3 research outputs found
Adhesion molecules and high-sensitivity C-reactive protein levels in patients with sickle cell beta-thalassaemia
Background and aim The primary symptoms of sickle cell disease (SCD)
arise from vaso-occlusive crises. The pathogenesis of these crises is
complex phenomenon where endothelial activation and damage has a major
role. Chronic inflammation also plays an important role in the
pathophysiology of SCD. We aimed to investigate endothelial activation
in Caucasian Greek patients with SCD by means of measuring adhesion
molecules and markers of inflammation. Subjects and methods Twenty-eight
patients with SCD aged 563 years were included in the study. Most of the
patients (23/28) were double heterozygotes for sickle
cell/beta-thalassaemia, while five patients (5/28) were sickle cell
homozygotes. Patients were treated with one/or more of hydroxyurea,
therapeutic phlebotomies, blood transfusion or splenectomy. Twenty
apparently healthy individuals matched for age and sex formed the
control group. Measurements of soluble intercellular adhesion
molecule-1, (sICAM-1), soluble vascular cell adhesion molecule-1
(sVCAM-1), P-selectin, E-selectin, soluble thrombomodulin (sTM) and
high-sensitivity C-reactive protein (hs-CRP) levels were performed using
immunoassays in both patients and healthy individuals. Results We found
that all endothelial adhesion molecules and hs-CRP were significantly
increased (P < 0 center dot 001) in patients with SCD compared with
controls, while sTM levels did not differ significantly (P > 0 center
dot 05) and this increase was not influenced by the treatment.
Conclusion Our findings demonstrate the high degree of endothelial
activation and damage seen in sickle cell patients even in steady-state
condition, as well as the important chronic inflammation underlying the
pathophysiology of this widespread disease
Data on eNOS T786 and G894T polymorphisms and peripheral blood eNOS mRNA levels in Sickle Cell Disease
In this article, we present data on endothelial Nitric Oxide Synthase (eNOS) gene T786C and G894T polymorphisms in Greek steady-state Sickle Cell Disease patients in comparison to healthy controls. Moreover, eNOS mRNA levels were determined in peripheral blood samples from 18 patients and 9 controls. This article complements our recently published article named “Prognostic value of eNOS T786C and G894T polymorphisms in Sickle Cell Disease” (I. Armenis, V. Kalotychou, R. Tzanetea, Z. Kontogeorgiou, D. Anastasopoulou, M. Mantzourani, M. Samarkos, K. Pantos, K. Konstantopoulos, I. Rombos, 2016) [1]