Brain vascular lesions: a clinicopathologic, immunohistochemistry, and ultrastructural approach
| Autor: | Miguel Ángel Collado-Ortiz, Martha Lilia Tena-Suck, Alma Dalia Hernández, Marisol Galván Navarrete, Citlaltepetl Salinas-Lara |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Adult
Male CD31 Pathology medicine.medical_specialty Vascular smooth muscle Adolescent CD34 Biology Mural cell Pathology and Forensic Medicine Lesion Young Adult medicine Humans Hyaline Aged Central Nervous System Vascular Malformations General Medicine Middle Aged Immunohistochemistry Microscopy Electron Hemosiderin Female medicine.symptom Biomarkers |
| Zdroj: | Annals of Diagnostic Pathology. 18:193-198 |
| ISSN: | 1092-9134 |
| DOI: | 10.1016/j.anndiagpath.2014.01.005 |
| Popis: | Brain vascular malformations are relatively common lesions that cause serious neurologic disability or death in a significant proportion of individuals bearing them. The purpose of this study was to analyze the clinicopathologic and immunohistochemistry these lesions, looking for common antibodies expressed such as CD31, CD34, CD15, factor VIII, nestin, vimentin, vascular endothelial grow factor (VEGF), vascular endothelial grow factor receptor-2 (VEGF-R2), glial fibrillar acidic protien (GFAP), and fibroblastic grow factor β (β-FGF) and ultrastructure in endothelial cells as well as in vessel walls. Fifty cases of vascular lesions were included in this study: 29 (58%) of them were arteriovenous malformations and 21 (52%) were brain cavernomas. Twenty-six (52%) patients were women and 24 (48%) men. The age range was from 13 to 68 years (mean age, 35.86 ± 15.19 years). The size of the lesions ranged between 1 and 8 cm (3 ± 1.65 cm), and parieto-occipital lesions had a bigger size. Evolution time varied from 1 month to 1 year (mean, 7.5 months). There was a significant statistical correlation between age and sex (P = -035), rupture of lesion (P = .015), brain hemorrhage (P = .033), necrosis (P = .011), hemosiderin deposit (P = .042), VEGF (P = .015), and VEGFR (P = .037), as well as localization of rupture (P = .017), loss of consciousness (P = .000), visual deficit (P = .026), hyaline vessels (P = .000), and CD31 (.009). Interactions between endothelial cells and mural cells (pericytes and vascular smooth muscle cells) in blood vessel walls have recently come into focus as central processes in the regulation of vascular formation, stabilization, remodeling, and function in brain vascular lesions. However, the molecular mechanisms that underlie the formation and growth of brain arteriovenous malformations are still poorly understood. |
| Databáze: | OpenAIRE |
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