Tratamiento de la hipertensión arterial en accidente cerebrovascular

Revisión sistemática de la literatura en la que se discuten las controversias del manejo de la presión arterial en las emergencias neurológicas agudas cerebrovasculares como accidente cerebrovascular isquémico, hemorrágico y hemorragia subaracnoidea.

Factores de riesgo asociados al diagnostico de asfixia perinatal en el Hospital Universitario Mayor Méderi, Bogota, 2010-2011.

Objetivo: Determinar los factores de riesgo de anteparto, intraparto y fetales asociados a asfixia perinatal en los recién nacidos del servicio de neonatología del Hospital Universitario Mayor Méderi de Bogotá, 2010-2011. Materiales y métodos: Estudio de casos y controles pareado por fecha de nacimiento, con una relación 1:5(51:306). Las asociaciones se evaluaron con la prueba de ji-cuadrado de Mantel y Haenszel o Test de Fisher para datos pareados, con OR e intervalo de confianza del 95%, el análisis multivariado con un modelo de regresión logística condicional. Resultados: Los factores de riesgo con asociación significativa fueron: - Ante parto: Antecedentes patológicos maternos (OR=6.00,IC95%:1.55-23.19,p=0.013), primigestación (OR=1.91,IC95%:1.02-3.56,p=0,090), -Intraparto: Abruptio de placenta (OR=25,00,IC95%:2.92-213.99,p=0.001), hemorragia del tercer trimestre (OR=12.50,IC95%:2.43-64.43,p=0.001), Oligohidramnios(OR=6.25,IC95%:1.68-23.28,p=0.001), taquicardia fetal (OR=7.66,IC95%:1.67-35.04,p=0.011), monitoreo fetal intraparto anormal (OR=10.33,IC95%:4.38-24.34,p=0.001), expulsivo prolongado(OR=13.00,IC95%:4.63-36.46,p=0.001), fiebre materna(p<0.001), corioamnionitis(p<0.001), convulsiones maternas(p<0.001), bradicardia fetal (p=<0.001), -Fetales: Género masculino(OR=1.87,IC95%:1.02-3.44,p=0.026), edad gestacional por BALLARD igual ó <36semanas(OR=4.78(IC95%:2.21-10.35,p=0.001), vía del nacimiento instrumentado(OR=18,80,IC95%:3.69-39.55,p=0.001), líquido amniótico hemorrágico o teñido de meconio(OR= 9.00,IC95%:3.01-26.85,p=0.001), circular de cordón(OR=9.00,IC95%:3.59-22.52,p=0.001), peso al nacer igual ó <2500 gramos (OR=8.88,IC95%:3.73-21.15,p=0.001). Los subrayados y el síndrome hipertensivo asociado al embarazo se encontraron significativos en análisis multivariado. Conclusiones: Los factores de riesgo para asfixia perinatal fueron: antecedentes patológicos maternos, primigestación, abruptio de placenta, hemorragia del tercer trimestre, oligohidramnios, monitoreo fetal intraparto anormal, taquicardia y bradicardia fetal, expulsivo prolongado, corioamnionitis, fiebre materna, convulsiones maternas, género masculino, edad gestacional por BALLARD igual ó <36 semanas, vía del nacimiento instrumentado, líquido amniótico hemorrágico o teñido de meconio, circular de cordón, peso al nacer igual ó <2500 gramos.

Escala de Fisher como factor predictor de hidrocefalia en hemorragia subaracnoidea espontanea

Objetivo. Determinar si la cantidad de sangre y su localización es el espacio subaracnoideo, medible con la escala de Fisher en las primeras 24 horas de ocurrido el ictus hemorrágico, es un factor predictor para el desarrollo de hidrocefalia en pacientes con diagnóstico de hemorragia subaracnoidea (HSA) espontánea, vistos en el Hospital Universitario Clínica San Rafael (HUCSR) con seguimiento de 12 meses. Métodos. 251 pacientes fueron incluidos en una cohorte retrospectiva. La asociación entre la escala de Fisher y el desarrollo de hidrocefalia en pacientes con HSA espontánea fue analizada a través de un análisis bivariado y multivariado. Resultados. La edad promedio de los pacientes fue de 55,5 ± 15 años; con predominancia en el sexo femenino 65,7%. La prevalencia de hidrocefalia fue de 27,1% en la cohorte y la etiología de la HSA fue en su mayoría por ruptura de aneurismas de arterias cerebrales; 78,5%. La sobrevida a 12 meses fue de 65,7%. Tanto el grado 4 en la escala de Fisher como Hunt-Hess III se asocian con el desarrollo de hidrocefalia: ORA; 2.93 IC 95%: 1.51-5.65, P <0.001, ORA 2.83 IC 95%: 1.31-6.17 P=0.008 respectivamente. Conclusión. La presencia de sangrado Intraventricular o intraparenquimatoso ( Fisher 4) en las primeras 24 horas, asociado a un deterioro neurológico al ingreso Hunt-Hess III están asociados con el desarrollo de hidrocefalia en los 251 pacientes evaluados con diagnóstico de HSA espontánea; hallazgos consistentes con lo reportado en la literatura mundial.

Descripción del estado acido base en pacientes con quemaduras térmicas agudas: serie de casos

Introducción: Los pacientes con lesiones térmicas presentan alteraciones fisiológicas complejas que hacen difícil la caracterización del estado ácido-base y así mismo alteraciones electrolíticas e hipoalbuminemia que pudieran estar relacionados con un peor pronóstico. Se ha estudiado la base déficit (BD) y el lactato, encontrando una gran divergencia en los resultados. Por lo anterior, el análisis físico-químico del estado ácido-base podría tener un rendimiento superior a los métodos tradicionales. Metodología: Se realizó el análisis de una serie de casos de 15 pacientes mayores de 15 años, con superficie corporal quemada mayor al 20% que ingresaron a una unidad de cuidado intensivo (UCI) de quemados, dentro de las siguientes 48 horas del trauma. Para el análisis se utilizaron tres métodos distintos: 1) método convencional basado en la teoría de Henderson-Hasselbalch, 2) anión-gap (AG) y anión-gap corregido por albúmina, 3) análisis físico-químico del estado ácido-base según la teoría de Stewart modificado por Fencl y Figge. Resultados: Por el método de Henderson-Hasselbalch, 8 pacientes cursaron con acidosis metabólica, 4 pacientes con una BD leve, 5 pacientes con una BD moderada y 5 pacientes con una BD severa. El AG resultó menor a 16 mmol/dl en 10 pacientes, pero al corregirlo por albumina sólo 2 pacientes cursaron con AG normal. La diferencia de iones fuertes (DIF) se encontraba anormalmente elevada en la totalidad de los pacientes. Conclusión:El análisis del AG corregido por albumina y el análisis físico-químico del estado ácido-base, podrían tener mayor rendimiento al identificar las alteraciones metabólicas de estos pacientes.

Factores de riesgo para morbilidad materna extrema en gestantes

Introducción: La morbilidad materna extrema es un término usado para definir cualquier condición obstétrica severa que amenaza la vida y requiere una intervención médica urgente con el fin de prevenir la probable muerte materna. Con el presente estudio se pretendió evaluar los factores de riesgo para morbilidad materna extrema en las gestantes del Hospital Universitario Mayor. Metodología Se realizó un estudio de casos y controles, comparando pacientes con MME y sin MME en una relación de 1:1. Se realizó un muestreo aleatorio simple teniendo en cuenta 95% de la población apareadas por diagnóstico de ingreso. Resultados Se incluyeron un total de 110 pacientes (55 en cada grupo). Ambas poblaciones fueron comprables. Ser de estrato socioeconómico bajo (p 0,000), haber tenido 2 o menos partos (p 0,000), ser tipo de sangre negativo (p0.000) realizar entre 0-3 controles prenatales (p 0,000), tener antecedente de preeclampsia (p 0,000), hipotiroidismo (p 0,000), o trastorno bipolar (p 0,000), son factores de riesgo significativos para presentar MME. Entre los factores protectores están tener más de tres partos OR 0,60 (IC95%: 0,17-0,82, p=0,00) y 7 o más controles prenatales OR 0,23 (IC95%: 0,09-0,55, p=0,000). Resultados concordantes con la literatura Discusión: Es importante dar a conocer los resultados del presente estudio para promover las campañas de prevención primaria, secundaria y terciaria con el fin de evitar las altas complicaciones que se pueden presentar en las mujeres en edad fértil de nuestra población.

Riesgo cardiovascular de trabajadores de una empresa de hidrocarburos. 2014

Objetivo: Determinar el riesgo cardiovascular de los trabajadores de una empresa de hidrocarburos (E.H) mediante la aplicación de la escala Framingham REGICOR durante el año 2014. Métodos: Se realizó un estudio descriptivo tipo corte transversal a partir de los registros de 700 trabajadores de una empresa de hidrocarburos que tenían una historia clínica laboral con información completa. Resultados: La edad promedio fue de 33,6 años (σ 9,1). Se encontró una prevalencia de HTA (1,4%), tabaquismo (5,7%), hábito de tomar licor (66,4%) y exceso de peso (61,6%). La prevalencia de hipertensión arterial y tabaquismo fue de 1.71% y 5.7% respectivamente, de hipercolesterolemia el 39,00%, de hipertrigliceridemia del 30,14% y el 20,00% de los trabajadores son obesos. El 3,00% (21) de los trabajadores fueron clasificados como de riesgo moderado de sufrir un evento isquémico o hemorrágico en un periodo de 10 años. A pesar que ningún trabajador fue clasificado como riesgo alto, se recomienda se realicen actividades tendientes a que a los trabajadores generen conciencia sobre los riesgos de desarrollar un evento cardiovascular si no se modifican los estilos de vida.

Genetic characterization of tick-borne flaviviruses: new insights into evolution, pathogenetic determinants and taxonomy

Here, we analyze the complete coding sequences of all recognized tick-borne flavivirus species, including Gadgets Gully, Royal Farm and Karshi virus, seabird-associated flaviviruses, Kadam virus and previously uncharacterized isolates of Kyasanur Forest disease virus and Omsk hemorrhagic fever virus. Significant taxonomic improvements are proposed, e.g. the identification of three major groups (mammalian, seabird and Kadam tick-borne flavivirus groups), the creation of a new species (Karshi virus) and the assignment of Tick-borne encephalitis and Louping ill viruses to a unique species (Tick-borne encephalitis virus) including four viral types (i.e. Western Tick-borne encephalitis virus, Eastern Tick-borne encephalitis virus, Turkish sheep Tick-borne encephalitis virus and Louping ill Tick-borne encephalitis virus). The analyses also suggest a complex relationship between viruses infecting birds and those infecting mammals. Ticks that feed on both categories of vertebrates may constitute the evolutionary bridge between the three distinct identified lineages.

Development of peptide-conjugated morpholino oligomers as pan-arenavirus inhibitors

Members of the Arenaviridae are a threat to public health and can cause meningitis and hemorrhagic fever, yet treatment options remain limited by a lack of effective antivirals. In this study, we found that peptide-conjugated phosphorodiamidate morpholino oligomers (PPMO) complementary to viral genomic RNA were effective in reducing arenavirus replication in cell cultures and in vivo. PPMO complementary to the Junín virus genome were designed to interfere with viral RNA synthesis, translation, or both. However, only PPMO designed to potentially interfere with translation were effective in reducing virus replication. PPMO complementary to sequence that is highly conserved across arenaviruses and located at the 5’-termini of both genomic segments were effective against Junín, Tacaribe, Pichinde and Lymphocytic Choriomeningitis arenavirus-infected cell cultures, and suppressed viral titers in the livers of LCMV-infected mice. These results suggest that arenavirus 5’-genomic-termini represent promising targets for pan-arenavirus antiviral therapeutic development.

Lonomia obliqua (Lepidoptera, Saturniidae) caterpillar bristle extract induces direct lysis by cleaving erythrocyte membrane glycoproteins

Lonomia obliqua caterpillar bristle extract induces hemolysis in vitro on washed human and rat erythrocytes, in either the absence or presence of exogenous lecithin. In the former condition, phospholipases A(2) are key enzymes involved in hemolysis. However, the mechanism whereby this extract causes direct hemolysis is not known. Thus, the aim of this study was to investigate the hemolytic mechanism of the crude extract of the caterpillar L obliqua on human erythrocytes in the absence of lecithin. The extract significantly increased the erythrocyte osmotic fragility and promoted the removal of glycophorins A and C, and band 3 from the erythrocyte membrane. The use of Ca(2+) and Mg(2+) ions significantly potentiated glycoprotein removal, remarkably of erythrocyte band 3. The composition of fatty acids was analyzed by HPLC in both L obliqua caterpillar bristle extract and human erythrocyte membranes incubated with the extract. The levels of unsaturated fatty acids were remarkably augmented in erythrocytes incubated with the extract than in control erythrocytes, modifying thereby the saturated/unsaturated fatty acid ratio. Altogether, evidence is provided here that the interplay of at least three mechanisms of action accounts for the direct activity of the bristle extract on erythrocyte membrane, leading to hemolysis: the removal of glycoproteins and band 3; the insertion of fatty acids; and the action of phospholipases. Such mechanisms might affect erythrocyte flexibility and deformability, which may induce hemolysis by increasing erythrocyte fragility. However, whether the direct hemolytic activity of L obliqua caterpillar is the major cause of intravascular hemolysis during envenomation still needs further investigation. (C) 2010 Elsevier Ltd. All rights reserved.

TUMOR NECROSIS FACTOR IS NOT ASSOCIATED WITH INTESTINAL ISCHEMIA/REPERFUSION-INDUCED LUNG INFLAMMATION

Intestinal ischemia-reperfusion (I/R) injury may cause acute systemic and lung inflammation. Here, we revisited the role of TNF-alpha in an intestinal I/R model in mice, showing that this cytokine is not required for the local and remote inflammatory response upon intestinal I/R injury using neutralizing TNF-alpha antibodies and TNF ligand-deficient mice. We demonstrate increased neutrophil recruitment in the lung as assessed by myeloperoxidase activity and augmented IL-6, granulocyte colony-stimulating factor, and KC levels, whereas TNF-alpha levels in serum were not increased and only minimally elevated in intestine and lung upon intestinal I/R injury. Importantly, TNF-alpha antibody neutralization neither diminished neutrophil recruitment nor any of the cytokines and chemokines evaluated. In addition, the inflammatory response was not abrogated in TNF and TNF receptors 1 and 2-deficient mice. However, in view of the damage on the intestinal barrier upon intestinal I/R with systemic bacterial translocation, we asked whether Toll-like receptor (TLR) activation is driving the inflammatory response. In fact, the inflammatory lung response is dramatically reduced in TLR2/4-deficient mice, confirming an important role of TLR receptor signaling causing the inflammatory lung response. In conclusion, endogenous TNF-alpha is not or minimally elevated and plays no role as a mediator for the inflammatory response upon ischemic tissue injury. By contrast, TLR2/4 signaling induces an orchestrated cytokine/chemokine response leading to local and remote pulmonary inflammation, and therefore disruption of TLR signaling may represent an alternative therapeutic target.

NITRIC OXIDE MEDIATES LUNG VASCULAR PERMEABILITY AND LYMPH-BORNE IL-6 AFTER AN INTESTINAL ISCHEMIC INSULT

Acute lung injury following intestinal I/R depends on neutrophil-endothelial cell interactions and on cytokines drained from the gut through the lymph. Among the mediators generated during I/R, increased serum levels of IL-6 and NO are also found and might be involved in acute lung injury. Once intestinal ischemia itself may be a factor of tissue injury, in this study, we investigated the presence of IL-6 in lymph after intestinal ischemia and its effects on human umbilical vein endothelial cells (HUVECs) detachment. The involvement of NO on the increase of lung and intestinal microvascular permeability and the lymph effects on HUVEC detachment were also studied. Upon anesthesia, male Wistar rats were subjected to occlusion of the superior mesenteric artery during 45 min, followed by 2-h intestinal reperfusion. Rats were treated with the nonselective NO synthase (NOS) inhibitor L-NAME (N(omega)-nitro-L-arginine methyl ester) or with the selective inhibitor of iNOS aminoguanidine 1 h before superior mesenteric artery occlusion. Whereas treatment with L-NAME during ischemia increased both IL-6 levels in lymph and lung microvascular permeability, aminoguanidine restored the augmented intestinal plasma extravasation due to ischemia and did not induce IL-6 in lymph. On the other hand, IL-6 and lymph of intestinal I/R detached the HUVECs, whereas lymph of ischemic rats upon L-NAME treatment when incubated with anti-IL-6 prevented HUVEC detachment. It is shown that the intestinal ischemia itself is sufficient to increase intestinal microvascular permeability with involvement of iNOS activation. Intestinal ischemia and absence of constitutive NOS activity leading to additional intestinal stress both cause release of IL-6 and increase of lung microvascular permeability. Because anti-IL-6 prevented the endothelial cell injury caused by lymph at the ischemia period, the lymph-borne IL-6 might be involved with endothelial cell activation. At the reperfusion period, this cytokine does not seem to be modulated by NO.

Small bowel injury associated to allergy is triggered by platelet-activating factor, mast cells, neutrophils and protected by nitric oxide

Allergy to components of the diet is followed by gut inflammation which in children, sometimes progress to mucosal lesions and anaphylaxis. In newborns suffering of cow`s milk allergy, bloody stools, rectal. bleeding and ulcerations are found. The rat systemic anaphylaxis is a suitable model to study the intestinal lesions associated to allergy. In the present study we used this model to investigate some mechanisms involved. We found that 15 min after antigen challenge of sensitized rats, hemorrhagic lesions develop in the small intestine. The lesions were more severe in jejunum and ileum compared to duodenum. Pretreatment of the rats with a platelet-activating factor-receptor antagonist (WEB-2170) reduced the lesions whereas inhibition of endogenous nitric oxide by L-NAME, greatly increased the hemorrhagic lesions and mortality. Both, lesions and mortality were reversed by L-arginine. The hemorrhagic lesions were also significantly reduced by the mast cell stabilizers, disodium cromoglycate and ketotifen as well as by neutrophils depletion (with anti-PMN antibodies) or inhibition of selectin binding (by treatment with fucoidan). Thus, the intestinal hemorrhagic lesions in this model are dependent on ptatelet-activating factor, mast cell granule-derived mediators and neutrophils. Endogenous nitric oxide and supplementation with L-arginine has a protective role, reducing the lesions and preventing mortality. These results contributed to elucidate mechanisms involved in intestinal lesions which could be of relevance to human small bowel injury associated to allergy. (c) 2007 Elsevier B.V. All rights reserved.

BnP1, a novel P-I metalloproteinase from Bothrops neuwiedi venom: Biological effects benchmarking relatively to jararhagin, a P-IIISVMP

Snake venom metalloproteinases (SVMPs) have been extensively studied and their effects associated with the local bleeding observed in human accidents by viper snakes. Representatives of P-I and P-III classes of SVMPs similarly hydrolyze extracellular matrix proteins or coagulation factors while only P-III SVMPs induce significant hemorrhage in experimental models. In this work, the effects of P-I and P-III SVMPs on plasma proteins and cultures of muscle and endothelial cells were compared in order to enlighten the mechanisms involved in venom-induced hemorrhage. To reach this comparison, BnP1 was isolated from B. neuwiedi venom and used as a weakly hemorrhagic P-I SVMPs and jararhagin was used as a model of potently hemorrhagic P-III SVMP. BnP1 was isolated by size exclusion and anion-exchange chromatographies, showing apparent molecular mass of approximately 24kDa and sequence similarity with other members of SVMPs, which allowed its classification as a group P-I SVMP. The comparison of local effects induced by SVMPs showed that BnP1 was devoid of significant myotoxic and hemorrhagic activities and jararhagin presented only hemorrhagic activity. BnP1 and jararhagin were able to hydrolyze fibrinogen and fibrin, although the latter displayed higher activity in both systems. Using HUVEC primary cultures, we observed that BnP1 induced cell detachment and a decrease in the number of viable endothelial cells in levels comparable to those observed by treatment with jararhagin. Moreover, both BnP1 and jararhagin induced apoptosis in HUVECs while only a small increase in LDH supernatant levels was observed after treatment with jararhagin, suggesting that the major mechanism involved in endothelial cell death is apoptosis. Jararhagin and BnP1 induced little effects on C2C12 muscle cell cultures, characterized by a partial detachment 24h after treatment and a mild necrotic effect as evidenced by a small increase in the supernatants LDH levels. Taken together, our data show that P-I and P-III SVMPs presented comparable effects except for the hemorrhagic activity, suggesting that hydrolysis of coagulation factors or damage to endothelial cells are not sufficient for induction of local bleeding. (C) 2007 Elsevier Ltd. All rights reserved.

Evolutionary history of Dengue virus type 4: Insights into genotype phylodynamics

Dengue virus type 4 (DENV-4) circulates in tropical and subtropical countries from Asia and the Americas. Despite the importance of dengue virus distribution, little is known about the worldwide viral spread. Following a Bayesian phylogenetic approach we inferred the evolutionary history of 310 isolates sampled from 37 countries during the time period 1956-2008 and the spreading dynamics for genotypes I and II. The region (tropical rainforest biome) comprised by Malaysia-Thailand was the most likely ancestral area from which the serotype has originated and spread. Interestingly, cross-correlation analysis on demographic time series with the Asian sequences showed a statistically significant negative correlation that could be suggestive of competition among genotypes within the same serotype. (C) 2011 Elsevier B.V. All rights reserved.

Identification of enteropathogenic and enterohaemorrhagic Escherichia coli strains by immunoserological detection of intimin

Aims: To evaluate the sensitivity and specificity of polyclonal and monoclonal antibodies (Mabs) against intimin in the detection of enteropathogenic and enterohaemorrhagic Escherichia coli isolates using immunoblotting. Methods and Results: Polyclonal and Mabs against the intimin-conserved region were raised, and their reactivities were compared in enteropathogenic E. coli (EPEC) and enterohaemorrhagic E. coli (EHEC) isolates using immunoblotting analysis. In comparison with rat antiserum, rabbit anti-intimin IgG-enriched fraction had a stronger recognition pattern to a wide spectrum of intimin types in different EPEC and EHEC serotypes. On the other hand, murine monoclonal IgG2b specific to intimin, with dissociation constant of 1 center dot 3 x 10-8 mol l-1, failed in the detection of some of these isolates. Conclusion: All employed antibodies showed 100% specificity, not reacting with any of the eae-negative isolates. The sensitivity range was according to the employed antisera, and 97% for rabbit anti-intimin IgG-enriched fraction, followed by 92% and 78% sensitivity with rat antisera and Mab. Significance and Impact of the Study: The rabbit anti-intimin IgG-enriched fraction in immunoblotting analysis is a useful tool for EPEC and EHEC diagnoses.