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Published on: October 22, 2020
CYP1A1, smoking and venous thromboembolism
Jin Zhu1, Wen-Jie Zheng, Fan-Cui Kong
1Beijing Chao-Yang Hospital affiliated with Beijing Capital Medical University, Beijing, China.
Thrombosis and Haemostasis
|July 29, 2010
Summary
Genetic variations in the CYP1A1 Ile462Val gene increase susceptibility to smoking-induced venous thromboembolism (VTE) in Chinese populations. Smokers with this variant face a doubled risk of VTE, highlighting gene-environment interactions.
Area of Science:
- Genetics
- Environmental Health
- Cardiovascular Disease Epidemiology
Background:
- The CYP1A1 enzyme metabolizes tobacco carcinogens, suggesting a role in smoking-related diseases.
- Venous thromboembolism (VTE) risk is influenced by genetic factors and environmental exposures like smoking.
Purpose of the Study:
- To investigate if genetic polymorphisms in the CYP1A1 gene modify the risk of developing VTE.
- To explore the interaction between CYP1A1 gene variants and smoking in VTE development.
Main Methods:
- A case-control study involving 425 Chinese VTE patients and 527 controls.
- Analysis of CYP1A1 MspI and Ile462Val polymorphisms using the Amplification Refractory Mutation System (ARMS).
- Statistical analysis adjusted for age, gender, weight, contraceptives, and smoking status.
Main Results:
- The CYP1A1 Ile462Val AG variant and combined AG+GG variant were significantly associated with VTE risk.
- This association remained significant after adjusting for smoking.
- Smokers carrying the Ile462Val AG+GG variant showed a more than two-fold increased risk of VTE (OR=2.805).
Conclusions:
- Genetic variations in CYP1A1 Ile462Val contribute to susceptibility to smoking-induced VTE in Chinese populations.
- Gene-environment interactions, specifically between CYP1A1 variants and smoking, are crucial in VTE development.
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