Luís Belo

Fetal lipoprotein changes in pre-eclampsia

Objective. To evaluate the impact of maternal lipid changes upon the fetus in pre‐eclampsia (PE) by evaluating lipid profile simultaneously in maternal and umbilical cord blood (UCB). Design. Case‐control study performed on healthy and pre‐eclamptic pregnant women and their neonates. Setting. The Department of Obstetrics and Gynecology, Hospital S. Joao and Faculty of Pharmacy, Porto, Portugal. Samples. Forty‐two healthy pregnancies and 46 pregnancies complicated with PE. Methods. Total cholesterol (TChol), HDL‐cholesterol (HDLc), LDL‐cholesterol (LDLc) and triglycerides (TG) levels were determined using enzymatic methods. Apolipoprotein (apo) A‐I, apoB and lipoprotein (a) [Lp(a)] values were measured by immunoturbidimetry. Main outcome measures. Fetal and maternal plasma levels of TChol, HDLc, LDLc, TG, apoA‐I, apoB and Lp(a). Results. Pre‐eclamptic women presented significantly higher values for TChol, LDLc, HDLc, TG, apoA‐I and apoB compared to normal pregnant women. In the UCB from pre‐eclamptic pregnancies, we observed significantly lower values for HDLc and apoA‐I, and significantly higher TG concentrations and LDLc/HDLc ratio when compared to normal cases. A positive correlation was observed between maternal TG levels and proteinuria, a marker of PE severity (r =0.40, p <0.01). Conclusions. Our data suggest that pre‐eclamptic pregnancy is associated with an enhanced hyperlipidemia, which seems to have a negative impact on fetal lipid profile, as reflected by a higher atherogenic LDLc/HDLc ratio and higher TG levels. These children, born of women with PE, may deserve a closer clinical follow‐up later in life.

Relationship between maternal and cord blood hemostatic disturbances in preeclamptic pregnancies

Endothelial cell activation or damage is believed to play a key role in preeclampsia (PE) and may underlie the hemostatic changes observed in this syndrome. The aim of this study was to evaluate a relationship between maternal and cord blood hemostatic disturbances in preeclamptic pregnancies. We measured the plasma levels of tissue plasminogen activator (tPA) antigen and of plasminogen activator inhibitor type 1 (PAI-1) antigen, both markers of hemostatic and endothelial function, and fibrin fragment D-dimer. Maternal blood from uncomplicated (n=42) and PEc pregnancies (n=44) were collected before delivery, and umbilical cord blood (UCB) immediately after delivery. In preeclamptic cases, UCB presented significantly higher tPA values and significantly lower PAI-1/tPA ratio. Preeclamptic women also presented significantly higher tPA, as well as PAI-1 values, when compared with normal pregnant women; no significant difference was found for D-dimer. In preeclamptic women, proteinuria (a marker of PE severity) correlated positively and significantly with tPA and PAI-1 antigen levels. An inverse relationship between maternal tPA antigen levels and fetal birth weigh in PE was also observed. Our data show that the hemostatic maternal disturbances observed in preeclamptic women have similarities with the UCB circulation, and that endothelial dysfunction is the most plausible underlying cause. Moreover, maternal hemostatic disturbances seem to be associated with the severity of PE. Further studies are needed to strength the values of tPA and PAI-1 as markers of severity in PE.

Leukocyte Count versus C-Reactive Protein Levels in Obese Portuguese Patients Aged 6-12 Years Old

Objectives: to evaluate whether total and differential WBC counts are altered in young obese patients (aged 6-12 years) and if a relationship exists between WBC counts and the severity of obesity as well as with CRP level. Materials and Methods: a group of 77 obese patients [32 males and 45 females] and 19 controls [7 males and 12 females] were studied. Total WBC count was performed by using an automatic blood cell counter. Blood cell morphology and WBC differential count were evaluated in Wright stained blood films. The plasma levels of CRP were evaluated by immunoturbidimetry. Results: obese participants presented with a statistically significant higher neutrophil percentage and CRP levels when compared to controls; the median CRP value was about 5 times higher than that observed in controls. Absolute neutrophil count and neutrophil/lymphocyte ratio were also higher in patients, though without statistical significance. The parameters that were statistically significant related with adiposity markers were neutrophil count and CRP levels. The neutrophil count was positively and statistically correlated with body mass index (BMI), BMI z-score, waist circumference and waist/height ratio, and also with CRP levels. In multiple regression analysis, the only variable that remained statistically associated with neutrophil count was CRP (neutrophil count = 2.612 + 0.439lnCRP; standardised coefficient/beta: 0.384, P=0.001). When performing multiple regression without CRP, the only variable that remained statistically associated with neutrophil count was BMI. Conclusions: our results demonstrated in obese patients aged 6-12 years, a significant change in the differential leukocyte count towards neutrophilia, together with a significant higher CRP concentration, and that absolute neutrophil count correlates with obesity markers and with CRP levels. Our data also indicate that neutrophil count, a current clinically used low-cost parameter, may be used as an obesity-related inflammatory marker in young obese patients.

rhEPO for the Treatment of Erythropoietin Resistant Anemia in Hemodialysis Patients – Risks and Benefits

Anemia is a common complication in hemodialysis (HD) patients, mainly due to the insuffi‐ cient production of erythropoietin (EPO) by the failing kidneys [1]. Anemia itself can worsens cardiac function, cognitive function, exercise capacity and quality of life, and it has been independently associated with increased mortality and progression of renal disease [2, 3]. A successful management of anemia is, therefore, crucial, as it may improve clinical outcome. The introduction of recombinant human EPO (rhEPO) therapy to treat anemia of chronic kidney disease (CKD) patients reduced anemia, improving patients’ quality of life [3]. There is, however, a marked variability in the response to this therapy and 5-10% of patients develop resistance to rhEPO therapy [4]. Resistance to rhEPO therapy has been associated to inflam‐ mation, oxidative stress and “functional” iron deficiency, as major causes.