Protein S activity in sickle cell anaemia patients in steady state and crisis

Ebele Uche; Olufunto Kalejaiye; Festus Olowoselu; Timothy Ekwere; Rafatu Bamiro; Abdulateef Kareem; Benjamin Augustine; Odebiyi Hassan; Abdulhafeez Balogun; Akinsegun Akinbami

doi:10.18203/issn.2454-2156.IntJSciRep20223370

Authors

Ebele Uche Department of Haematology and Blood Transfusion, Lagos State University, College of Medicine, Lagos, Nigeria
Olufunto Kalejaiye Department of Medicine, College of Medicine, College of Medicine, University of Lagos, Lagos, Nigeria
Festus Olowoselu Department of Haematology and Blood transfusion, College of Medicine, College of Medicine, University of Lagos, Lagos, Nigeria
Timothy Ekwere Department of Haematology, College of Health Sciences, University of Uyo, Akwa Ibom State. Nigeria
Rafatu Bamiro Department of Haematology and Blood Transfusion. General Hospital Marina, Lagos, Nigeria
Abdulateef Kareem Department of Family Medicine, Lagos State University Teaching Hospital, Lagos, Nigeria
Benjamin Augustine Department of Haematology and Blood Transfusion, Ahmadu Bello University Zaria, Kaduna State, Nigeria
Odebiyi Hassan Department of Haematology and Blood Transfusion, Federal Medical Center, Birnin Kudu, Jigawa State, Nigeria
Abdulhafeez Balogun Newday Medical Centre, Akure, Ondo State, Nigeria
Akinsegun Akinbami Department of Haematology and Blood Transfusion, Lagos State University, College of Medicine, Lagos, Nigeria

DOI:

https://doi.org/10.18203/issn.2454-2156.IntJSciRep20223370

Keywords:

Protein S, Sickle cell anaemia, Crisis, Steady state, Control

Abstract

Background: In sickle cell anaemia, there is an ever-present risk for haemostatic abnormalities which may result in reduced levels of naturally occurring coagulation inhibitors. Protein S is a Vitamin-K dependent, γ-carboxy glutamic acid-containing glycoprotein that potentiates the action of protein C when activated resulting in anticoagulation. This study measured serum Protein S activity in SCA patients during vaso-occlusive crisis and in steady-state, and this was compared with the activity in HbAA controls with a view to establishing if Protein S plays a role in VOC in SCA patients.

Methods: This was an analytical prospective study comprised of 30 HbSS patients and 30 HbAA controls. Using ELISA method, Protein S levels were measured in the HbSS study group during crisis and in the HbAA control group; When the HbSS patients were in steady state, Protein S levels were also measured.

Results: Protein S levels were highest in the HbAA control group (5.27+0.47 ng/ml) followed by the HbSS patients in steady state (5.08+0.56 ng/ml) and lowest in the HbSS patients in crisis (4.96+0.97 ng/ml). However, this difference was not statistically significant.

Conclusions: Protein S levels are reduced in HbSS patients when compared with HbAA controls, and the levels are lower during a VOC compared with steady state.

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