title: Bevacizumab as a treatment option for radiation-induced cerebral necrosis.
abstract: Radiation necrosis of normal CNS tissue represents one of the main risk factors of brain irradiation, occurring more frequently and earlier at higher total doses and higher doses per fraction. At present, it is believed that the necrosis results due to increasing capillary permeability caused by cytokine release leading to extracellular edema. This process is sustained by endothelial dysfunction, tissue hypoxia, and subsequent necrosis. Consequently, blocking the vascular endothelial growth factor (VEGF) at an early stage could be an option to reduce the development of radiation necrosis by decreasing the vascular permeability. This might help to reverse the pathological mechanisms, improve the symptoms and prevent further progression. A patient with radiationinduced necrosis was treated with an anti-VEGF antibody (bevacizumab), in whom neurologic signs and symptoms improved in accordance with a decrease in T1-weighted fluid-attenuated inversion recovery signals. Our case report together with the current literature suggests bevacizumab as a treatment option for patients with symptoms and radiological signs of cerebral necrosis induced by radiotherapy.
authors.affiliation: Department of Radiation Oncology, University Hospital Düsseldorf, Düsseldorf, Germany.
authors.forename: Christiane
authors.initials: C
authors.lastname: Matuschek
authors.forename: Edwin
authors.initials: E
authors.lastname: Bölke
authors.forename: Jens
authors.initials: J
authors.lastname: Nawatny
authors.forename: Thomas K
authors.initials: TK
authors.lastname: Hoffmann
authors.forename: Matthias
authors.initials: M
authors.lastname: Peiper
authors.forename: Klaus
authors.initials: K
authors.lastname: Orth
authors.forename: Peter Arne
authors.initials: PA
authors.lastname: Gerber
authors.forename: Ethelyn
authors.initials: E
authors.lastname: Rusnak
authors.forename: Guido
authors.initials: G
authors.lastname: Lammering
authors.forename: Wilfried
authors.initials: W
authors.lastname: Budach
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018906:Antineoplastic Agents, Alkylating / Q000008:administration & dosage / Q000009:adverse effects; D001254:Astrocytoma / Q000188:drug therapy / Q000473:pathology / Q000532:radiotherapy* / Q000601:surgery; D000068258:Bevacizumab; D001812:Blood-Brain Barrier / Q000528:radiation effects; D001921:Brain / Q000473:pathology / Q000528:radiation effects* / Q000601:surgery; D001929:Brain Edema / Q000188:drug therapy / Q000473:pathology; D001932:Brain Neoplasms / Q000188:drug therapy / Q000473:pathology / Q000532:radiotherapy* / Q000601:surgery; D017024:Chemotherapy, Adjuvant; D003131:Combined Modality Therapy; D003606:Dacarbazine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives; D006801:Humans; D008297:Male; D009336:Necrosis; D009364:Neoplasm Recurrence, Local / Q000188:drug therapy / Q000473:pathology / Q000532:radiotherapy* / Q000601:surgery; D009460:Neurologic Examination / Q000187:drug effects / Q000528:radiation effects; D011832:Radiation Injuries / Q000188:drug therapy* / Q000473:pathology; D016634:Radiosurgery / Q000009:adverse effects; D011879:Radiotherapy Dosage; D011880:Radiotherapy Planning, Computer-Assisted; D018714:Radiotherapy, Adjuvant; D000077204:Temozolomide; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors*; D055815:Young Adult
chemical_list: D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018906:Antineoplastic Agents, Alkylating; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; D003606:Dacarbazine; D000077204:Temozolomide