RESUMO
A case of 31-year old woman who underwent emergency caesarean section (CS) following suspicion of the HELLP syndrome was reported. She developed arterial hypertension in 33rd week. In 38th week of her gestation elevated liver enzymes and positive albumin in urine were reported and pathological flow in umbilical artery and fetal aorta was found on ultrasound. The HELLP score was 12 and the HELLP syndrome was diagnosed. The pregnancy was terminated by CS for fetal distress and the HELLP syndrome. Two hours after the section she developed massive uterine bleeding with the signs of hemorrhagic shock. Despite of replacement therapy laboratory data worsened. DIC was diagnosed. Recombinant factor VIIa was administrated; after several minutes bleeding decreased and laboratory data normalized.
Assuntos
Cesárea/efeitos adversos , Fator VIIa/farmacologia , Síndrome HELLP/complicações , Hemorragia Uterina/tratamento farmacológico , Adulto , Feminino , Humanos , Gravidez , Choque Hemorrágico , Hemorragia Uterina/etiologiaRESUMO
The purpose of this investigation was to make a comprehensive study of intravascular lipofysis, including extrahepatic lipoprotein lipase and hepatic triglyceride lipase in the serum, and the responsiveness of the heparin system in insulin resistance. Patients with arterial hypertension (n = 14), type 2 diabetes mellitus (n = 16), or metabolic syndrome (n = 10) were found to have higher serum lipolytic activity, triglyceridemia, lipidemia (in type 2 diabetes mellitus and metabolic syndrome) and hyperglycemia (in type 2 diabetes mellitus) than controls (10 healthy donors). Excessive blood intracellular reserve heparin secretion-induced release of extrahepatic lipoprotein lipase and hepatic triglyceride lipase into the vascular bed as a prerequisite for increasing the baseline level of lipolytic activity in insulin resistance pathology is discussed. The effects ofheparin (50 U/ml of serum) and insulin (2 U/ml of serum) on total lipoprotein lipase activity were not revealed in vitro. It is suggested that enhanced extracellular lipofysis and depleted endogenous heparin system result in the body's insulin resistance.