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1.
Rev. colomb. ortop. traumatol ; 35(2): 141-146, 2021. ilus.
Article in Spanish | LILACS, COLNAL | ID: biblio-1378599

ABSTRACT

Introducción El objetivo del estudio es pormenorizar los factores asociados a fracturas de cadera, prestando especial atención a las necesidades de transfusión de hemoderivados y sus factores de riesgo, así como su modificación a través del tratamiento preoperatorio mediante la administración de hierro intravenoso. Materiales y métodos Estudio observacional prospectivo de 119 pacientes ingresados por fractura de cadera. Descripción detallada del protocolo para la optimización prequirúgica de estos pacientes. Se recopilaron datos epidemiológicos, valores analíticos, así como datos acerca de la administración de hierro intravenoso y necesidad de transfusión. Resultados El 31,09% de los pacientes se encontraban antiagregados y el 21,85% estaban anticoagulados en el momento de la admisión. La hemoglobina media al ingreso fue de 12,5g/dl. El 43,2% se transfundieron durante la estancia hospitalaria. En el análisis de los factores de riesgo para la transfusión demostramos estadísticamente que tanto la hemoglobina al ingreso (p<0.001), como los diagnósticos previos de anemia crónica, hipertensión arterial e insuficiencia renal, tienen una relación con la necesidad de transfusión intrahospitalaria. Encontramos una relación estadísticamente significativa entre la administración de hierro y la cantidad de concentrados de hematíes trasfundidos (p<0.005). Los requerimientos de transfusión sanguínea fueron mayores en las fracturas extracapsulares que en las intracapsulares (p=0,024). Discusión Los pacientes con fractura de cadera presentan frecuentemente bajos niveles de hemoglobina al ingreso, así como comorbilidades y tratamientos que predisponen al desarrollo de anemia perioperatoria. La optimización preoperatoria de estos pacientes mediante la administración de hierro intravenoso podría reducir las necesidades transfusionales.


Background Aim of the study is to describe the elements associated with hip fractures about needs for transfusion of blood products and their risk factors, as well as their modification through preoperative treatment through the administration of intravenous iron. Material and methods A Cohort study of 119 patients admitted for hip fracture was conducted. Detailed description of the protocol for the pre-surgical optimization of these patients, epidemiological data, analytical values, as well as data on intravenous iron administration and need for transfusion were collected. Results 31.09% of the patients were using platelet aggregation inhibitors and 21.85% were were using anticoagulants at the time of admission. The mean hemoglobin on admission was 12.5g / dl. 43.2% were transfused during the hospital stay. In the analysis of risk factors for transfusion, we statistically demonstrated that both hemoglobin on admission (p <0.001), as well as previous diagnoses of chronic anemia, arterial hypertension, and renal failure, are related to the need for intra-hospital transfusion. We found a statistically significant relationship between iron administration and the amount of packed red blood cells transfused (p <0.005). Blood transfusion requirements were higher in extra-capsular than in intra-capsular fractures (p=0.024). Discussion Patients with hip fracture frequently present low hemoglobin levels upon admission, as well as comorbidities and treatments that predispose to the development of perioperative anemia. Preoperative optimization of these patients by administering intravenous iron could reduce transfusion requirements.


Subject(s)
Humans , Hip Fractures , Blood Transfusion , Hemoglobins , Iron , Anticoagulants
2.
Rev. cuba. anestesiol. reanim ; 13(1): 64-72, ene.-abr. 2014.
Article in Spanish | LILACS | ID: lil-739143

ABSTRACT

Introducción: las terapias de anticoagulación y antiagregación son frecuentemente utilizadas en pacientes cardiópatas. La conducción anestésica de estos pacientes tiene peculiaridades que de no cumplirlas puede llevar a complicaciones severas o a la muerte del paciente. Objetivo: revisar la conducta anestésica ante un paciente cardiópata anticoagulado para cirugía no cardiaca electiva y de urgencia. Método: se hizo una revisión de las características del paciente cardiópata anticoagulado, se analizaron las causas de la anticoagulación y se valoró la interrupción o no del tratamiento anticoagulante ante procederes mayores, menores, electivos y urgentes. Se detalla la monitorización intraoperatoria y la reiniciación del tratamiento anticoagulante post-cirugía. Conclusiones: el éxito de la cirugía no cardiaca del paciente cardiópata anticoagulado, sólo es posible gracias al conocimiento y cumplimiento de las particularidades de estos pacientes. No es posible improvisar ante estos casos, que implican una gran responsabilidad médica y legal para el anestesiólogo.


Introduction: therapies of anti coagulation and anti aggregation are frequently used in cardiopath patients. The anesthetic conduction of these patients has some peculiarities which in case they are not fulfilled they may lead to severe complications or even the death of the patient. Objective: to revise the anesthetic conduct in front of cardiopath patients and is anti coagulated for elective or emergent non cardiac surgery. Method: a revision of the characteristics of this patient was carried out, the causes of anti coagulation were analyzed , the causes of anti coagulation were analyzed as well as the causes of anti coagulation and the interruption or not of the anti coagulant treatment ante main, minor, elective or urgent procedures. The intra operative monitoring is detailed and the reinitiating of post surgery anti coagulant treatment. Conclusion: the success of the non cardiac surgery of the cardiopath patient and takes an anti coagulant treatment is only possible thanks to the knowledge and fulfillment of particularities of this patient. It is not possible to improvise with these cases which explain a great medical legal responsibility for the anesthesiologist.

3.
Experimental Neurobiology ; : 36-44, 2014.
Article in English | WPRIM | ID: wpr-187156

ABSTRACT

Huntington's disease (HD) is a late-onset and progressive neurodegenerative disorder that is caused by aggregation of mutant huntingtin protein which contains expanded-polyglutamine. The molecular chaperones modulate the aggregation in early stage and known for the most potent protector of neurodegeneration in animal models of HD. Over the past decades, a number of studies have demonstrated molecular chaperones alleviate the pathogenic symptoms by polyQ-mediated toxicity. Moreover, chaperone-inducible drugs and anti-aggregation drugs have beneficial effects on symptoms of disease. Here, we focus on the function of molecular chaperone in animal models of HD, and review the recent therapeutic approaches to modulate expression and turn-over of molecular chaperone and to develop anti-aggregation drugs.


Subject(s)
Huntington Disease , Models, Animal , Molecular Chaperones , Neurodegenerative Diseases
4.
Rev. colomb. cardiol ; 19(1): 25-32, ene.-feb. 2012.
Article in Spanish | LILACS | ID: lil-648038

ABSTRACT

Objetivo: realizar una revisión estructurada de la interacción clopidogrel y omeprazol, establecer su relevancia clínica y generar recomendaciones prácticas respecto al tema. Método: revisión estructurada en PubMed/MedLine de trabajos publicados en los últimos diez años, utilizando como estrategia clopidogrel AND omeprazole. La información se agrupó y complementó acorde con el método utilizado para la cuantificación del efecto y con la determinación de un posible efecto de clase. Resultados: la búsqueda generó 35 artículos, de ellos se incluyeron 18 (cinco valoraron la interacción in-vitro, seis la interacción in-vivo y diez la interacción como un efecto de clase). Siete estudios reportaron pérdida del efecto antiagregante, mientras que tres no encontraron una alteración relevante del mismo. Conclusiones: la evidencia de la relevancia clínica de la interacción clopidogrel y omeprazol no es concluyente. Se recomienda seguir las indicaciones de las agencias regulatorias y, en algunos casos, sustituir omeprazol por pantoprazol.


Objective: to perform a structured review of the clopidogrel and omeprazole interaction, establish its clinical relevance and generate practical recommendations on the subject. Method: a structured review on PubMedLine of studies published in the last ten years, using clopidogrel AND omeprazole as strategy. The information was grouped and complemented according to the method used to quantify the effect and with the determination of a possible class effect. Results: the search generated 35 articles, of which 18 were included (five assessed the in-vitro interaction, six the in-vivo interaction and ten analyzed the interaction as a class effect). Seven studies reported loss of the platelet anti-aggregation effect, while three found no significant alteration of the effect. Conclusions: the evidence of the clinical relevance of clopidogrel and omeprazole interaction is nor conclusive. It is recommended to follow the regulatory agencies indications, and in some cases replace omeprazole for pantoprazole.


Subject(s)
Pharmacokinetics , Platelet Aggregation Inhibitors
5.
Chinese Pharmacological Bulletin ; (12): 45-48, 2005.
Article in Chinese | WPRIM | ID: wpr-857393

ABSTRACT

Aim: To study the effect of PLC on rabbit platelet cAMP, and then to explore the mechanism of PLC anti-aggregation to platelet. Method: Rabbit platelets removed of red cells were treated with PSS, ASA and different dose of PLC respectively and induced by ADP respectively. cAMP was extracted by trichloroacetic acid. The concentration of cAMP of differently treated platelets was determined by RIA (radioimmunoassay). Result: When rabbit platelets were treated with PSS, the concentration of cAMP at static state was 20.16 ± 0.91 pmol/109 platelets; when the platelets were treated with PSSinverted commasASA 668 μ mol·L-1, 5,10,15,20 and 25 U PLC·ml-1, the concentration of cAMP of determined at activated state induced by ADP was 13.85 ± 1.14, 16.27 ± 0.36, 18.74 ± 0.55, 19.80 ± 0.52, 20.49 ± 0.43, 22.55 ± 0.61 and 24.24 ± 0.85 (pmol/109 platelets) respectively. Compared with PSS, enhanced rates (%) of ASA 668 μmol·L-1, 5, 10, 15, 20, 25 U PLC·ml-1 to the concentration of cAMP were 17.47, 35.31, 42.96, 47.94, 62.82, 75.02 respectively. Conclusion: PLC has significant effects on the concentration of cAMP of rabbit platelets (P < 0.01), and increases cAMP dose-dependantly(P < 0.01). All these indicate PLC can enhance the concentration of cAMP. This may be one of the important reason why PLC can inhibit platelet aggregation.

6.
Chinese Pharmacological Bulletin ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-555259

ABSTRACT

Aim To study the effect of PLC on rabbit and human platelet actin polymerization, and then to explore the mechanism of PLC anti-aggregation to platelet. Methods Platelets of rabbit and human were treated with PSS, ASA and different doses of PLC respectively and then were extracted by Triton abstraction. The relative concentration of actin of differently treated platelets induced by ADP was determined by SDS-PAGE and spectrophotometre. Results For rabbit platelets were treated with PSS, the relative concentration of actin determined at static state was 1.682?0.319; when the platelets were treated with ASA 668 ?mol?L -1,PLC 5,10,15,20 and 25 U?ml -1, the relative concentration of actin determined at activated state induced by ADP was 2.450?0.562,1.089?0.322,1.727?0.442,1.450?0.324,1.161?0.306, 0.857?0.242 and 0.692?0.187 respectively. Compared with PSS, inhibition rates (%) of ASA 668 ?mol?L -1, PLC 5, 10, 15, 20, 25 U?ml -1 to the relative concentration of actin were 55.55,29.51, 40.82,52.61, 65.02,71.76 respectively.For human platelets were treated with PSS, the relative concentration of actin determined at static state was 1.358?0.376; when the platelets were treated with ASA 668 ?mol?L -1,PLC 5,10,15,20 and 25 U?ml -1, the relative concentration of actin determined at activated state induced by ADP was 2.445?0.750, 1.096?0.344, 1.705?0.507,1.437?0.416, 1.165?0.355, 0.845?0.257 and 0.679?0.198 respectively. Compared with PSS, inhibition rates (%) of ASA 668 ?mol?L -1, PLC 5, 10, 15, 20, 25 U?ml -1 to the relative concentration of actin were 55.17,30.27, 41.23,52.35, 65.44, 72.23 respectively. Conclusion PLC has significant effects on actin polymerization of rabbit and healthy human platelets (P

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