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González-Conejero Hilla, Rocío

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González-Conejero Hilla, Rocío
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Universidad de Murcia. Departamento de Medicina
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    Neutrophil extracellular traps and von Willebrand factor are allies that negatively influence COVID-19 outcomes
    (Wiley, 2021-01) Águila Martínez, Sonia; Fernández-Pérez, M. P.; Reguilón-Gallego, L.; de Los Reyes-García, A. M.; Miñano, A.; Bravo-Pérez, C.; García-Barberá, N.; Gómez-Verdú, J. M.; Martínez, C.; Morena Barrio, María Eugenia de la; Corral de la Calle, Javier; Bernal Morell, Enrique; Herranz Marín, María Teresa; Vicente García, Vicente; González-Conejero Hilla, Rocío; Lozano Almela, María Luisa; Medicina Interna
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    Genetic variants of the extra-large stimulatory Gs protein alpha-subunit and risk of thrombotic and haemorrhagic disorders
    (Wiley, 2004-04-27) González-Conejero Hilla, Rocío; Corral de la Calle, Javier; Guerrero López, José Antonio; Iniesta Valera, Juan Antonio; Rivera Pozo, José; Arriba de la Fuente, Felipe de; Vicente García, Vicente; Medicina Interna
    A polymorphism of the gene encoding the extra-large stimulatory G-protein a-subunit (XLas), originally identified in three patients with a bleeding tendency, involved a 36-bp insertion and two missense changes. A paternallyinherited insertion displayed a moderate platelet Gsa over-expression, which lead to platelet hypo-reactivity. These data prompted us to investigate the genetic, functional and clinical relevance of this polymorphism in the Mediterranean population. We included 414 healthy subjects and three case/ control studies: 263 consecutive patients with a first episode of primary intracerebral haemorrhage, 195 patients with deep venous thrombosis, and 104 patients with cerebrovascular disease. Controls were selected by approximating criteria to match selected risk factors to patients. Moreover, we performed studies of platelet function. We developed a simple method to determine the methylated allele, by digestion of genomic DNA with Sma I before polymerase chain reaction amplification. We identified two new rare variants, resulting from the loss of repeat units 7 and 5. The AB genotype was present in 3Æ6% of healthy population and the prevalence of the B allele was similar among cases and controls. Accordingly, the non-methylated B allele did not modify either the expression of platelet Gsa or the platelet response to Gs-agonists. Thus, our study suggests a minor functional role of XLas polymorphism in thrombotic or in haemorrhagic disorders.
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    Biological assessment of aspirin efficacy on healthy individuals: heterogeneous response or aspirin failure?
    (2004-12-16) González-Conejero Hilla, Rocío; Rivera Pozo, José; Corral de la Calle, Javier; Acuña, Carmen; Vicente, Vincente; Guerrero López, José Antonio; Medicina Interna; Facultad de Medicina
    Background and Purpose— The widespread use of aspirin requires clarification of the aspirin resistance phenomenon. Most studies on this field are focused on patients which may affect the action of aspirin. Methods— We evaluated the biological efficacy of aspirin in healthy subjects. Results— Agonist–induced platelet aggregation was fully abrogated by 100 mg of aspirin in all individuals. By contrast, with the platelet function analyzer-100 device, 33.3% of the subjects displayed no response. This failure was overcome by 500 mg or by in vitro treatment of blood with 30 μmol/L acetylsalicylic acid. Intake of 100 mg of aspirin efficiently reduced by 75% the level of 11-dehydro thromboxane B2 (11-dTxB2) in all cases. However, variability on the pre-aspirin level (range 72.4 to 625.9 ng/mmol creatinine) led to substantial differences in the residual amount of the metabolite between subjects treated with aspirin (range 12.9 to 118.0 ng/mmol creatinine). Finally, there was no influence of platelet glycoprotein IIb/IIIa (Pro33Leu), platelet glycoprotein Ia/IIa, (C807T), and FXIII (Val34Leu) polymorphisms on the efficacy of aspirin. However, the cyclooxygenase (Cox)-1 50T allele associated with higher level of 11-dTxB2, both before and after aspirin. Moreover, the Cox-2 −765C variant displayed a slightly higher reduction in 11-dTxB2 level on treatment with aspirin. Conclusions— Our findings suggest that full resistance of healthy subjects to aspirin is rather unlikely. However, differences in aspirin absorption, or pharmacokinetic, or other unrecognized factors may lead to lack of effect of low dose of aspirin in some subjects when using tests like platelet function analyzer-100. Whether Cox polymorphisms are thrombotic risk factor for patients under aspirin will require further research.
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    Latent and polymeric antithrombin: Clearance and potential thrombotic risk
    (Frontiers Media, 2007) Guerrero López, José Antonio; Corral de la Calle, Javier; Rivera Pozo, José; Miñano, Antonia; Alberca, Ignacio; Hernández Espinosa, David; Ordóñez, Adriana; Martínez, Constantino; Navarro-Núñez, Leyre; González-Conejero Hilla, Rocío; Lozano Almela, María Luisa; Vicente García, Vicente; Medicina Interna
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