Key result
H+H+ LPL-Hind III polymorphism links to ~10-fold greater severe hypertriglyceridemia risk vs H-H- genotype.
Why the study?
Polymorphisms in the LPL and APO CII genes have been linked to severe hypertriglyceridemia in several populations, but their frequency in Kurdish patients was unknown.
Are LPL-Hind III and APO CII-Ava II gene polymorphisms associated with severe hypertriglyceridemia in Kurdish patients?
Case-Control (n=100)
No
Are LPL-Hind III and APO CII-Ava II gene polymorphisms associated with severe hypertriglyceridemia in Kurdish patients?
Odds Ratio: 10.5 (95% CI 2.01–54.83)
p-value: p=0.002
The H+H+ LPL-Hind III and A1A1 APO CII-Ava II polymorphisms are highly frequent in Kurdish patients with severe hypertriglyceridemia and may serve as hereditary indicators of vulnerability to this condition.
Background Polymorphisms in the lipoprotein lipase (LPL) and apolipoprotein CII (APO CII) genes have been linked to severe hypertriglyceridemia in several populations. This study investigated the frequency of LPL-Hind lll and APO Cll-Ava ll polymorphism among Kurdish patients with severe hypertriglyceridemia. Methodology We investigated LPL-Hind lll and APO Cll-Ava ll gene polymorphism in a sample of Kurdish patients receiving treatment at Azadi Teaching Hospital in Duhok, Kurdistan Region, Iraq. We included a total of 100 subjects in this study, of which 64 had severe hypertriglyceridemia, and 36 had normotriglyceridemia. There were 56 males and 44 females. We used the polymerase chain reaction-restriction fragment length polymorphism technique to determine the polymorphism of the LPL-Hind lll and APO Cll-Ava ll genes. Results In those with severe hypertriglyceridemia, the most frequent alleles were H+H+ LPL-Hind lll polymorphism (42, 65.6%) followed by A1A1 APO Cll-Ava ll polymorphism (30, 46.9%), whereas these frequencies were 16 (44.4%) and 6 (16.7%) in those with normotriglyceridemia, respectively. The H+H+ genotype group had considerably higher triglyceride levels and lower high-density lipoprotein cholesterol levels compared with the H−H− genotype group. A similar pattern was observed when comparing the A1A1 and A2A2 genotype groups, with both patterns being statistically significant. Conclusions Our results showed a high frequency of H+H+ LPL-Hind III polymorphism in those with hypertriglyceridemia, which may be a hereditary indicator of vulnerability to this condition in the Kurdish population.
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Hussein et al. (2023) conducted a case-control in Severe hypertriglyceridemia (n=100). H+H+ LPL-Hind III polymorphism vs. H-H- genotype was evaluated on Severe hypertriglyceridemia (OR 10.50, 95% CI 2.01-54.83, p=0.002). The H+H+ LPL-Hind III polymorphism was significantly associated with severe hypertriglyceridemia in the Kurdish population, demonstrating an odds ratio of 10.50 compared to the H-H- genotype.
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