Gallai V, Caso V, Paciaroni M, Cardaioli G, Arning E, Bottiglieri T, Parnetti L
Neuroscience Department, University of Perugia, Perugia, Italy.
Stroke. 2001 Mar;32(3):714-8. doi: 10.1161/01.str.32.3.714.
The pathogenesis of cervical artery dissection (CAD) remains unknown in most cases. Hyperhomocyst(e)inemia [hyperH(e)], an independent risk factor for cerebrovascular disease, induces damage in endothelial cells in animal cell culture. Consecutive patients with CAD and age-matched control subjects have been studied by serum levels of homocyst(e)ine and the genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR).
Twenty-six patients with CAD, admitted to our Stroke Unit (15 men and 11 women; 16 vertebral arteries, 10 internal carotid arteries), were compared with age-matched control subjects. All patients underwent duplex ultrasound, MR angiography, and/or conventional angiography.
Mean plasma homocyst(e)ine level was 17.88 micromol/L (range 5.95 to 40.0 micromol/L) for patients with CAD and 6.0+/-0.99 micromol/L for controls (P:<0.001). The genetic analysis for the thermolabile form of MTHFR in CAD patients showed heterozygosity in 54% and homozygosity in 27%; comparable figures for controls were 40% (P:=0.4) and 10% (P:=0.1), respectively.
Mild hyperH(e) might represent a risk factor for cervical artery dissection. The MTHFR mutation is not significantly associated with CAD. An interaction between different genetic and environmental factors probably takes place in the cascade of pathogenetic events leading to arterial wall damage.
在大多数情况下，颈动脉夹层（CAD）的发病机制仍不清楚。高同型半胱氨酸血症[高H（e）]是脑血管疾病的一个独立危险因素，在动物细胞培养中可诱导内皮细胞损伤。我们通过检测同型半胱氨酸的血清水平和5,10-亚甲基四氢叶酸还原酶（MTHFR）的基因型，对连续的CAD患者和年龄匹配的对照者进行了研究。
将入住我们卒中单元的26例CAD患者（15例男性和11例女性；16例椎动脉，10例颈内动脉）与年龄匹配的对照者进行比较。所有患者均接受了双功超声、磁共振血管造影和/或传统血管造影检查。
CAD患者的平均血浆同型半胱氨酸水平为17.88微摩尔/升（范围5.95至40.0微摩尔/升），对照组为6.0±0.99微摩尔/升（P<0.001）。对CAD患者中MTHFR热不稳定型的基因分析显示，杂合子占54%，纯合子占27%；对照组的相应数字分别为40%（P=0.4）和10%（P=0.1）。
轻度高H（e）可能是颈动脉夹层的一个危险因素。MTHFR突变与CAD无显著相关性。在导致动脉壁损伤的一系列致病事件中，不同的遗传和环境因素之间可能存在相互作用。
