Treatment-induced neoangiogenesis in cerebral arteriovenous malformations

U Sure; N Butz; A M Siegel; H D Mennel; S Bien; H Bertalanffy

doi:10.1016/s0303-8467(01)00112-3

Treatment-induced neoangiogenesis in cerebral arteriovenous malformations

Clin Neurol Neurosurg. 2001 Apr;103(1):29-32. doi: 10.1016/s0303-8467(01)00112-3.

Authors

U Sure¹, N Butz, A M Siegel, H D Mennel, S Bien, H Bertalanffy

Affiliation

¹ Neurochirurgische Klinik, Philipps-Universität, Baldingerstrasse, 35033, Marburg, Germany. sure@post.med.uni-marburg.de

PMID: 11311473
DOI: 10.1016/s0303-8467(01)00112-3

Abstract

We investigated the angiogenetic and proliferative activity of the endothelium of 30 consecutive surgical cases of AVM treated at our institution by immunohistochemical detection of the PCNA, MIB-1, Flk-1 and VEGF antibodies. Endothelial positive immunostaining was observed in 87% of the cases for PCNA, in 20% for MIB-1, and in 80% for Flk-1. Of 22 individuals treated with incomplete embolization prior to surgery, 17 showed an expression of VEGF (77%), but only two of the eight patients (25%) who were treated without prior embolization exhibited such an immunoreaction (P=0.0086). The proliferation and growth of cerebral AVMs is documented by endothelial expression of PCNA and MIB-1. The statistically significantly higher expression of VEGF in partially obliterated (embolized) AVMs is most likely caused by transient regional hypoxia within the AVM nidus that mediates neoangiogensis. It points out the clinical relevance of a complete occlusion in order to avoid neovascularization associated with subsequent morbidity and mortality.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Antigens, Nuclear
Brain / blood supply*
Brain Chemistry*
Embolization, Therapeutic / adverse effects*
Embolization, Therapeutic / methods
Endothelial Growth Factors / biosynthesis
Humans
Immunohistochemistry
Intracranial Arteriovenous Malformations / pathology
Intracranial Arteriovenous Malformations / surgery
Intracranial Arteriovenous Malformations / therapy*
Ki-67 Antigen
Lymphokines / biosynthesis
Neovascularization, Pathologic / metabolism*
Nuclear Proteins / biosynthesis
Proliferating Cell Nuclear Antigen / biosynthesis
Receptor Protein-Tyrosine Kinases / biosynthesis
Receptors, Growth Factor / biosynthesis
Receptors, Vascular Endothelial Growth Factor
Secondary Prevention
Up-Regulation
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors

Substances

Antigens, Nuclear
Endothelial Growth Factors
Ki-67 Antigen
Lymphokines
Nuclear Proteins
Proliferating Cell Nuclear Antigen
Receptors, Growth Factor
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Receptor Protein-Tyrosine Kinases
Receptors, Vascular Endothelial Growth Factor