Clinical biomarkers in sickle cell disease

Abstract

Sickle cell disease (SCD) is a hereditary blood disorder caused by a single gene. Various blood and urine biomarkers have been identified in SCD which are associated with laboratory and medical history. Biomarkers have been proven helpful in identifying different interconnected disease-causing mechanisms of SCD, including hypercoagulability, hemolysis, inflammation, oxidative stress, vasculopathy, reperfusion injury and reduced vasodilatory responses in endothelium, to name just a few. However, there exists a need to establish a panel of validated blood and urine biomarkers in SCD. This paper reviews the current contribution of biochemical markers associated with clinical manifestation and identification of sub-phenotypes in SCD.

GlycA is not a useful biomarker of inflammation in sickle cell disease

“…However, haptoglobin is a scavenger of free hemoglobin and becomes rapidly depleted during intravascular hemolysis. The negative correlation between the plasma GlycA level and LDH, an indirect marker of hemolysis, supports this hypothesis . Our data, therefore, suggest that hemolysis in SCD nullifies GlycA as a valid biomarker of inflammation in SCD.…”

Antisickling Effects of Quercetin may be Associated with Modulation of Deoxyhaemoglobin, 2, 3-bisphosphoglycerate mutase, Redox Homeostasis and Alteration of Functional Chemistry in Human Sickle Erythrocytes.

“…The superoxide radical dismutase's to hydrogen peroxide, which amasses and reacts with methemoglobin to produce hydroxyl radical via Fenton's and Haber Weiss reactions. These are of course the hallmarks of oxidative damage as part of the secondary metabolic complications associated with SCD (Damanhouri et al, 2015). Therefore, this study was aimed at examining the antisickling effects of quercetin via modulation of deoxy-haemoglobin, redox homeostasis and alteration of functional chemistry in human sickle erythrocytes using in silico and in vitro models while championing preventive and curative approaches.…”

Dictatorial streaming of biomarkers in some diseases

“…Up-regulation: HbS, HbF, HbSF, MCV, HbA2, ISCs, CD36 (glycoprotein IV), integrin a4b1 (very late activation antigen-4) to VCAM-1 and fibronectin, integrin α4β1, leukocyte adhesion molecules (L-selectin and αMβ2), CRP, ESR, sPLA2, IL-2, -3, -6, -8, -10, urinary cysteinyl LTE4, PGE2, CA 15-3, sCD40 ligand, HSP-70, ferritin, angiopoietin 1/2, stromal derived factor 1, TNF-α, TNFR-1, LDH-1, haptoglobin, Hb, reticulocyte count, RBC survival, blood coagulation, GSH/GSSG, stroke, BP, renal disease, TG, LDH, FMD, VEGF, PGF, ET-1, vitamin D, ALP, TRV, NT-proBNP, cTnI, PIT, HJBs, pitted RBCs (Damanhouri et al, 2015).…”