez Gómez1, Munther A. Khamashta2, Antonio Rodriguez-Ariza3, Jose Antonio Gonzalez-Reyes4, Jose Manuel Villalba5, Eduardo Collantes-Estevez1 and Mª Jose Cuadrado6, 1Rheumatology Unit, IMIBIC-Reina Sofia University Hospital, Cordoba, Spain, 2Lupus Research Unit, The Rayne Institute, St Thomas Hospital, Kings College London School of Medicine, London, United Kingdom, 3Oncology Service and Research Unit, IMIBIC-Reina Sofia Hospital, Cordoba, Spain, 4Cell Biology, Physiology, and Immunology, University of Cordoba, Agrifood Campus of International Excelence (ciA3), Cordoba, Spain, 5Cell Biology, Physiology and Immunology, University of Cordoba, Agrifood Campus of International Excelence (ciA3), Cordoba, Spain, 6Lupus Research Unit, The Rayne Institute, London, United Kingdom

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: antiphospholipid syndrome, thrombosis and treatment

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Session Information

Title: Antiphospholipid Syndrome

Session Type: Abstract Submissions (ACR)

Background/Purpose

To investigate the beneficial effects of in vivoubiquinol (Q) supplementation on athero-thrombosis prevention in APS patients.

Methods

The study was performed on 10 APS patients randomized to receive either Q (200 mg/day) or placebo for one month. Blood was drawn at time 0 and at the end of the treatment. Studies were conducted in plasma and purified leukocytes subsets. Plasma Q levels and various prothrombotic/proinflammatory parameters and oxidative stress biomarkers were evaluated. Endothelial activity analysis was performed by Laser-Doppler flowmetry measurement of post ischemic reactive hyperemia.

Results

All patients completed the intervention, which increased significantly plasma Q levels. CD14highCD16- classical monocyte count was not significantly changed after Q treatment but CD14highCD16+ intermediate monocytes and CD14dimCD16high non-classical monocytes were decreased. Q treatment decreased significantly Tissue Factor (TF) expression levels in total monocytes, and more notably in CD14highCD16+ intermediate monocytes which also displayed a more robust reduction of intracellular IKK levels. Only this monocytes subset exhibited IL-8 reduction after intervention. Q supplementation produced a significant reduction in both the levels of peroxides and the percentage of monocytes with altered mitochondrial membrane potential (ΔΨm), and in six of the ten patients evaluated endothelial function was improved as shown by a significant amelioration in the highest perfusion value after occlusion was released, expressed as a percentage of change vs rest flow value (RF-PF). Q effects were particularly relevant in APS patients suffering from arterial thrombosis (AT) in comparison to those with venous thrombosis (VT) or obstetrical manifestations (OM) since TF expression, being particularly higher at baseline in AT patients, showed a more pronounced decline and endothelial function was better improved.

Correlation studies showed that reduced monocyte TF expression after Q treatment were related to both decreased peroxides levels and increased plasma Q levels. The decrease of CD14dimCD16high non-classical monocytes count was related to the reduction in the percentage of cells with altered ΔΨm as well as with the increase in RF-PF value. Improvement in endothelial function was further related to reduction of peroxide levels and to reduced TF expression on non-classical monocytes.

Conclusion

Q supplementation at 200 mg/d significantly reduced TF expression and oxidative stress markers in monocytes from APS patients, which were further related to an improvement on endothelial function. Our results support the potential impact of Q in the prevention of atherothrombosis in APS patients.

Supported by: CTS-7940, PI12/01511, Spanish Rheumatology Society, KANEKA Corporation.


Disclosure:

C. Lopez-Pedrera,
None;

C. Perez-Sanchez,
None;

Aguirre Zamorano,
None;

N. Barbarroja,
None;

P. Ruiz-Limon,
None;

Y. Jiménez Gómez,
None;

M. A. Khamashta,
None;

A. Rodriguez-Ariza,
None;

J. A. Gonzalez-Reyes,
None;

J. M. Villalba,
None;

E. Collantes-Estevez,
None;

M. J. Cuadrado,
None.

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