33 research outputs found
Dificultades en la clasificación del síndrome metabólico: El ejemplo de los adolescentes en México
OBJETIVO. Determinar la diferencia entre las definiciones del National Cholesterol Education Program Adult Treatment Panel (ATPIII) y de la International Diabetes Federation (IDF) para síndrome metabólico (SM) en adolescentes mexicanos. MATERIAL Y MÉTODOS. Estudio transversal en 575 adolescentes de 14 a 16 años. Se utilizaron pruebas t de Student, ji cuadrada y correlación de Spearman. RESULTADOS. La prevalencia de SM fue mayor por ATPIII (18.6%) versus IDF (8.2%) (p<0.001), con 41.1% de concordancia. CONCLUSIONES. Existe una diferencia estadística de la prevalencia del SM en adolescentes mexicanos entre las dos definiciones
Rituximab therapy for chonic and refractory immune thrombocytopenic purpura: a long-term follow-up analysis
The aim of this study was to evaluate the long-term response to rituximab in patients with chronic and refractory immune thrombocytopenic purpura (ITP). Adults with ITP fail to respond to conventional therapies in almost 30% of cases, developing a refractory disease. Rituximab has been successfully used in these patients. We used rituximab at 375 mg/m2, IV, weekly for a total of four doses in 18 adult patients. Complete remission (CR) was considered if the platelet count was >100 × 109/l, partial remission (PR) if platelets were >50 × 109/l, minimal response (MR) if the platelet count was >30 × 109/l and <50 × 109/l, and no response if platelet count remained unchanged. Response was classified as sustained (SR) when it was stable for a minimum of 6 months. Median age was 43.5 years (range, 17 to 70). Median platelet count at baseline was 12.5 × 109/l (range, 3.0 to 26.3). CR was achieved in five patients (28%), PR in five (28%), MR in four (22%), and two patients were classified as therapeutic failures (11%). Two additional patients were lost to follow-up. The median time between rituximab therapy and response was 14 weeks (range, 4 to 32). SR was achieved in 12 patients (67%). There were no severe adverse events during rituximab therapy. During follow-up (median, 26 months; range, 12 to 59), no other immunosuppressive drugs were used. In conclusion, rituximab therapy is effective and safe in adult patients with chronic and refractory ITP. Overall response rate achieved is high, long term, and with no risk of adverse events
Protein C activation peptide inhibits the expression of ICAM-1, VCAM-1, and interleukin-8 induced by TNF-a in human dermal microvascular endothelial cells
Activated protein C (APC) is generated from the cleavage of protein C by thrombin coupled to thrombomodulinand, subsequently, is released as protein C activation peptide (papC). The aim of this study was toevaluate the effect of papC on human dermal microvascular endothelial cells (HMEC-1), activated with 5 ng//mL TNF-a. Flow cytometry showed that papC inhibited the expression of VCAM-1 and ICAM-1, after activationwith TNF-a. Similarly, RT-PCR analysis revealed that 2 and 4 pM papC inhibited the expression of VCAM-1and IL-8 mRNA in TNF-a-treated HMEC-1. In addition, the expression of endothelial nitric oxide synthase(eNOS) increased in HMEC-1 treated with papC, compared to those without treatment. Furthermore, Jurkatcell adhesion to HMEC-1 induced by TNF-a was significantly inhibited after the addition of papC, compared toHMEC-1 without papC (p = 0.03). Finally, a control peptide analog to papC showed no effect on the expressionof ICAM and VCAM on the surface of HMEC-1. In conclusion, our results suggest that papC exerts antiinflammatoryeffects on endothelial cells.Activated protein C (APC) is generated from the cleavage of protein C by thrombin coupled to thrombomodulinand, subsequently, is released as protein C activation peptide (papC). The aim of this study was toevaluate the effect of papC on human dermal microvascular endothelial cells (HMEC-1), activated with 5 ng//mL TNF-a. Flow cytometry showed that papC inhibited the expression of VCAM-1 and ICAM-1, after activationwith TNF-a. Similarly, RT-PCR analysis revealed that 2 and 4 pM papC inhibited the expression of VCAM-1and IL-8 mRNA in TNF-a-treated HMEC-1. In addition, the expression of endothelial nitric oxide synthase(eNOS) increased in HMEC-1 treated with papC, compared to those without treatment. Furthermore, Jurkatcell adhesion to HMEC-1 induced by TNF-a was significantly inhibited after the addition of papC, compared toHMEC-1 without papC (p = 0.03). Finally, a control peptide analog to papC showed no effect on the expressionof ICAM and VCAM on the surface of HMEC-1. In conclusion, our results suggest that papC exerts antiinflammatoryeffects on endothelial cells
Prevalence of Metabolic Syndrome Components in an Urban Mexican Sample: Comparison between Two Classifications
Background. The aim of this study was to examine the prevalence of metabolic syndrome (MS) components in an urban Mexican sample. Methods. A total of 854 subjects were included. Anthropometric, blood pressure measurements, clinical data, and overnight fasting blood samples were obtained from all subjects. Results. In accordance with definitions by the American Heart Association/ National Heart, Lung, and Blood Institute (AHA/NHLBI) and the International Diabetes Federation (IDF), the prevalence of MS among participants was 59.7 and 68.7%, respectively. The prevalence of MS was higher in women and in individuals older than 45 years of age. More than 40% of the subjects fulfilled four criterions of MS according to both definitions. Conclusions. There was a high prevalence of MS components in an urban Mexican sample. Therefore, strong strategies had to be developed for early detection of MS and its components to prevent DMT2 and atherothrombotic complications in these patients
Reduced proliferation of endothelial colony-forming cells in unprovoked venous thromboembolic disease as a consequence of endothelial dysfunction
Background
Venous thromboembolic disease (VTD) is a public health problem. We recently reported that endothelial colony-forming cells (ECFCs) derived from endothelial cells (EC) (ECFC-ECs) from patients with VTD have a dysfunctional state. For this study, we proposed that a dysfunctional status of these cells generates a reduction of its proliferative ability, which is also associated with senescence and reactive oxygen species (ROS).
Methods and results
Human mononuclear cells (MNCs) were obtained from peripheral blood from 40 healthy human volunteers (controls) and 50 patients with VTD matched by age (20−50 years) and sex to obtain ECFCs. We assayed their proliferative ability with plasma of patients and controls and supernatants of cultures from ECFC-ECs, senescence-associated β-galactosidase (SA-β-gal), ROS, and expression of ephrin-B2/Eph-B4 receptor. Compared with cells from controls, cells from VTD patients showed an 8-fold increase of ECFCs that emerged 1 week earlier, reduced proliferation at long term (39%) and, in passages 4 and 10, a highly senescent rate (30±1.05% vs. 91.3±15.07%, respectively) with an increase of ROS and impaired expression of ephrin-B2/Eph-4 genes. Proliferation potential of cells from VTD patients was reduced in endothelial medium [1.4±0.22 doubling population (DP)], control plasma (1.18±0.31 DP), or plasma from VTD patients (1.65±0.27 DP).
Conclusions
As compared with controls, ECFC-ECs from individuals with VTD have higher oxidative stress, proliferation stress, cellular senescence, and low proliferative potential. These findings suggest that patients with a history of VTD are ECFC-ECs dysfunctional that could be associated to permanent risk for new thrombotic events
Prevalence of Metabolic Syndrome Components in an Urban Mexican Sample: Comparison between Two Classifications
Background. The aim of this study was to examine the prevalence of metabolic syndrome (MS) components in an urban Mexican sample. Methods. A total of 854 subjects were included. Anthropometric, blood pressure measurements, clinical data, and overnight fasting blood samples were obtained from all subjects. Results. In accordance with definitions by the American Heart Association/ National Heart, Lung, and Blood Institute (AHA/NHLBI) and the International Diabetes Federation (IDF), the prevalence of MS among participants was 59.7 and 68.7%, respectively. The prevalence of MS was higher in women and in individuals older than 45 years of age. More than 40% of the subjects fulfilled four criterions of MS according to both definitions. Conclusions. There was a high prevalence of MS components in an urban Mexican sample. Therefore, strong strategies had to be developed for early detection of MS and its components to prevent DMT2 and atherothrombotic complications in these patients
Better detection of platelet aggregation in patients with metabolic syndrome using epinephrine and ADP
Alteraciones plaquetarias en la diabetes mellitus tipo 2
La diabetes mellitus es un grave problema de salud mundial. Las complicaciones vasculares son la principal causa de morbimortalidad. El diabético tiene una evolución aterotrombótica acelerada y peor que la de otras entidades clínicas; pese a ello, la hiperglucemia per se no explica por completo las complicaciones isquémicas que se observan en estos enfermos. La mayoría de los eventos isquémicos arteriales se precipitan por rotura de la placa ateroesclerótica, activación plaquetaria y la trombosis resultante. En la diabetes se producen diversas alteraciones del sistema de coagulación, como disfunción endotelial, hiperactividad plaquetaria, generación de trombina y fibrinólisis disminuida, eventos patológicos que favorecen la trombosis. La plaqueta es clave en la aterotrombosis diabética debido a que existe hipersensibilidad plaquetaria a agonistas y respuesta baja a los agentes antiplaquetarios terapéuticos, además de hiperactividad plaquetaria en sitios de daño endotelial, hiperagregabilidad, resistencia a los efectos inhibitorios de la insulina y una producción endotelial baja de prostaciclina y óxido nítrico. Estas alteraciones dependen del medio ambiente "tóxico" (hiperglucemia) o son intrínsecas a la plaqueta. Por todo lo anterior, la plaqueta es otro blanco de los efectos deletéreos de la resistencia a la insulina. Ya que la plaqueta es clave en la ateroesclerosis y en las complicaciones vasculares de la diabetes mellitus, esta revisión analiza las alteraciones plaquetarias características de esta enfermedad metabólica