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Published on: April 1, 2015
ASSESSMENT OF THROMBOSPONDIN-1 IN SICKLE CELL VASOOCCLUSIVE CRISIS AND ITS RELATIONSHIP WITH PLATELET INDICES AND
I T Lawrence1, B Augustine1, A I Mamman1
1Department of Haematology and Blood Transfusion, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria. Email: : greytidisha@gmail.com.
Introduction:
Thrombospondin-1 (TSP-1) is a key protein product of activated platelets which is significantly increased in sickle cell vaso-occlusive crisis (VOC) and other inflammatory conditions. This study aims to determine TSP-1 levels and their relationship with platelet indices and inflammation.
Objective:
To evaluate TSP-1 levels in sickle cell anaemia (SCA) patients and assess their relationship with platelet indices and inflammation.
Methods:
This hospital-based cross-sectional comparative study was conducted in North Western Nigeria from July to December 2022. The study included 120 participants: 80 adults with SCA (40 in VOC) and 40 in steady state (SS)), matched with 40 healthy controls (HbAA). TSP-1 levels were measured using ELISA and haematological parameters were obtained from an automated analyzer. Analysis of variance was used to compare groups and determinants of TSP-1 variability were analyzed using multiple logistic regression. Statistical significance was at p ≤0.05.
Results:
The mean TSP-1 level was significantly higher in VOC patients (406.0 ± 164.6 ng/mL) compared to SS patients (312.4 ± 145.6 ng/mL) and HbAA controls (192.3 ± 121.2 ng/mL) (p < 0.001). In the SS group, TSP-1 negatively correlated with mean platelet volume (MPV; r = -0.38, p = 0.02) and platelet-large cell ratio (P-LCR; r = -0.36, p = 0.02). White blood cell count (WBC) was the only predictor of TSP-1 variability (β = 10.301, t = 3.843, p < 0.001).
Conclusion:
Elevation of TSP-1 during VOC indicates its potential as a biomarker for crisis episodes. In SS patients, TSP-1 is associated with platelet indices, suggesting its role in platelet activation. WBC is a key predictor of TSP-1 variability, emphasizing the influence of inflammation.
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