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Published on: July 17, 2021
Apolipoprotein E gene polymorphisms are associated with primary hyperuricemia in a Chinese population
Jie Wu1, Ling Qiu1, Xiu-zhi Guo1
1Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Science, Beijing, China.
The Apolipoprotein E (APOE) ε2 allele and APOE-ε2ε3 genotype are linked to higher serum uric acid levels. Individuals with the APOE-ε2 allele show an increased risk of developing hyperuricemia.
Area of Science:
- Genetics
- Human Health
- Biochemistry
Background:
- Primary hyperuricemia is a significant public health issue.
- It is associated with gout, metabolic syndrome, hypertension, and cardiovascular disease.
- Understanding genetic factors like Apolipoprotein E (APOE) polymorphisms is crucial for managing hyperuricemia.
Purpose of the Study:
- To investigate the genetic association between Apolipoprotein E (APOE) polymorphisms and hyperuricemia.
- To assess the risk of hyperuricemia in relation to specific APOE genotypes and alleles in a Chinese population.
Main Methods:
- A case-control study involving 770 subjects (356 hyperuricemic cases, 414 normouricemic controls) from China.
- Biochemical tests were performed on collected blood samples, including uric acid and lipid levels.
- Multi-ARMS PCR was used to determine APOE genotypes and analyze allele frequencies.
Main Results:
- The APOE-ε2ε3 genotype and APOE-ε2 allele were significantly more frequent in hyperuricemic cases compared to controls.
- This association was observed in both male subjects and across different ethnic groups (Han and Hui).
- Multivariate logistic regression confirmed that carriers of the APOE-ε2ε3 genotype and ε2 allele had a significantly higher risk of hyperuricemia (OR=2.194 and OR=2.099, respectively).
Conclusions:
- The APOE-ε2ε3 genotype and APOE-ε2 allele are significantly associated with elevated serum uric acid levels.
- Individuals carrying the APOE-ε2 allele have an increased risk of developing hyperuricemia.
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