Our results suggest that sleep breathing disorders, predominantly obstructive, seem to be common in PD and those events correlate with the severity of the disease.

Atenolol use may be associated with growth retardation when given in pregnancy, although the relationship to trimester of initiation, duration of treatment, and its use as monotherapy is still uncertain. To compare the obstetric and fetal outcome between women receiving atenolol (as monotherapy) and other antihypertensive drug monotherapies, and also to investigate the effect of duration of treatment on fetal growth, we performed a retrospective cohort study of 312 pregnancies in 223 women attending an Antenatal Hypertension Clinic. Atenolol (as monotherapy) was given in 78 pregnancies (25.0%), other types of antihypertensive drugs as monotherapy were given in 53 pregnancies (17.0%), and multiple drug combinations were given in 90 pregnancies (28.8%). In 91 pregnancies (29.2%) no antihypertensive drugs were given. Atenolol was found to be associated with lower birth weight and ponderal index values, with a trend toward a higher prevalence of preterm (<37 weeks) delivery and small-for-gestational-age babies when compared to other antihypertensive drugs as monotherapy, or to no treatment. The adverse effect of atenolol was more pronounced in women receiving the drug earlier in their pregnancy, and continuing the drug for a longer duration. In conclusion, atenolol should be avoided in the early stages of pregnancy and given with caution at the later stages, as it is associated with fetal growth retardation, which is related to duration of treatment.

Obesity and adherence to the Mediterranean diet patterns are factors related independently to indices of AS even in 12-year-old children.

There is a number of publications evaluating the eosinophil count and the neutrophil-to-lymphocyte count ratio for diagnosis, prognosis or monitoring of patients. Of special interest is the use of these parameters for discrimination between the different causes of fever (e.g. bacterial versus viral vs. non-infectious causes of fever) and for monitoring the efficacy of therapy and predict the course of the patient. However, pitfalls in previous study designs prevent applicability to clinical practice. Here, we provide a short review of the relevant literature and summarize important factors that should be taken into account when designing studies, with special attention to the selection of a proper and clinically meaningful study population and the effects of the stress response and of corticosteroids.

Background: Thrombogenesis, angiogenesis, and endothelial damage/dysfunction are components in the pathogenesis of atherosclerosis. Objective: To investigate the relation of these variables to atherosclerotic disease severity and the possible interrelations between the three. Methods: 111 patients attending for coronary angiography were studied (85 male, 26 female; mean (SD) age, 61.6 (10.0) years). Plasma concentrations of von Willebrand factor (vWf, a marker of endothelial damage/dysfunction), vascular endothelial growth factor (VEGF, associated with angiogenesis), soluble VEGF receptor Flt-1 (sFlt-1), and tissue factor (TF, a key component of coagulation) were measured by an enzyme linked immunosorbent assay. Following angiography, disease severity was assessed by the number of coronary vessels diseased (. 50% stenosis) and by a coronary atheroma score. Results: All indices were raised in the patients compared with 34 healthy controls except sFlt-1, which was lower in the patients. No significant correlations were found between the coronary atheroma score and values of vWf (Spearman correlations: r = 0.21, p = 0.83), VEGF (r = 0.11, p = 0.27), or TF (r = 20.04, p = 0.68). However, there was an inverse correlation between plasma sFlt-1 and coronary atheroma score (r = 20.19, p = 0.049). The number of vessels diseased had no relation to any marker. Correlations were found between TF and VEGF (r = 0.25, p = 0.008) and between TF and sFlt-1 (r = 0.42, p , 0.001) in the patients. Conclusions: Despite evidence of abnormal angiogenesis (VEGF and sFlt-1), thrombogenesis (TF), and endothelial damage/dysfunction (vWf) in the patients with coronary artery disease, there was no correlation between VEGF, sFlt-1, vWf, or TF and angiographically defined disease severity.