Abstract

VCAM-1, a protein expressed on endothelial cells, increases the risk of vasooclusion in SCD patients through adhesion of sickle red blood cells. Suboptimal zinc status and iron overload due to blood transfusion have been implicated in disease severity through oxidative stress. However, the influence of these factors on VCAM-1 has not been previously investigated. We measured sVCAM-1, zinc, hemoglobin [Hb], hematocrit [Hct], and serum ferritin in 76 SCD children and 96 non-SCD children, mean age 7.73 y and 11.24 y, respectively. Although mean zinc levels of both groups were within the normal range (≈14.5 μmol/l), 14.5 % of SCD and 11% of non-SCD children had levels below normal (10.7 μmol/L). As expected, mean Hb and Hct of SCD children were below normal and serum ferritin levels were 2–3 fold higher than those usually seen in healthy children. Mean sVCAMs1 levels of SCD children (837 μg/l) were higher than those of controls (627 μg/l) (p <0.0001). Differences persisted after taking into account age, Hb phenotypes, and inflammation (α1-acid glycoprotein >1g/l and C-reactive protein >10 mg/l). sVCAM-1 negatively correlated with serum (r=−0.444) and red blood cells zinc (r=−0.242, p <0.05), but not acute phase proteins. Hb and Hct, but not serum ferritin levels tended to inversely correlate with sVCAM-1 in children with SS and Sβthal Hb phenotypes (r≤−0.3364, p >0.05). Data suggest that zinc, but not body high iron stores may modulate SCD clinical status through VCAM-1 expression, and zinc supplementation may be beneficial in these patients. Funds: Pediatrics

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