Probucol and ticlopidine: effect on platelet and monocyte activation markers in hyperlipidemic patients with and without type 2 diabetes
Autor: | Hisato Nakamori, Nobuyuki Takahashi, Shosaku Nomura, Kohichi Yamada, Takayuki Kajiura, Norihito Inami, Nobuyuki Tsuda |
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Rok vydání: | 2004 |
Předmět: |
Male
medicine.medical_specialty Ticlopidine Combination therapy Probucol Hyperlipidemias Type 2 diabetes Sensitivity and Specificity Monocytes Reference Values Malondialdehyde Internal medicine Diabetes mellitus Hyperlipidemia medicine Humans Prospective Studies Platelet activation Aged Probability Analysis of Variance business.industry Type 2 Diabetes Mellitus Middle Aged Platelet Activation medicine.disease P-Selectin Endocrinology Diabetes Mellitus Type 2 Drug Therapy Combination Female E-Selectin Cardiology and Cardiovascular Medicine business Biomarkers medicine.drug |
Zdroj: | Atherosclerosis. 174:329-335 |
ISSN: | 0021-9150 |
Popis: | We investigated the effects of probucol and ticlopidine on circulating levels of platelet activation markers, microparticles, soluble selectins, and malondialdehyde-low density lipoprotein (MDA-LDL) in hyperlipidemic patients with or without type 2 diabetes. There were significant differences in the levels of CD62P, PAC-1, annexin V, PDMP, MDMP, sP-selectin, sE-selectin and MDA-LDL between the hyperlipidemic patients and the controls. In particular, these markers were significantly increased in hyperlipidemic patients who had type 2 diabetes. In the hyperlipidemic patients with diabetes, MDA-LDL was decreased by both monotherapy with probucol and combination therapy (probucol and ticlopidine). In these patients, CD62P, PAC-1, annexin V, MDMP, PDMP, sP-selectin, and sE-selectin were also significantly decreased after treatment. The decreases of CD62P, PAC-1, annexin V, PDMP and sP-selectin were greater combination therapy than with monotherapy. These findings suggest that administration of probucol and ticlopidine to hyperlipidemic patients with type 2 diabetes may help to prevent the development of cardiovascular complications caused by modified LDL, selectins, or activated platelets and monocytes. |
Databáze: | OpenAIRE |
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