PDF(Pubmed)
Abstract：
UNASSIGNED: Spontaneous cervical artery dissection (sCAD) is a rare vasculopathy whose trigger is still unknown. We hypothesized that autoimmunity against components of the vascular wall might play a critical role in sCAD and examined anti-collagen type I antibodies in patients with sCAD, acute ischemic stroke, patients with thromboendarterectomy, and controls.
UNASSIGNED: Fifty-seven patients with sCAD (age 45.7 ± 10.2 years, female 18 (31.6%)) were prospectively enrolled in four German stroke centers. Blood samples were collected at baseline, at day 10 ± 3, and after 6 ± 1 months. Patients with ischemic stroke not related to CAD (n=54, age 56.7 ± 13.7 years, female 15 (27.8%)), healthy probands (n=80, age 57.4 ± 12.9 years, female 56 (70%)), and patients undergoing thromboendarterectomy of the carotid artery (n=9, age 70.7 ± 9.3 years, female 2 (22.2%)) served as controls. Anti-collagen type I antibodies were determined by enzyme-linked immunosorbent assays (ELISAs).
UNASSIGNED: Patients with acute sCAD had higher serum levels of anti-collagen type I antibodies (33.9 ± 24.6 µg/ml) than probands (18.5 ± 11.0 µg/ml; p <0.001) but lower levels than patients with ischemic stroke not related to sCAD (47.8 ± 28.4 µg/ml; p=0.003). In patients with sCAD, serum levels of anti-collagen type I antibodies were similar in the acute, subacute, and chronic phase. Levels of anti-collagen type I antibodies significantly correlated with circulating collagen type I (rho=0.207, p=0.003).
UNASSIGNED: Anti-collagen type I antibodies seem not to represent a trigger for acute sCAD or ischemic stroke but may rather be linked to the metabolism and turnover of collagen type I.
UNASSIGNED: Fifty-seven patients with sCAD (age 45.7 ± 10.2 years, female 18 (31.6%)) were prospectively enrolled in four German stroke centers. Blood samples were collected at baseline, at day 10 ± 3, and after 6 ± 1 months. Patients with ischemic stroke not related to CAD (n=54, age 56.7 ± 13.7 years, female 15 (27.8%)), healthy probands (n=80, age 57.4 ± 12.9 years, female 56 (70%)), and patients undergoing thromboendarterectomy of the carotid artery (n=9, age 70.7 ± 9.3 years, female 2 (22.2%)) served as controls. Anti-collagen type I antibodies were determined by enzyme-linked immunosorbent assays (ELISAs).
UNASSIGNED: Patients with acute sCAD had higher serum levels of anti-collagen type I antibodies (33.9 ± 24.6 µg/ml) than probands (18.5 ± 11.0 µg/ml; p <0.001) but lower levels than patients with ischemic stroke not related to sCAD (47.8 ± 28.4 µg/ml; p=0.003). In patients with sCAD, serum levels of anti-collagen type I antibodies were similar in the acute, subacute, and chronic phase. Levels of anti-collagen type I antibodies significantly correlated with circulating collagen type I (rho=0.207, p=0.003).
UNASSIGNED: Anti-collagen type I antibodies seem not to represent a trigger for acute sCAD or ischemic stroke but may rather be linked to the metabolism and turnover of collagen type I.
摘要：
■自发性颈动脉夹层（sCAD）是一种罕见的血管病变，其触发因素尚不清楚。我们假设针对血管壁成分的自身免疫可能在sCAD中起关键作用，并检查了sCAD患者的抗I型胶原抗体。急性缺血性卒中,血栓内膜切除术患者，和控制。
■57例sCAD患者（年龄45.7±10.2岁，女性18人(31.6%)前瞻性纳入德国4个卒中中心.在基线时收集血样，在第10±3天和6±1个月后。与CAD无关的缺血性卒中患者（n=54，年龄56.7±13.7岁，女性15（27.8%）），健康先证者(n=80，年龄57.4±12.9岁，女性56（70％），和接受颈动脉血栓内膜切除术的患者（n=9，年龄70.7±9.3岁，女性2（22.2％）作为对照。通过酶联免疫吸附测定(ELISA)确定抗I型胶原抗体。
■急性sCAD患者的血清抗I型胶原抗体水平（33.9±24.6µg/ml）高于先证者（18.5±11.0µg/ml；p<0.001），但低于与sCAD无关的缺血性卒中患者（47.8±28.4µg/ml；p=0.003）。在sCAD患者中，血清抗I型胶原抗体水平在急性，亚急性，慢性阶段。抗I型胶原蛋白抗体的水平与循环I型胶原蛋白显着相关（rho=0.207，p=0.003）。
抗I型胶原抗体似乎不代表急性sCAD或缺血性卒中的触发因素，但可能与I型胶原的代谢和周转有关。
■57例sCAD患者（年龄45.7±10.2岁，女性18人(31.6%)前瞻性纳入德国4个卒中中心.在基线时收集血样，在第10±3天和6±1个月后。与CAD无关的缺血性卒中患者（n=54，年龄56.7±13.7岁，女性15（27.8%）），健康先证者(n=80，年龄57.4±12.9岁，女性56（70％），和接受颈动脉血栓内膜切除术的患者（n=9，年龄70.7±9.3岁，女性2（22.2％）作为对照。通过酶联免疫吸附测定(ELISA)确定抗I型胶原抗体。
■急性sCAD患者的血清抗I型胶原抗体水平（33.9±24.6µg/ml）高于先证者（18.5±11.0µg/ml；p<0.001），但低于与sCAD无关的缺血性卒中患者（47.8±28.4µg/ml；p=0.003）。在sCAD患者中，血清抗I型胶原抗体水平在急性，亚急性，慢性阶段。抗I型胶原蛋白抗体的水平与循环I型胶原蛋白显着相关（rho=0.207，p=0.003）。
抗I型胶原抗体似乎不代表急性sCAD或缺血性卒中的触发因素，但可能与I型胶原的代谢和周转有关。
