Elevated homocysteine and crises state in patients with sickle cell anemia: A comparative study

Abstract

Background: High plasma concentration of homocysteine (Hcy) is a well-established risk factor for several disorders, including cardiovascular disease, stroke, venous thrombosis, and arteriosclerosis. Folic acid deficiency leads to an increase in homocysteine. This study aimed to test whether elevated serum homocysteine, diminished folate, and B12 levels correlate with the frequency of crisis in sickle cell disease (SCD). Methods: This was a comparative cross-sectional study conducted on 110 adults consisting of participants with SCD in vaso-occlusive crises (VOC), SCD in hyperhemolytic crises (HHC), SCD in steady-state (SS), and healthy controls. Serum homocysteine, folate, and B12 levels were determined using the Enzyme-linked immunosorbent assay method. The level of statistical significance was defined as P < 0.05, at a 95% confidence interval. Results: The mean age of all participants was 25.5 ± 5.8 years. There was a statistically significant difference in mean serum homocysteine levels with mean levels of (11.9 ± 4.5, 13.1 ± 5.4, 10.3 ± 2.3, 9.9 ± 2.5 μmol/L) in participants in VOC, HHC, SS, and controls, respectively (P = 0.016). With a cut-off of <15 μmol/L, hyperhomocysteinemia was seen in 31.% and 26.7% of participants in HHC and VOC, respectively. Conversely, no participant in the SS or the control group had hyperhomocysteinemia. Serum folate (nmol/L) level was lower, though not significantly, in the HHC group than in the other groups, with 9.9 ± 5.5 versus 12.7 ± 6.8, 11.8 ± 4.1 and 12.7 ± 2.2 nmol/L for the VOC, SS, and control group, respectively (P = 0.121). A significant inverse correlation was found between homocysteine and folate (correlation coefficient − 0.589 and P < 0.001) in all study participants. Conclusion: This study reveals significantly higher homocysteine levels in participants with sickle anemia in vaso-occlusive and hyperhemolytic crises (HHCs), highlighting homocysteine and folate role in the pathogenesis of these events.