Symbiant Medical Center Alkmaar

Alkmaar, Netherlands

Symbiant Medical Center Alkmaar

Alkmaar, Netherlands
SEARCH FILTERS
Time filter
Source Type

Background: Cerebral vascular malformations were investigated for the presence of the glucose transporter protein GLUT1, which is normally expressed in endothelial cells of the pre-existing microvasculature of the brain and absent in the vasculature of the choroid plexus and extracranial vasculature without a barrier function. Extracranial arteriovenous malformations (AVM) are known to show an absence of GLUT1 expression which distinguishes them from infantile hemangioma of skin and soft tissue. The expression of GLUT1 in cerebrovascular malformations is not systematically investigated. Methods: Paraffin-embedded sections of cerebral AVM (4), including one choroid plexus AVM, cerebral cavernous malformations (CCM, 3) and extracranial (facial) AVM (3) were immunostained with anti-CD31 and GLUT1 in doublestaining procedure which was further analyzed with the use of spectral analysis software. Results: All 7 cases of cerebral vascular malformations showed colocalization of GLUT1/CD31 of endothelial cells of the vessels within the malformation. Only in the extracranial AVM expression of GLUT1 was completely absent. Conclusion: Cerebral AVM differ from extracranial AVM by their endothelial immunoexpression of GLUT1, indicating that the vessels of these malformations retain the endothelial phenotype of the local vascular beds from which they are derived during embryogenesis©2012 Dustri-Verlag Dr. K. Feistle ISSN 0722-5091.


Cerebral vascular malformations were investigated for the presence of the glucose transporter protein GLUT1, which is normally expressed in endothelial cells of the pre-existing microvasculature of the brain and absent in the vasculature of the choroid plexus and extracranial vasculature without a barrier function. Extracranial arteriovenous malformations (AVM) are known to show an absence of GLUT1 expression which distinguishes them from infantile hemangioma of skin and soft tissue. The expression of GLUT1 in cerebrovascular malformations is not systematically investigated. Paraffin-embedded sections of cerebral AVM (4), including one choroid plexus AVM, cerebral cavernous malformations (CCM, 3) and extracranial (facial) AVM (3) were immunostained with anti-CD31 and GLUT1 in doublestaining procedure which was further analyzed with the use of spectral analysis software. All 7 cases of cerebral vascular malformations showed colocalization of GLUT1/CD31 of endothelial cells of the vessels within the malformation. Only in the extracranial AVM expression of GLUT1 was completely absent. Cerebral AVM differ from extracranial AVM by their endothelial immunoexpression of GLUT1, indicating that the vessels of these malformations retain the endothelial phenotype of the local vascular beds from which they are derived during embryogenesis.


Meijer-Jorna L.B.,Symbiant Medical Center Alkmaar | Van Der Loos C.M.,University of Amsterdam | Teeling P.,University of Amsterdam | De Boer O.J.,University of Amsterdam | And 3 more authors.
Journal of Cutaneous Pathology | Year: 2012

Background: Areas of microvascular proliferation have been observed in a subpopulation of symptomatic congenital vascular malformations later in life. We investigated whether this angiogenic response is followed by a stage of maturation. Methods: Resections of vascular malformations (n = 15), infantile hemangiomas (IHs) (n = 8) and pyogenic granulomas (PGs) (n = 5) were studied. Histopathologically, all lesions were screened for presence of foci of immature and/or mature microvessels. These areas were further studied immunohistochemically for differential expression of several angiogenic factors, cell cycle-dependent proteins, p53 and active caspase3. Immunostains were scored semiquantitatively. Results: Immature microvessel areas were present in five vascular malformations (all of the arteriovenous type), five IHs and five PGs; these lesions also contained transitions between immature and mature microvessels. Conglomerates of mature microvessels were found in 19 cases (6 vascular malformations, 5 PGs and 8 IHs). Expression of vascular endothelial growth factor-A, angiopoietin-1, Ki-67, p16 and p21/27 ratios were overall significantly lower in mature areas than in immature areas including those in vascular malformations. P53 and caspase3 expression was scarce in all lesions. Conclusions: Microvascular areas in vascular malformations appear to follow the same pattern of vascular proliferation and maturation as seen in other microvascular lesions of skin and soft tissue. Copyright © 2012 John Wiley & Sons A/S.


PubMed | Symbiant Medical Center Alkmaar
Type: Journal Article | Journal: Clinical neuropathology | Year: 2012

Cerebral vascular malformations were investigated for the presence of the glucose transporter protein GLUT1, which is normally expressed in endothelial cells of the pre-existing microvasculature of the brain and absent in the vasculature of the choroid plexus and extracranial vasculature without a barrier function. Extracranial arteriovenous malformations (AVM) are known to show an absence of GLUT1 expression which distinguishes them from infantile hemangioma of skin and soft tissue. The expression of GLUT1 in cerebrovascular malformations is not systematically investigated.Paraffin-embedded sections of cerebral AVM (4), including one choroid plexus AVM, cerebral cavernous malformations (CCM, 3) and extracranial (facial) AVM (3) were immunostained with anti-CD31 and GLUT1 in doublestaining procedure which was further analyzed with the use of spectral analysis software.All 7 cases of cerebral vascular malformations showed colocalization of GLUT1/CD31 of endothelial cells of the vessels within the malformation. Only in the extracranial AVM expression of GLUT1 was completely absent.Cerebral AVM differ from extracranial AVM by their endothelial immunoexpression of GLUT1, indicating that the vessels of these malformations retain the endothelial phenotype of the local vascular beds from which they are derived during embryogenesis.


PubMed | Symbiant Medical Center Alkmaar
Type: Journal Article | Journal: Journal of the American Academy of Dermatology | Year: 2013

Episodes of microvascular proliferation associated with volume expansion have been observed in arteriovenous malformations (AVMs) of skin and soft tissue.We sought to investigate the relationship between a microvascular proliferative response and flow velocity in AVMs.Resection specimens of 80 AVMs were clinically categorized as either high- or low-flow lesions, and histopathologically screened for the presence of microvessels, inflammation, thrombosis, or a combination of these. Immunohistochemistry was performed with endoglin (CD105), von Willebrand factor, and fibrinogen antibodies.Clinically, 37 AVMs were classified as high-flow lesions and 43 as low-flow lesions. In 81% of high-flow lesions microvascular proliferations were seen versus in 14% of low-flow lesions (P < .005). In high-flow lesions, which were embolized before surgery (30% of all), 88% showed microvascular proliferation, 88% inflammation, and 33% thrombosis. However, similar vasoproliferative responses were also observed in nonembolized AVM (69% high-flow and 14% low-flow lesions). Endoglin was more frequently expressed in high-flow lesions. Extracellular von Willebrand factor staining was found in most lesions, irrespective of flow type or presence of microvascular proliferations.The study was carried out at a single tertiary referral center.Microvascular proliferative masses in AVMs appear to be strongly associated with high-flow characteristics. This could be explained to some extent by previous therapeutic embolization and/or inflammation in the lesion. However, occurrence of similar microvascular responses in AVM that were not embolized before surgery suggests that the biomechanical effects of high flow in these lesions may also have an angiogenic effect.


PubMed | Symbiant Medical Center Alkmaar
Type: Journal Article | Journal: Journal of cutaneous pathology | Year: 2012

Areas of microvascular proliferation have been observed in a subpopulation of symptomatic congenital vascular malformations later in life. We investigated whether this angiogenic response is followed by a stage of maturation.Resections of vascular malformations (n = 15), infantile hemangiomas (IHs) (n = 8) and pyogenic granulomas (PGs) (n = 5) were studied. Histopathologically, all lesions were screened for presence of foci of immature and/or mature microvessels. These areas were further studied immunohistochemically for differential expression of several angiogenic factors, cell cycle-dependent proteins, p53 and active caspase3. Immunostains were scored semiquantitatively.Immature microvessel areas were present in five vascular malformations (all of the arteriovenous type), five IHs and five PGs; these lesions also contained transitions between immature and mature microvessels. Conglomerates of mature microvessels were found in 19 cases (6 vascular malformations, 5 PGs and 8 IHs). Expression of vascular endothelial growth factor-A, angiopoietin-1, Ki-67, p16 and p21/27 ratios were overall significantly lower in mature areas than in immature areas including those in vascular malformations. P53 and caspase3 expression was scarce in all lesions.Microvascular areas in vascular malformations appear to follow the same pattern of vascular proliferation and maturation as seen in other microvascular lesions of skin and soft tissue.

Loading Symbiant Medical Center Alkmaar collaborators
Loading Symbiant Medical Center Alkmaar collaborators