Kim Grace H, Hahn David K, Kellner Christopher P, Hickman Zachary L, Komotar Ricardo J, Starke Robert M, Mack William J, Mocco J, Solomon Robert A, Connolly E Sander
Department of Neurological Surgery, Columbia College of Physicians and Surgeons, Neurological Institute of New York, 630 W 168th St, Room 5-454, New York, NY 10032, USA.
Stroke. 2008 Aug;39(8):2274-9. doi: 10.1161/STROKEAHA.107.512442. Epub 2008 Jun 5.
The role of abnormal angiogenesis in the formation and progression of cerebral arteriovenous malformations (AVMs) is unclear. Previous studies have demonstrated increased local expression of vascular endothelial growth factor (VEGF) in AVM tissue and increased circulating levels of VEGF in AVM patients. We sought to further investigate the role of VEGF in AVM pathophysiology by examining changes in plasma VEGF levels in patients undergoing treatment for AVMs.
Three serial blood samples were obtained from 13 AVM patients undergoing treatment: (1) before any treatment, (2) 24 hours postresection, and (3) 30 days postresection. Plasma VEGF concentrations were measured via commercially available enzyme-linked immunosorbent assay (ELISA). For controls, blood samples were obtained from 29 lumbar laminectomy patients.
The mean plasma VEGF level in AVM patients at baseline was 36.08+/-13.02 pg/mL, significantly lower than that of the control group (80.52+/-14.02 pg/mL, P=0.028). Twenty-four hours postresection, plasma VEGF levels dropped to 20.09+/-4.54 pg/mL, then increased to 66.81+/-26.45 pg/mL 30 days later (P=0.048). The mean plasma VEGF concentration 30 days after resection was no longer significantly different from the control group (P=0.33).
Plasma VEGF levels in 13 AVM patients were unexpectedly lower than controls, dropped early after AVM resection, then significantly increased 30 days later. These results support the key role of abnormal angiogenesis in AVM pathophysiology and suggest that a disruption in systemic VEGF expression may contribute to the natural history of these lesions.
异常血管生成在脑动静脉畸形（AVM）形成和进展中的作用尚不清楚。先前的研究表明，AVM组织中血管内皮生长因子（VEGF）的局部表达增加，且AVM患者循环中VEGF水平升高。我们试图通过检测接受AVM治疗患者血浆VEGF水平的变化，进一步研究VEGF在AVM病理生理学中的作用。
从13例接受治疗的AVM患者中采集三份连续血样：（1）任何治疗前；（2）切除后24小时；（3）切除后30天。通过市售酶联免疫吸附测定（ELISA）法检测血浆VEGF浓度。作为对照，从29例腰椎椎板切除术患者中采集血样。
AVM患者基线时血浆VEGF平均水平为36.08±13.02 pg/mL，显著低于对照组（80.52±14.02 pg/mL，P = 0.028）。切除后24小时，血浆VEGF水平降至20.09±4.54 pg/mL，然后在30天后升至66.81±26.45 pg/mL（P = 0.048）。切除后30天血浆VEGF平均浓度与对照组不再有显著差异（P = 0.33）。
13例AVM患者的血浆VEGF水平意外低于对照组，AVM切除后早期下降，然后在30天后显著升高。这些结果支持异常血管生成在AVM病理生理学中的关键作用，并表明全身VEGF表达的破坏可能有助于这些病变的自然病程。
