TY - JOUR
T1 - Association between peripheral vascular endothelial dysfunction and livedoid vasculopathy
AU - Yang, Chih Hsun
AU - Shen, Su Chin
AU - Hui, Rosaline Chung Yee
AU - Huang, Yu Huei
AU - Chu, Pao-Hsien
AU - Ho, Wan Jing
PY - 2012/7
Y1 - 2012/7
N2 - Background: Livedoid vasculopathy (LV) is a disease characterized by multiple painful and recurrent ulcerations on the feet, accompanied by atrophic scars. Many researchers suggest that a hypercoagulable status is the pathogenetic factor for LV. However, the cause of LV remains elusive. Objective: We sought to determine if endothelial dysfunction is present in patients with LV. Methods: This prospective study included 16 patients with LV and active ulcers and 16 matched control subjects. We reviewed detailed clinical parameters, including antinuclear antibody, high-sensitivity C-reactive protein, protein C, protein S, homocysteine, anti-SSA, anti-SSB, anticardiolipin antibody, and serum lipid profiles. Flow-mediated vasodilation of the brachial artery was used as an indicator of vascular endothelial function using high-resolution 2-dimensional ultrasonic imaging. Results: Blood pressure, blood biochemistry, high-sensitivity C-reactive protein, and homocysteine were not significantly different in patients with LV and control subjects. Nitroglycerin-mediated vasodilation was not significantly different in patients with LV and control subjects. However, flow-mediated vasodilation was much less in patients with LV than in the control group (3.58 ± 2.32% vs 7.51 ± 2.40%, P <.001). Limitations: The study was performed at a single site with a limited sample size. Conclusion: Peripheral vascular endothelial dysfunction was demonstrated in patients with LV by reduction of brachial flow-mediated vasodilation.
AB - Background: Livedoid vasculopathy (LV) is a disease characterized by multiple painful and recurrent ulcerations on the feet, accompanied by atrophic scars. Many researchers suggest that a hypercoagulable status is the pathogenetic factor for LV. However, the cause of LV remains elusive. Objective: We sought to determine if endothelial dysfunction is present in patients with LV. Methods: This prospective study included 16 patients with LV and active ulcers and 16 matched control subjects. We reviewed detailed clinical parameters, including antinuclear antibody, high-sensitivity C-reactive protein, protein C, protein S, homocysteine, anti-SSA, anti-SSB, anticardiolipin antibody, and serum lipid profiles. Flow-mediated vasodilation of the brachial artery was used as an indicator of vascular endothelial function using high-resolution 2-dimensional ultrasonic imaging. Results: Blood pressure, blood biochemistry, high-sensitivity C-reactive protein, and homocysteine were not significantly different in patients with LV and control subjects. Nitroglycerin-mediated vasodilation was not significantly different in patients with LV and control subjects. However, flow-mediated vasodilation was much less in patients with LV than in the control group (3.58 ± 2.32% vs 7.51 ± 2.40%, P <.001). Limitations: The study was performed at a single site with a limited sample size. Conclusion: Peripheral vascular endothelial dysfunction was demonstrated in patients with LV by reduction of brachial flow-mediated vasodilation.
KW - endothelial dysfunction
KW - endothelium-dependent flow-mediated vasodilation
KW - livedoid vasculopathy
UR - https://www.scopus.com/pages/publications/84862275657
U2 - 10.1016/j.jaad.2011.07.021
DO - 10.1016/j.jaad.2011.07.021
M3 - 文章
AN - SCOPUS:84862275657
SN - 0190-9622
VL - 67
SP - 107
EP - 112
JO - Journal of the American Academy of Dermatology
JF - Journal of the American Academy of Dermatology
IS - 1
ER -