C-reactive protein, genetic susceptibility, and the long-term risk of venous thromboembolism in patients with past cancer

Yunlong Guan; Zeyu Gan; Si Li; Xi Cao; Ao Zeng; Jing Li; Wei Gong; Jun Deng; Xingjie Hao

doi:10.1055/a-2495-1350

C-reactive protein, genetic susceptibility, and the long-term risk of venous thromboembolism in patients with past cancer

Thromb Haemost. 2024 Dec 3. doi: 10.1055/a-2495-1350. Online ahead of print.

Authors

Yunlong Guan¹, Zeyu Gan², Si Li¹, Xi Cao¹, Ao Zeng¹, Jing Li³, Wei Gong³, Jun Deng⁴, Xingjie Hao¹

Affiliations

¹ Department of Epidemiology and Biostatistics, School of Public Health, Huazhong University of Science and Technology Tongji Medical College, Wuhan, China.
² School of Medicine and Health Management, Huazhong University of Science and Technology Tongji Medical College, Wuhan, China.
³ Department of Oncology, Xiangyang Central Hospital, Xiangyang, China.
⁴ Institute of Hematology, Huazhong University of Science and Technology Tongji Medical College Union Hospital, Wuhan, China.

PMID: 39626789
DOI: 10.1055/a-2495-1350

Abstract

Background: Several studies indicated that C-reactive protein (CRP) is associated with the risk of venous thromboembolism (VTE) in general population. But CRP appears to be unrelated to VTE events in newly diagnosed cancer patients. However, as the survival time of cancer patients increases, the effect of CRP on the long-term risk of VTE may change. We aimed to investigate the association between CRP and VTE in cancer survivors, and further assess the modification effect of genetic susceptibility.

Methods: Cox proportional hazards model was used to evaluate the association between serum CRP levels and VTE risk, as well as to investigate the joint effect of CRP and genetic susceptibility. The Kaplan-Meier curve and the restricted cubic spline were used to visualize the relationship between CRP and VTE.

Results: This study included 30,145 participants with cancer diagnosis at baseline in the UK Biobank. Over a follow-up period of 344,636 person-years, a total of 1,151 VTE events were recorded. Participants were divided into four groups based on the quartiles of CRP levels. The adjusted hazard ratios (95% CIs) of Q1, Q2, Q3, and Q4 were 1.00, 1.20 (0.99-1.44), 1.25 (1.04-1.50), and 1.51 (1.25-1.82), respectively. For those with high genetic risk of VTE, high CRP had an additional increased risk for VTE.

Conclusion: CRP can be used as a predictive biomarker for VTE risk in cancer survivors, especially for those with high genetic risk. Future research can explore whether prevention and treatment strategies for VTE can be developed based on CRP for cancer survivors.