[Venous thromboembolism and liver cirrhosis]. / Enfermedad tromboembólica venosa y cirrosis hepática.

OBJECTIVE: despite the endogenous coagulopathy of cirrhosis, some patients do experience thrombophilic states. The American College of Chest Physicians failed to address the prevention and treatment of venous thromboembolism (VTE) occurring among these patients. This study aims to describe the characteristics of cirrhotics patients hospitalized in the last 15 years, and to use the experience gained. MATERIAL AND METHOD: we retrospectively reviewed all admissions for cirrhosis in our hospital from 1992 to 2007. A total of 17 patients had non-portal venous thromboembolic disease. We recorded risk factors, epidemiological and laboratory data, thrombosis characteristics, and treatment complications. RESULTS AND CONCLUSIONS: approximately 0.8% of all hospitalized patients with cirrhosis had a non-portal VTE despite the elevated INR and low platelet count. We found low serum albumin, acquired antithrombin III, protein C and protein S deficiency, presence of antiphospholipid antibodies, and hyperhomocisteinemia in blood tests. Many patients had hemorragic complications during anticoagulation therapy, and 35% needed blood transfusions.

Enfermedad tromboembólica venosa y cirrosis hepática / No disponible

Objetivos: la enfermedad tromboembólica venosa (ETV) espoco frecuente en la cirrosis hepática, no estando su tratamientocontemplado en las guías del American College of Chest Physicians.El objetivo del presente trabajo es aportar la experiencia depacientes cirróticos con ETV hospitalizados en nuestro centro enlos últimos 15 años.Material y método: de enero de 1992 a diciembre de 2007fueron hospitalizados en nuestro centro 2.074 pacientes con cirrosishepática. Presentaron una ETV no esplácnica 17, siendoellos la población a estudio. Se recogen datos epidemiológicos yanalíticos: hemograma, VSG, química hemática, coagulación,trombofilia congénita, anticuerpos antifosfolípidos (AAFL) y homocisteinemia.Se valoran factores de riesgo adquiridos, característicasde la trombosis, el tratamiento y las complicaciones.Resultados y conclusiones: la ETV no esplácnica se observaen el 0,8% de pacientes cirróticos. En ellos es frecuente observarhipoalbuminemia, disminución de factores anticoagulantes(ATIII, PC, y PS), presencia de AAFL e hiperhomocisteinemia, asícomo la presencia de factores de riesgo adquiridos: intervencionesquirúrgicas, insuficiencia venosa, inmovilización e infecciones.Tras la anticoagulación, se observan complicaciones hemorrágicasmayores en el 35% de los pacientes

Objective: despite the endogenous coagulopathy of cirrhosis,some patients do experience thrombophilic states. The AmericanCollege of Chest Physicians failed to address the prevention andtreatment of venous thromboembolism (VTE) occurring amongthese patients. This study aims to describe the characteristics ofcirrhotics patients hospitalized in the last 15 years, and to use theexperience gained.Material and method: we retrospectively reviewed all admissionsfor cirrhosis in our hospital from 1992 to 2007. A total of17 patients had non-portal venous thromboembolic disease. Werecorded risk factors, epidemiological and laboratory data, thrombosischaracteristics, and treatment complications.Results and conclusions: approximately 0.8% of all hospitalizedpatients with cirrhosis had a non-portal VTE despite the elevatedINR and low platelet count. We found low serum albumin,acquired antithrombin III, protein C and protein S deficiency,presence of antiphospholipid antibodies, and hyperhomocisteinemiain blood tests. Many patients had hemorragic complicationsduring anticoagulation therapy, and 35% needed blood transfusions

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension.

The objective of the present study was to analyze the impact of metabolic syndrome (MS) and its individual components on oxidative stress (OX) and on the activity of antioxidant enzymes of patients with essential hypertension. One hundred and eighty-seven hypertensives, 127 (61.9%) of them having criteria for MS according to the International Diabetes Federation criteria and 30 healthy normotensive subjects were included. OX status was assessed by measuring glutathione oxidized/glutathione reduced and reactive oxygen species-induced byproducts of lipid peroxidation, malondialdehyde, and DNA damage, 8-oxo-dG genomic and mitochondrial. Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase (SOD) and catalase (CAT) was measured in plasma and glutathione peroxidase 1 in hemolysed erythrocytes. In mononuclear cells, total-SOD activity, CAT and glutathione peroxidase 1, were assessed as well. The OX state in both blood and peripheral mononuclear cells observed in hypertensives were not enhanced by the addition of components of the so-called MS. Likewise, the reduction in the activity of antioxidant enzymes, both extracellular and cytoplasmic, was not affected by the presence of additional components of the MS. Neither the number of components nor the individual addition of each of them, low high-density lipoprotein, triglycerides, abdominal obesity or fasting glucose, further impact in the OX abnormalities observed in those with only hypertension in absence of other components. In conclusion, the present data indicates that contribution of MS components to the OX burden generated by high blood pressure is minimal.