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Review [Platelet activation and hypercholesterolemia in the pathogenesis of deep vein thrombosis] 2006
Martínez M, Labiós M, Gabriel F. · Departamento de Biopatología Clínica, Hospital Universitario La Fe, Valencia, España. · Med Clin (Barc). · Pubmed #17169286 No free full text.
Abstract: Currently it is accepted that deep vein thrombosis is a multifactorial event in which the presence of activated platelets and also plasmatic lipids seems to play a pivotal role that it is not well established in the scientific bibliography. Due to the non consensus state about these topics between the different groups working in these aspects, the topic involving deep vein thrombosis-platelets-lipids, and also their interactions, still is an interesting area of investigation, in which it is necessary to carry out studies with the aim of establishing risk factors, initial diagnostic methods and clinical assays to probe the efficacy of new therapies.
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Clinical Conference Effect of a modified fibrate (Biniwas Retard) on hemorheological alterations in hyperlipemic patients. 1999
Labios M, Martínez M, Vayá A, Gabriel F, Guiral V, Aznar J. · Hypertension Unit, Hospital Clínico Universitario, Valencia, Spain. · Clin Hemorheol Microcirc. · Pubmed #10599590 No free full text.
Abstract: The effect of a binifibrate (Biniwas Retard, Wasserman) on the plasma lipids and hemorheological profile of 30 primary hyperlipemic patients was studied. Our results indicate that the patients under study had evident rheological alterations as well as the expected lipid alterations. Treatment with Biniwas (2 x 550 mg/day) for six months not only substantially improved the alterations in the lipid balance but also tended to normalize the patients' hemorheological alterations, and there was a statistically significant correlation between the two effects. Apart from the decrease in plasma viscosity (1.20 +/- 0.05 vs 1.29 +/- 0.07 mPa.s, p < 0.001), the most noteworthy effects of Biniwas treatment were the decrease in red blood cell aggregability (8.7 +/- 1.2 vs 9.3 +/- 1.1, p < 0.05) and increased deformability (55 +/- 3 vs 47 +/- 5%, p < 0.001). Both changes may be due to modifications in the lipid composition of the erythrocyte membrane due to cell-plasma lipid exchange.
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Article [Musculoskeletal adverse effects of levofloxacin] free! 2006
Rivero M, Otermin I, Pereda A, Cía M, Martínez M. · Clínica Ubarmin, Elcano, Navarra. · Rev Esp Quimioter. · Pubmed #17235408 links to free full text
This publication has no abstract.
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Article Effect of atorvastatin upon platelet activation in hypercholesterolemia, evaluated by flow cytometry. 2005
Labiós M, Martínez M, Gabriel F, Guiral V, Martínez E, Aznar J. · Department of Internal Medicine, Clinic University Hospital, Valencia, Spain. · Thromb Res. · Pubmed #15668185 No free full text.
Abstract: Hyperlipidemia is a well established risk factor for cardiovascular disease and atherothrombotic events, in which platelet activation also plays a significant role. However, very few studies have addressed platelet activation in hypercholesterolemia, the potential effect of lipid lowering drugs upon platelet hyperfunction, and the question of whether changes in the latter are correlated to normalization of plasma lipids. This study used whole blood flow cytometry to assess in vivo and in vitro platelet activation in a group of 33 patients with hypercholesterolemia, and also the ex vivo effect of atorvastatin (20 mg/day) upon such activation. A control group of 40 normolipidemic volunteers matched in terms of age, sex and added risk factors to the patient group was used. The results showed that hypercholesterolemic patients had in vivo a significantly greater percentage of GPIIb/IIIa- and phosphatidylserine-positive platelets compared with the control group (4.62+/-3.51% and 2.58+/-1.19% versus 2.73+/-1.08% and 1.54+/-0.68%, respectively). In vitro response of CD62 expression to thrombin was also greater in the patients than in the controls (92.51+/-6.00% versus 89.63+/-10.72%, p<0.05). Atorvastatin therapy normalized platelet hyperfunction in the patients studied and reduced GPIIb/IIIa response to ADP (from 82.65+/-6.43% to 75.84+/-4.89%, p<0.01). A significant correlation can be seen between such normalization and the decrease in plasma levels of total and LDL cholesterol.
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Article Plasma lipids and blood fluidity in patients with polygenic hypercholesterolaemia treated with fluvastatin. 2002
Piñon F, Merino JF, Ferrer JC, Martínez M, Vayá A, Aznar J. · Endocrinology and Nutrition Department, "LA FE" University Hospital, Valencia, Spain. · Clin Hemorheol Microcirc. · Pubmed #12454376 No free full text.
Abstract: The clinical benefit brought about by HMG-CoA reductase inhibitors (statins) may not entirely be due to their lipid-lowering effect. Further investigation is necessary in order to determine the significance of ancillary effects to the clinical benefit of statin treatment. We studied 27 polygenic hypercholesterolaemia (PHC) patients before and 3 and 6 months after fluvastatin treatment. A control group of 38 normal, sex and age matched, subjects were also studied. The following parameters were measured: haematimetry, serum lipids and general biochemistry, apo-A/B and lipoproteins, fibrinogen, blood filterability, red blood cell aggregation, blood and plasma viscosity. PHC patients showed lower blood filterability (16.00+/-0.99 vs 19.90+/-2.90 microl/s), higher plasma fibrinogen (274.8+/-41.5 vs 241.6+/-43.2 mg/dl), increased erythrocyte aggregation at low shear stress (8.10+/-1.15 vs 7.19+/-1.29) and increased plasma viscosity (1.26+/-0.06 vs 1.23+/-0.05 mPa.s). Notable lipid changes after 6 months fluvastatin treatment were not accompanied by measurable changes in the haemorheological alterations of the PHC patients.
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Article Thrombomodulin levels in asymptomatic familial hypercholesterolemia. 1999
Vayá A, Martínez M, Ballesta A, Martí R, Ortuño C, Aznar J. · Department of Clinical Pathology, La Fe Hospital, Valencia, Spain. · Clin Hemorheol Microcirc. · Pubmed #10416810 No free full text.
Abstract: In order to ascertain whether young asymptomatic patients with heterozygous familial hypercholesterolemia (FH) but without clinical signs of atherosclerosis have increased plasma thrombomodulin (TM) levels expressing early endothelial damage, we determined TM in 23 heterozygous FH subjects (aged 28-44 years, x: 32 +/- 6) and in a well matched control group (CG). In addition, carotid Doppler ultrasonography was done in all the patients and controls in order to assess the state of the vascular tree. Results show a tendency for FH subjects to have higher TM values than the CG (37.8 +/- 14.2 ng/ml vs. 30.1 +/- 11.2 ng/ml), although the differences are not statistically significant. When taken together the results of TM and carotid ultrasound, the sensitivity and specificity of the former were only 66% and 80%, respectively. The fact that only 66% of the FH patients with atherosclerotic injury had high TM values eliminates the possibility of using this as an early marker of atherosclerosis in FH individuals.
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