Apolipoproteins A1, B, and other prognostic biochemical cardiovascular risk factors in patients with beta-thalassemia major.

Objectives: The occurrence of cardiac iron deposition is one of the late effect of iron over load which causes cardiovascular disease (CVD) in patients who are affected by beta-thalassemia major. Evaluation of some cardiovascular risk factors plays a crucial role in prediction and prevention of CVD. Subjects and methods: This study consisted of 70 young adult subjects with beta-thalassemia major (beta-TM) (aged <30 years) and 71 age- and sex-matched healthy subjects as control group in the range of 20–30 years. Hematological and biochemical laboratory parameters including apolipoprotein (Apo)A1 and ApoB, oxidative stress biomarker pro-oxidant–antioxidant balance (PAB), homocysteine, serum high-sensitivity C-reactive protein (hs-CRP), and lipid profile were evaluated. Results: ApoA1, ApoB, lipid profiles, and homocysteine were significantly decreased in patients group (P < 0.001); however, very low-density lipoprotein and also mean corpuscular hemoglobin concentration (P > 0.05) were different. Some elements included ferritin (P < 0.001), PAB (P < 0.001), and ApoB/apoA1 ratio (P < 0.05) statistically increased in patients, whereas hs-CRP (P > 0.05) was not significantly different in study groups. Exception of high-density lipoprotein (P > 0.05), other lipid profiles, and apoB had a negative meaningful correlation with PAB (P < 0.05). Likewise, apoA1, apoB, apoB/A1 ratio with apoB and homocysteine showed a strong correlation (P < 0.05). We did not find a slight correlation between apoB/A1 ratio in the company of oxidative stress marker PAB (r = −0.366;P = 0.086). We found a statistical correlation between apoB/A1 and homocysteine (P < 0.05). Discussion: Higher level of some risk factors like PAB values, apoB/A1 ratio concentration, and lipid profiles is able to involve in the prognostic pathological consequences in patients with beta-thalassemia major. Even so, they contribute toward the gradual development of CVD. [ABSTRACT FROM AUTHOR]