Key result
The Hind III polymorphism of the LPL gene was not significantly associated with the development of ischemic stroke in the Iraqi population (OR 0.65).
Why the study?
Studies have suggested an association of LPL gene variants with cardiovascular and cerebrovascular diseases, but whether the Hind III polymorphism and serum LPL level associate with ischemic stroke in the Iraqi population was unknown.
Is the Hind III polymorphism of the LPL gene or serum LPL level associated with ischemic stroke in the Iraqi population?
Case-Control (n=100)
Is the Hind III polymorphism of the LPL gene or serum LPL level associated with ischemic stroke in the Iraqi population?
Odds Ratio: 0.65 (95% CI 0.287–1.472)
p-value: p=0.30
The Hind III polymorphism of the LPL gene and serum LPL levels are not associated with the development of ischemic stroke in the Iraqi population.
No association in this Iraqi cohort; leaves open LPL polymorphism's role in ischemic stroke risk.
Background: Lipoprotein lipase (LPL) plays an important role in plasma lipoprotein metabolism.An increasing number of studies have suggested an association of LPL gene variants with the risk ofcardiovascular and cerebrovascular diseases.Objective: To analyze whether Hind III polymorphism of LPL gene and serum LPL level are associatedwith ischemic stroke in Iraqi population.Method: Fifty ischemic stroke patients (clinical diagnosis and x-ray CT) and fifty controls were enrolled inthis case–control study. The LPL Hind III polymorphism was determined by PCR-RFLP technique and LPLmass level was estimated using a sensitive sandwich enzyme-linked immunosorbent assay (ELISA).Results: In the present research was not found any association between the Hindlll LPL gene polymorphismand acute ischemic stroke in the population studied; the allele and genotypic frequencies of the studiedpolymorphism was similar in cases and controls and followed the Hardy-Weinberg equilibrium. Therelationship between Hind III genotypes and the LPL mass level was analyzed using ANOVA and furtherconfirmed by Post-hoc analysis. there was no significant difference in LPL mass levels between the genotypegroups H+H+, H+H-, and H-H- (p value>0.05).Conclusions: The Hind III polymorphism of LPLis not a genetic marker for the development of ischemicstroke as well as not determinants of serum LPL level in the Iraqian sample used.
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Jaafer Mukdad Mohmmed (2020) conducted a case-control in Ischemic stroke (n=100). LPL gene Hind III polymorphism vs. Absence of polymorphism / Healthy controls was evaluated on Association of LPL Hind III polymorphism with ischemic stroke (Dominant model) (OR 0.65, 95% CI 0.287-1.472, p=0.30). The Hind III polymorphism of the LPL gene was not significantly associated with the development of ischemic stroke in the Iraqi population (OR 0.65).
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