This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a significant, reproducible, association with CVD (CEAP C ≥ 2 meta-odds ratio 1.31, 95% CI 1.27-1.34, P = 1 × 10<sup>-98</sup>, PHet = 0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.
There were also nonsignificant trends toward a higher incidence of EHIT in patients with a history of VTE (20% vs 10%; P = .06), worsening venous disease (Clinical, Etiology, Anatomy, Pathophysiology [CEAP] class >2, 37% vs 26%; P = .13), and history of tobacco use (43% vs 31%; P = .18).
The severity of varicose veins was divided into 2 groups according to CEAP (clinical, etiological, anatomical, and pathophysiological) classification: mild type of venous disease (C0-C2) and severe type of venous disease (C3-C6).
This study compared the nature and prevalence of thrombophilia in patients with varicose veins (VV, CEAP clinical [C] grade C(2) to C(3)) and patients with CVU (C(5) to C(6)) with an age- and sex-matched population without clinical or duplex ultrasound evidence of venous disease.
Accounting for age, obesity and family history of leg ulcer, odds ratios (ORs) of venous disease for elevated factor VIII, von Willebrand factor (VWF), D-dimer and for factor V Leiden were 1.4 (95% CI 0.9-2.1), 1.5 (CI 1.0-2.3), 1.7 (CI 1.1-2.8) and 1.1 (CI 0.5-2.4), respectively.
The frequency of the factor V Leiden gene mutation was significantly increased in patients with femoro-popliteal occlusive disease (n = 126), to 21.6% (t = 16.94; P< .001), and venous disease (n = 50), to 36.0% (t = 20.93; P< .001).
This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a significant, reproducible, association with CVD (CEAP C ≥ 2 meta-odds ratio 1.31, 95% CI 1.27-1.34, P = 1 × 10<sup>-98</sup>, PHet = 0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.
Therefore, upregulation of the CLOCK gene in the vessel walls of veins may be involved in the pathogenesis of VVs and the progression of venous disease.
Accounting for age, obesity and family history of leg ulcer, odds ratios (ORs) of venous disease for elevated factor VIII, von Willebrand factor (VWF), D-dimer and for factor V Leiden were 1.4 (95% CI 0.9-2.1), 1.5 (CI 1.0-2.3), 1.7 (CI 1.1-2.8) and 1.1 (CI 0.5-2.4), respectively.
Skin biopsies were obtained from the legs of patients with varying degrees of chronic venous disease and were assessed for procollagen gene expression by in-situ hybridization and for cell proliferation by immunolocalization of proliferating cell nuclear antigen.
The MTHFR 677TT mutation (RR: 6.92; 3.86-12.4) and its association with the 844ins68 insertion (RR: 21.9; 8.35-57.4), but not the isolated insertion (RR: 0.71), were more frequent in patients and controls with fasting hyperhomocysteinemia than in normohomocysteinemic subjects, irrespective of the type of occlusive disease (venous or arterial).
Immunohistochemical staining of skin biopsies revealed an increase in the expression of ICAM-1 and VCAM-1 on endothelial cells in an early stage of venous disease such as stasis dermatitis.
Immunohistochemical staining of skin biopsies revealed an increase in the expression of ICAM-1 and VCAM-1 on endothelial cells in an early stage of venous disease such as stasis dermatitis.