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Elevated serum homocysteine levels are associated with the development of chronic venous ulcers
Zhenyu Guo1, Xu Li1, Tao Wang1
1Department of Vascular Surgery, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai, China.
Insights
High homocysteine levels (HHcy) are linked to venous ulcer development in patients with varicose veins. This study found HHcy significantly associated with ulcer formation and progression, suggesting a potential therapeutic target.
Area of Science:
- Vascular Biology
- Clinical Medicine
- Biochemistry
Background:
- Venous ulceration is a complex condition.
- The role of hyperhomocysteinemia (HHcy) in venous ulcer development from varicose veins is not well-established.
Purpose of the Study:
- To investigate the correlation between HHcy and the formation of venous ulcers in patients with primary varicose veins.
- To explore the underlying mechanisms of HHcy-induced vascular changes.
Main Methods:
- Retrospective analysis of clinical data from 717 patients (106 with ulcers, 611 without).
- Multivariate logistic regression and propensity score matching were employed.
- In vitro experiments assessed HHcy's effect on endothelial cells and vascular smooth muscle cells.
Main Results:
- A significantly higher prevalence of HHcy was observed in patients with venous ulcers (46.2%) compared to controls (17.5%).
- HHcy was independently associated with venous ulceration in primary varicose veins (p < 0.001).
- Experimental data indicated HHcy induces endothelial dysfunction and vascular smooth muscle cell phenotypic switching.
Conclusions:
- Clinical and experimental evidence strongly implicates HHcy as a contributing factor in venous ulcer development.
- Further research is warranted to evaluate HHcy-lowering therapies for preventing venous ulcers in varicose vein patients.
Introduction:
Venous ulceration is a multifactorial disease, and whether hyperhomocysteinemia (HHcy) promotes deterioration from primary varicose veins to venous ulcers remains unproven.
Methods:
This study retrospectively analyzed clinical data from 717 patients to investigate the potential correlation between HHcy and primary varicose veins ulcer formation, including 611 patients without ulcers (control group) and 106 with ulcers (case group).
Results:
In this study, 46.2% (49/106) of patients in the case group and 17.5% (107/611, p < 0.001) in the control group suffered from HHcy. Multivariate logistic analysis revealed that HHcy was closely associated with the incidence of venous ulceration in patients with primary varicose veins (p < 0.001). Propensity score matching created 101 matched pairs of patients with and without ulcers, and the analysis pointed to a potential link between HHcy and ulcer formation in the context of primary varicose veins (p < 0.001). Additional experiments showed that HHcy could induce endothelial dysfunction and phenotypic switching of vascular smooth muscle cells.
Conclusion:
Both clinical and experimental findings implicated HHcy as a key factor in the development of venous ulceration. Further research is needed to appraise the effectiveness of HHcy-lowering therapy in the prevention of venous ulcers in patients with varicose veins.
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