Cardoso A

Does umbilical vein catheterization to exchange transfusion lead to portal vein thrombosis

Abstract The aetiopathology of extrahepatic portal vein obstruction is unknown. In retrospective studies, umbilical vein cannulation and sepsis have been alleged to cause portal thrombosis. This prospective study was undertaken to detect whether thrombosis and consequent obstruction of the splenoportal venous system develops after umbilical vein catheterization for exchange transfusion in newborns using Doppler ultrasound. Forty children (M = 24; F = 16) who had undergone exchange transfusion for hyperbilirubinaemia were studied at school age. Maximal duration of the venous umbilical cannulation was 120 min and sepsis did not occur. Clinical, biological and sonographic examinations were normal, except in 3 children. In 2 the left branch of portal vein could not be identified (normal variant). Conclusion Our results show that, in these children, umbilical vein catheterization did not lead to development of portal vein thrombosis. However, when other risk factors such as umbilical infection, traumatic catheterization are associated, children should be screened for obstruction of the portal vein.

Is Mitral Valve Prolapse a Congenital or Acquired Disease

The prevalence of mitral valve prolapse (MVP) at birth was studied in 1,734 consecutive newborns without congenital structural heart disease. We have not identified any case of an unequivocal pattern of MVP using auscultatory and echocardiographic diagnostic criteria. Our data argue for the concept that MVP is an acquired disease.

Pretransplant hyponatremia could be associated with a poor prognosis after liver transplantation.

INTRODUCTION Predicting the prognosis of hepatic cirrhosis is the most accurate method to achieve a fair allocation among the liver transplant waiting list thereby reducing overall mortality rates. AIM To study the survival rates of recipients who undergo liver transplantation in association with hyponatremia rates. METHODS This retrospective study used a prospectively collected database. The characteristics of liver donors and recipients were: age (years), Model for End-stage Liver Disease (MELD), MELD Na score, recipient body mass index (kg/m(2)), warm ischemia time (minutes), cold ischemia time (minutes), intensive care unit time (days), hemocomponents transfused, recipient glycemia (mg/dL) and serum sodium (mEq/L), Child-Pugh-Turcotte classification (points), and survival time (months). We analyzed all 318 consecutive liver transplantations from February 1994 to May 2010 divided into two groups: A (Na > 130 mEq/L) and B (Na ≤ 130 mEq/L). The Kaplan-Meier method was used to evaluate survival rate and the Cox regression test to identify predictive factors. RESULTS Hyponatremic patients displayed shorter survival (P = .04). The Cox regression for survival time showed that patients with low serum sodium values (group B) had: Child-Pugh scores with 1.13% plus risk of death for each point; cold ischemia time with 1.001% less risk of death for each minute; glycemia with 0.6% for each mg/dL; 0.66% use of cell-saver; plus a risk of death for each 100 mL plus 1.02% risk of death for each year of donor age. CONCLUSION Hyponatremic cirrhotic patients show more advanced stages of disease compared to normonatremic cirrhotics. They usually display metabolic or cirrhotic decompensation and comorbidities. When these symptoms were associated with the use of extended criteria donors, increased cold ischemia time, and intraoperative bleeding, we observed lower survival rates.

Prognostic Factors for Hepatocellular Carcinoma Recurrence: Experience With 83 Liver Transplantation Patients

INTRODUCTION Orthotopic liver transplantation (OLT) is a rational therapeutic option for early-stage hepatocellular carcinoma (HCC) providing a potential cure and improving survival. METHODS This retrospective study of a longitudinal cohort used an electronic database collected prospectively from September 1997 to May 2010. The variables were gender, age (years), and alpha-fetoprotein (AFP) level (ng/mL). In explanted livers we observed: microvascular or macrovascular invasion, number of nodules and their largest size, Edmondson-Steiner histological differentiation, incidental tumor transarterial chemoembolization (TACE), Milan criteria, and previous down-staging. RESULTS Five of 83 (6.0%) subjects including 68 (82%) males with a mean time to diagnosis of 9 months experienced tumor relapses. Mean patient age at HCC recurrence was 55.3 years for male and 44.6 years for female subjects. Vascular invasion was detected in 17/83 (20.5%) subjects, namely 2% of macrovascular invasion, and 52.5% with expanded Milan criteria due to an increased number and size of nodules in the explanted livers. An incidental tumor was observed in 29.5% of cases. Preoperative TACE treatment was performed in 13 (15.6%) patients. None of the patients who had a HCC recurrence had undergone TACE. AFP level at the time of recurrence was around 1,900 ng/mL. The predictive factor for mortality was nodule size (P=.04; hazard ratio=0.0269; confidence interval [CI], 95% 0.0094-0.299). CONCLUSION Patients with relapses showed the worst survival and tumor size was a predictive factor for recurrence.

Red Blood Cell Antigen Alloimmunization in Liver Transplant Recipients

Orthotopic liver transplantation (OLT) is a life-saving procedure for patients with end-stage liver disease. Transfusion support is an important part of OLT. Intraoperative transfusion of large volumes of blood products is recognized to be a poor prognostic factor, probably due to the negative effects of blood transfusions, such as transfusion reactions, infectious contamination of blood products, or immune modulation of the transfused patient. The aim of this study was to evaluate the frequency of alloimmunization and its specificity to red blood cell (RBC) antigens among patients undergoing OLT. We identified 74 RBC alloantibodies in 70 (23%) patients when the indirect antiglobulin test (IAT) was performed. The most common RBC alloantibodies were against Rh system antigens. The majority (41.9%) were directed against the E antigen. Despite the ethnic heterogeneity of our population there were no cases of intravascular hemolysis. The incidence of alloimmunization (23%) was slightly higher among patients than in the literature, most probably as a consequence of our ethnic heterogeneity.

HUMAN PARAOXONASE GENE POLYMORPHISM AND CORONARY ARTERY DISEASE RISK

BACKGROUND Complex diseases such as coronary artery disease (CAD), hypertension and diabetes are usually caused by individual susceptibility to multiple genes, environmental factors, and the interaction between them. The paraoxonase 1 (PON1) enzyme has been implicated in the pathogenesis of atherosclerosis and CAD. Two common polymorphisms in the coding region of the PON1 gene, which lead to a glutamine (Q)/arginine (R) substitution at position 192 and a leucine (L)/methionine (M) substitution at position 55, influence PON1 activity. Studies have investigated the association between these polymorphisms and CAD, but with conflicting results. AIMS 1) To evaluate the association between PON1 polymorphisms and CAD risk; and 2) to study the interaction between PON1 polymorphisms and others in different candidate genes. METHODS We evaluated the risk of CAD associated with PON1 Q192R and L55M polymorphisms in 298 CAD patients and 298 healthy individuals. We then evaluated the risk associated with the interaction of the PON1 polymorphisms with ACE DD, ACE 8 GG and MTHFR 1298AA. Finally, using a logistic regression model, we evaluated which variables (genetic, biochemical and environmental) were linked significantly and independently with CAD. RESULTS We found that the PON1 55MM genotype was more common in the CAD population, but this did not reach statistical significance as a risk factor for CAD, while PON1 192RR presented an 80% higher relative risk compared to the population without this polymorphism. The interaction between PON1 192RR and MTHFR 1298AA, sited in different genes, increased the risk for CAD, compared with the polymorphisms in isolation (OR=2.76; 95% CI=1.20-6.47; p=0.009), as did the association of PON1 192RR with ACE DD, which presented a 337% higher risk compared to the population without this polymorphic association (OR=4.37; 95% CI=1.47-13.87; p=0.002). Similarly, the association between PON1 192RR and ACE 8 GG was linked to an even higher risk (OR=6.23; 95% CI=1.67-27.37; p<0.001). After logistic regression, smoking, family history, fibrinogen, diabetes, Lp(a) and the association of PON1 192RR + ACE 8 GG remained in the regression model and proved to be significant and independent risk factors for CAD. In the regression model the latter association had OR=14.113; p=0.018. CONCLUSION When analyzed separately, the PON1 192RR genotype presented a relative risk for CAD 80% higher than in the population without this genotype. Its association with other genetic polymorphisms sited in different genes, coding for different enzymes and belonging to different physiological systems, always increased the risk for CAD. After correction for other conventional and biochemical risk factors, the PON1 192RR + ACE 8 GG association remained a significant and independent risk factor for CAD.