Umbilical cord serum activin A levels are increased in pre-eclampsia with impaired blood flow in the uteroplacental and fetal circulation.

The aims of the present study were to evaluate the umbilical cord serum activin A concentrations in complicated pregnancies and also to explore the relationship between activin A levels and blood flow velocity in fetal arteries. Umbilical cord blood samples were obtained postpartum after a full term uneventful gestation (control group, n=40), and from pregnancies complicated by gestational diabetes (n=13), preterm labour (n=18), or pre-eclampsia (n=19). Cord serum activin A levels were three-fold higher in pregnancies complicated by pre-eclampsia (1.17+/-0.14 ng/ml, p<0.01) than in the control group (0.43+/-0.03 ng/ml), but were unaltered in the diabetes and preterm labour groups. The pre-eclampsia group had a marked increase of umbilical artery pulsatility index (PI) and also a decrease of middle cerebral artery PI (p<0.01). Furthermore, activin A concentration correlated directly with the umbilical artery PI (r=0.540, p=0.021), with the length of stay in the Neonatal Intensive Care Unit (r=0.857, p<0.001) and also with cord blood pH (r=-0.886, p<0.001). In conclusion, umbilical cord serum activin A levels are increased in the presence of pre-eclampsia and provide an indirect marker of impaired blood flow in the uteroplacental and fetal circulation.

Different effect of statins on platelet oxidized-LDL receptor (CD36 and LOX-1) expression in hypercholesterolemic subjects.

Hydroxymethyl-glutaryl-CoA-reductase inhibitors (statins) reduce cardiovascular mortality by decreasing cholesterol as well as by non-lipid-related actions. Oxidized low-density lipoproteins (ox-LDL) are pro-atherogenic molecules and potent platelet agonists. CD36 and lectin-like ox-LDL receptor-1 (LOX-1) are specific ox-LDL receptors also expressed in platelets. This study was planned to address whether treatment with atorvastatin 10 mg/day, pravastatin 40 mg/day or simvastatin 20 mg/day could affect platelet CD36 and LOX-1 expression. Twenty-four patients for each treatment were evaluated after 3, 6, and 9 days and at 6 weeks for complete lipid profile (chromogenic), ox-LDL (ELISA), platelet P-selectin (P-sel), CD36, LOX-1 (FACS), and intracellular citrullin recovery (iCit) (HPLC). Data show hyperactivated platelets (P-sel absolute values, percent variation in activated cells, all p < 0.001), and CD36 and LOX-1 overexpression (all p < 0.001) in patients at baseline. P-sel, CD36, and LOX-1 were significantly decreased by atorvastatin and simvastatin (all p < 0.01) and related with iCit increase (r = 0.58, p < 0.001) and platelet-associated ox-LDL (r = 0.51, p < 0.01) at 9 days. Pravastatin reduced LOX-1 and P-sel (p < 0.05) at 6 weeks in relation with decreased LDL and ox-LDL (r = 0.39, p < 0.01 and r = 0.37, p < 0.01, respectively). These data suggest that atorvastatin and simvastatin reduce platelet activity by exposure of CD36 and LOX-1 before significant LDL reduction, whereas pravastatin action is detected later and in relation with LDL and ox-LDL lowering. Rapid and consistent reduction of CD36 and LOX-1 could be considered a direct anti-atherothrombotic mechanism related to the role of ox-LDL in platelet activation, platelet-endothelium interactions, and NO synthase activity.

CA 125 and CA 19-9 in peritoneal, cyst and amniotic fluids.

The concentrations of the tumour markers CA 125 and CA 19-9 were determined in peritoneal, cyst and amniotic fluids, with particular attention being paid to certain reliability criteria of the assay methods. The antigens were measured in undiluted samples and after several dilutions. A recovery test was also performed and protein content evaluated. The results show high levels of CA 125 in all fluids; in descending order of concentration: amniotic (2376-3891 U ml-1), peritoneal (379-4040 U ml-1) and cyst fluid (124-466 U ml-1). Amniotic, peritoneal and cyst fluid concentrations of CA 19-9 were found to be 314-1008 U ml-1, 26.7-2182 U ml-1 and 226-2988 U ml-1, respectively. Recovery was between 80 and 100% for all fluids. CA 125 was easily assayable in all fluids, except amniotic and peritoneal which required dilution even of the samples which fell within the range of the standard curve before dilution. The presence of CA 125 and CA 19-9 in amniotic and cyst fluids emphasizes the non-specificity of these molecules and suggests caution in the interpretation of the results.

Plasma and cyst fluid levels of delta 5 and delta 4 steroid hormones in women with gross cystic breast disease.

delta 5 and delta 4 steroid levels were studied in the plasma and cyst fluid of women with gross cystic breast disease (GCBD). In luteal phase a significant increase in plasma levels (mean +/- SEM) of DHA (11.2 +/- 2.4 ng/ml), DHAS (1.45 +/- 0.6 micrograms/ml) and cortisol 277 +/- 15.7 ng/ml) was found; in follicular phase the mean levels were 4.09 +/- 0.47 ng/ml for DHA, 0.65 +/- 0.08 microgram/ml for DHAS and 190 +/- 46.3 micrograms/ml for cortisol. The DHA/DHAS and cortisol/androstenedione ratios were significantly higher in the plasma and lower in the cyst fluid of GCBD patients, than in the plasma of controls; the androstenedione/DHA ratio was higher in the cyst fluid than in the plasma of controls. The hormonal situation of the GCBD patients thus differed from that of the controls both in the plasma and cyst fluid, particularly as regards the delta 5 steroids.

Prolactin changes after administration of agonist and antagonist dopaminergic drugs in puerperal women.

Prolactin (PRL) is an anterior pituitary hormone which plays a large part in the reproductive function of mammals. Its only well-documented effect in humans is that of initiating and maintaining lactation. Among hypothalamic neurotransmitters regulating the anterior pituitary function, dopamine (DA) is currently considered to correspond to the PRL-inhibiting factor. The central control mechanisms which induce high PRL levels in puerperal women are not well understood. To study DA tonus in puerperium we tested plasma PRL levels in different groups of puerperal subjects (6 per group) after acute administration of direct or indirect DA agonists or placebo: DA, L-dopa (a DA precursor), L-dopa plus carbidopa (a peripheral dopa-decarboxylase inhibitor), nomifensine (a DA-releasing and blocking or reuptake agent) and amphetamine (a DA releaser). The same tests with the same drug doses were performed on groups of healthy volunteers. A consistent reduction in plasma PRL levels after both direct and indirect DA agonist drugs compared to placebo was evident in puerperal and in control women. A different trend was only observed with the use of DA and amphetamine in puerperal subjects, who, unlike controls, failed to show a rebound in plasma PRL levels after the termination of drug infusion. These findings support the view that the inhibitory control of tuberoinfundibular neurons over PRL secretion is maintained in puerperium and changes in the affinity of DA receptors are related to the endocrine milieu which occurs during gestation.