Estudo de componentes da hemostasia em crianças portadoras de trombose da veia porta




Althoug venous thrombosis is rare in childhood, yet it is morbid and sometÍI!l~s fatal. Some factors such as infections, congenital anomalies, umbilical catheterism and genetical coagulation disorders have been linked to portal vein thrombosis (TVP). Hemostasis disorders have not been studied deeply and ve:ry few data is available. Having in mind to research some of the hemostasis components in TVP patients, it was suggested to study their coagulation. When , analyzing coagulation and fibrinolysis, a stretch of prothrombin time (TP) and thrombin time (TT) were noted in TVP patients, probably due to activated clotting, even though a D-dimmer increase was absent, or a proteic Syfithesis decrease. It was also noted that factors 11 and V decreased, thus causing a TP and TT increase, probably caused by a selective lowering or a fibrinolysis increase. Fibrinogen was reduced probably because of its functional disorder, leading to a dysfibrinogenemia, or lowering the proteic synthesis or even by a local intravascular clotting or primary fibrinolysis. Our data shows that in TVP patients the vitamin K metabolism was unaffected since the activated partial thromboplastin time (TTP A) was nonnal, except for a decrease of the factor II, which depends of this vitamin. The nonnal protein C (PROT C) and protein S (PROT S) levels in patients,strengthened this finding. Hyperfibrinolysis found by a lysis area in fibrin plates (ALPF) increase and an euglobulin lisys time (TLE) shortening could have leed to a selective factor V decrease. A local intravascular clotting may have occurred since it is assumed that coagulation activation and fibrinolysis are simultaneous even though D-dimmer increase was absent. Factor V Leiden, although being the most frequent hereditary disorder for VenS>1,lS thrombosis, was not the found in our group of patients, and probable is not related to TVP. One patient showed low PROT C levels which were not congenital since his parents had nonnal PROT C levels. This defficiency was a consequence and not the TVP cause. His lower factor V, pre albumin levels, TT and TP stretching suggested a decrease of the proteic synthesis. LUPUSII anticoagulant was found in one patient and may be assumed as the TVP cause. Lower pre albumin levels may mean either a synthesis decrease caused by modulation or disordered synthesis. The most pr?bable causes for factor II and V decrease, TP as well as TT length are synthesis modulation or consumption brought by activated coagulation. Consequently, plasmatic levels of various components of coagulation and fibrinolysis in TVP patients were determined by studying some hemostasis parameters. Congenital defiencies of coagulation inhibitors in TVP ethiology were not found


trombose hemostase crianças

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