NEUROCHEMICAL JOURNAL, cilt.18, sa.3, ss.515-520, 2024 (SCI-Expanded)
Hemoglobinopathies
are commonly occurring genetic disorders worldwide. The aim of this
study is to determine the biochemical predictors of cerebrovascular
complications in pediatric patients with sickle cell anemia. We
investigated the relationship between levels of neurological damage
markers, such as Serum S100 calcium-binding protein B (S100B), Glial
Fibrillary Acidic Protein (GFAP), and Neuron-Specific Enolase (NSE), and
radiological findings in these patients. A total of 72 SCD patients and
30 healthy children were included in the study. Clinical and laboratory
findings were recorded. Time-averaged maximum mean velocity (TAMMV)
values were obtained from transcranial Doppler ultrasonography imaging
(TCDI) of the middle cerebral artery. Serum levels of S100B, GFAP, and
NSE were measured using the ELISA method both in the SCD group and the
control group. Among the patients, 51 had sickle cell anemia (HbSS), 21
had HbS beta 0 thalassemia, with 32 (44.4%) being female and 40 (55.6%)
male. Their mean age was 12.68 +/- 4.56 (ranging from 3 to 24) years
old. S100B, GFAP, and NSE serum levels were significantly higher in the
SCD group compared to the control group. It was observed that serum
levels of S100B, NSE, and GFAP were higher in the group with TAMMV >=
170 cm/s. As known, in patients with SCD, the disruption of the
blood-brain barrier begins with the occurrence of vaso-occlusive events.
Hence, the risk of cerebrovascular events increases. Our study's
indication that serum levels of S100B, GFAP, and NSE could be used in
predicting or detecting cerebrovascular events in the early stages is
noteworthy.