Increased soluble selectins as a reflection of activated platelets and endothelium in Legg-Calve-Perthes disease.

J Pediatr Hematol Oncol

*Department of Orthopaedics and Traumatology ‡Section of Hematology, Department of Internal Medicine, Hacettepe University, Sihhiye, Ankara †Department of Internal Medicine, Acibadem University, Istanbul, Turkey.

Published: October 2014

Background And Aim: Legg-Calve-Perthes disease (LCPD) is still an enigma. Hemostatic abnormalities have been indicated in the pathogenesis. We had previously demonstrated enhanced tissue factor pathway inhibitor response, increased global fibrinolytic capacity, and an increase in thrombomodulin in patients with LCPD compared with healthy individuals. These studies emphasized the role of vascular endothelium in pathogenesis of the LCPD. P-selectin is expressed on activated platelets and endothelial cells, and E-selectin is expressed on activated endothelial cells. The aim of this study was to assess circulating E-selectin and P-selectin levels in LCPD patients, which might reflect an endothelium activation and/or injury.

Materials And Methods: The study included 85 pediatric patients. Group I consisted of 55 patients with LCPD and group II (control) consisted of 30 healthy children. Peripheral venous blood concentrations of E-selectin and P-selectin levels were measured with a commercially available assay.

Results: Mean age was 8.41±2.73 years in group I and 8.83±2.92 years in group II. Both E-selectin and P-selectin levels were higher in LCPD patients in comparison with the age-matched controls. E-selectin was 54.92±18.84 pg/mL in group I, 45.54±15.31 pg/mL in group II and P-selectin was 46.40±20.35 pg/mL in group I, 36.92±9.84 pg/mL in group II (P=0.022 and P=0.019, respectively).

Conclusions: On the basis of our results, two important endothelium and platelet markers, E-selectin and P-selectin, are upregulated in LCPD. Our results suggested that activated platelets and possibly endothelial activation, as reflected by enhanced P-selectin/E-selectin kinetics, might contribute to the microvascular thrombosis and/or inflammation of LCPD.

Download full-text PDF

Source
http://dx.doi.org/10.1097/MPH.0000000000000203DOI Listing

Publication Analysis

Top Keywords

e-selectin p-selectin
16
pg/ml group
16
activated platelets
12
p-selectin levels
12
legg-calve-perthes disease
8
lcpd
8
patients lcpd
8
expressed activated
8
platelets endothelial
8
endothelial cells
8

Similar Publications

Sialyl Lewis Glycomimetics as E- and P-Selectin Antagonists Targeting Hyperinflammation.

ACS Med Chem Lett

January 2025

Bioorganic Chemistry Laboratory, Institut de recherches cliniques de Montréal (IRCM), Montréal, Québec H2W 1R7, Canada.

Inflammatory disorders, such as sepsis, pancreatitis, and severe COVID-19, often cause immune dysfunction and high mortality. These conditions trigger excessive immune cell influx, leading to cytokine storms, organ damage, and compensatory immune suppression that results in immunoparalysis, organ dysfunction, and reinfection. Controlled and reversible immunosuppression limiting immune cell recruitment to inflammation sites could reduce hyperinflammation and prevent immune exhaustion.

View Article and Find Full Text PDF

Sickle cell disease (SCD) is a devastating hemolytic disease, marked by recurring bouts of painful vaso-occlusion, leading to tissue damage from ischemia/reperfusion pathophysiology. Central to this process are oxidative stress, endothelial cell activation, inflammation, and vascular dysfunction. The endothelium exhibits a pro-inflammatory, pro-coagulant, and enhanced permeability phenotype.

View Article and Find Full Text PDF

The systemic inflammatory response after cardiopulmonary bypass has been widely studied. However, there is a paucity of studies that focus on the local inflammatory changes that occur in the pericardial cavity. The purpose of this study is to assess the inflammatory mediators in the pericardial fluid of patients undergoing cardiac surgery.

View Article and Find Full Text PDF

Drugs blocking the renin-angiotensin-aldosterone system may offer benefit on endothelial function, inflammation, and hemostasis in addition to the effects of reducing blood pressure. We have shown antithrombin effects by treatment with the angiotensin converting enzyme (ACE) inhibitor ramipril. As thrombin is a key inducer of platelet aggregation, we hypothesized that treatment with ramipril could modulate platelet reactivity and endothelial glycocalyx (eGCX) function.

View Article and Find Full Text PDF

Increased thrombin generation in kidney transplant recipients with donor-specific antibodies directed against human leukocyte antigens.

Front Immunol

November 2024

Division of Clinical Laboratory Sciences, Department of Laboratory Medicine, Faculty of Medicine, Kálmán Laki Doctoral School, University of Debrecen, Debrecen, Hungary.

Introduction: The development of anti-HLA donor specific antibodies (DSAs) is associated with poor outcomes in kidney transplant recipients. It is surmised that an interaction between DSAs and the graft endothelium cause tissue injury, however, the exact underlying pathomechanism and optimal management of patients with DSAs remain undetermined.

Aims: We hypothesized that in kidney transplant recipients the presence of DSAs induce hemostasis alterations, including hypercoagulability, as assessed by the thrombin generation assay (TGA).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!