RESUMEN
INTRODUCTION AND OBJECTIVES: For long, bleeding in cirrhotic patients has been associated with acquired coagulation disorders. The aim of our study was to investigate the impact of acquired coagulation disorders on bleeding risk in cirrhotic patients. MATERIALS AND METHODS: Blood samples were collected from 51 cirrhotic patients with (H+) or without (H-) bleeding events and 50 controls matched by age and sex. Thrombin generation was assessed as endogenous thrombin potential (ETP). Hemostatic balance was assessed by means of ratios of pro- to anticoagulant factors and by ETP ratio with/without protein C (PC) activator (ETP ratio). RESULTS: Bleeding events occurred in 9 patients (17.6%). Compared with controls, VIII/anticoagulant factors, VII/PC and XII/PC were significantly higher in (H+) patients. No significant difference as regards all ratios across patient groups was detected. ETP ratio was significantly higher in (H+) patients than in controls (p=0.017). However, there was no significant difference between patient groups as regards ETP ratio. CONCLUSION: Hemostatic balance is shifted toward a hypercoagulability state even in cirrhotic patients who experienced bleeding. These findings provide evidence against traditional concept of hemostasis-related bleeding tendency in cirrhotic patients.
Asunto(s)
Trastornos de la Coagulación Sanguínea/sangre , Hemorragia/sangre , Cirrosis Hepática/sangre , Trombofilia/sangre , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Pruebas de Coagulación Sanguínea , Estudios de Casos y Controles , Factor VII/metabolismo , Factor VIII/metabolismo , Factor XII/metabolismo , Humanos , Persona de Mediana Edad , Tiempo de Tromboplastina Parcial , Proteína C/metabolismo , Tiempo de Protrombina , Riesgo , Trombina/metabolismo , Adulto JovenRESUMEN
We describe a new δ-globin variant, Hb A2-Tunis [δ46(CD5)Gly â Glu; HBD: c.140G>A]. This hemoglobin (Hb) variant displayed a faster electrophoretic mobility than normal Hb A2 and was expressed at 3.2%. The molecular defect was characterized by DNA sequencing analysis. Hb A2-Tunis was found in a carrier of a ß(0)-thalassemia (ß(0)-thal) [IVS I-1 (ß143, G>A); HBB: c.92 + 1G>A] and Hb C [ß6(A3)Glu â Lys; HBB: c.19G>A], presenting with a normal Hb A2 level. Phenotype and genotype investigations revealed that the patient has a total Hb A2 level of 7.1% that was expected for a ß-thalassemia (ß-thal) minor carrier.
