Relation between haptoglobin polymorphism and oxidative stress status, lipid profile, and cardiovascular risk in sickle cell anemia patients

OBJECTIVE: The haptoglobin (Hp) gene located on chromosome 16q22 exhibits a polymorphism that can impact its capacity to inhibit the deleterious oxidative activity of free hemoglobin. We aimed to determine the influence of Hp polymorphism on oxidative stress, lipid profile, and cardiovascular risk in Cameroonian sickle cell anemia patients (SCA patients). METHOD: The Hp genotypes of 102 SCA patients (SS), 60 healthy individuals (AA), and 55 subjects with sickle cell trait (AS) were determined by allele‐specific PCR, and the blood parameters were assessed using standard methods. RESULTS: Hp2‐2 genotype was significantly (P < .05) present in SS (54%) than in AS (42%) and AA (38%). Levels of catalase and cell reactive protein were higher, while levels of total antioxidant capacity, triglycerides, low‐density lipoprotein cholestetol, blood pressure, Framingham score, and body mass index were lower in the SCA patients. These parameters appeared to be unrelated to the haptoglobin genotypes. SCA patients with Hp1‐1 genotype presented a higher oxidative stress index (0.53 ± 0.31) than those with Hp2‐1 (0.33 ± 0.18). Lipid profile and cardiovascular risk were not significantly different between various Hp genotypes in SCA patients. CONCLUSION: Haptoglobin polymorphism did not affect lipid profile, cardiovascular risk, and oxidative stress status of SCA patients. Nevertheless, SCA patients with Hp1‐1 genotype tended to be more prone to oxidative stress than those with Hp2‐1.