Altered Adhesion Molecule Expression of Leukocytes of SCD Patients in Crisis and Steady StateNagina Parmar1, Jamie Hutchison2, Gemma Vomiero3, Ashok Kumar6, Mohamed Abdelhaleem4, Isabelle Gaboury5,Melanie Kirby-Allen7 and Robert J. Klaassen5*
- *Corresponding Author:
- Robert Klaassen
Department of Pediatrics, Division of Hematology/Oncology
Children’s Hospital for Eastern Ontario (CHEO), Rm 5109
401 Smyth Rd, Ottawa, ON. K1H 8L, Canada
Tel: (613)737-7600 Extn. 2210
E-mail: [email protected]
Received date: February 17, 2015; Accepted date: March 26, 2015; Published date: March 30, 2015
Citation: Parmar N, Hutchison J, Vomiero G, Kumar A, Abdelhaleem M, et al. (2015) Altered Adhesion Molecule Expression of Leukocytes of SCD Patients in Crisis and Steady State. J Blood Disord Transfus 6:262. doi: 10.4172/2155-9864.1000262
Copyright: © 2015 Parmar N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Sickle cell disease (SCD) patients experience ischemic events resulting from vaso-occlusion of both macro-and microcirculation. A risk factor associated with increased morbidity and mortality is leukocytosis in the absence of infection. This study investigated the role of leukocytes in the pathogenesis of acute sickle cell crisis.
Procedure: Children were enrolled at two tertiary care centers in three groups: hemoglobin SS (Hb SS) patients admitted to hospital with an acute crisis, non-crisis or steady state SS patients, and sickle cell screen negative, racematched controls. Flow cytometry measured cell surface expression of adhesion molecules.
Results: 28 Hb SS and 10 control patients were enrolled. Elevated white blood and platelet counts were observed for the crisis children (P<0.01) compared to healthy control children. There was a significant increase in the expression of adhesion molecules on neutrophils and monocytes (CD11, CD 18 and CD-62L) in children in steady state (P<0.05) compared to crisis, and healthy children. 71% of crisis children were receiving non-steroidal anti-inflammatory drugs (NSAIDs) or hydroxycarbamide, whereas none of the patients in steady state were receiving these drugs.
Conclusion: Further investigation is needed to explain these findings, but is likely due to the use of NSAIDs and hydroxycarbamide in our crisis patients.