title: Corticosteroid therapy in a patient with cerebral amyloid angiopathy-related inflammation.
abstract: We studied longitudinal changes of the levels of anti-amyloid β (anti-Aβ) antibody, amyloid β (Aβ) protein, and interleukin 8 (IL-8) in cerebrospinal fluid (CSF) of a patient with cerebral amyloid angiopathy-related inflammation (CAA-ri) in whom steroid treatment resulted in clinical improvement. The diagnosis of CAA-ri was established with brain biopsy. Levels of anti-Aβ 42 antibody, Aβ 40, Aβ 42 and IL-8 in CSF were measured in the CAA-ri patient at 23 time points in the 8-month clinical course. These CSF samples were divided into 2 groups: those obtained before (n = 12) and those after (n = 11) oral corticosteroid therapy was started. We compared these levels between CSF samples obtained before and after therapy. The mean levels of anti-Aβ 42 antibody and IL-8 were significantly higher in CSF samples of the CAA-ri patient before oral corticosteroid therapy than those after therapy. A positive correlation was noted between levels of anti-Aβ 42 antibodies and IL-8 in CSF of this patient. There were no significant differences of mean levels of Aβ 40 and Aβ 42 between CSF samples obtained before and after oral corticosteroid therapy. It was possible that the autoinflammatory process with anti-Aβ 42 antibodies and IL-8 may have been involved in the pathogenesis of CAA-ri, and that corticosteroid therapy directly affected levels of anti-Aβ 42 antibody and IL-8. In summary, CAA-ri encephalopathy is a relapsing or progressive disorder and may be treatable by adequate immunosuppressive therapy. The anti-Aβ 42 antibody in CSF is a useful biological marker for therapeutic monitoring of CAA-ri.
authors.affiliation: Department of Neurology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu, 501-1194, Japan. kimura1@gifu-u.ac.jp
authors.forename: Akio
authors.initials: A
authors.lastname: Kimura
authors.forename: Takeo
authors.initials: T
authors.lastname: Sakurai
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Yoshikura
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Masao
authors.initials: M
authors.lastname: Takemura
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takahashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Inuzuka
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000368:Aged; D000369:Aged, 80 and over; D016229:Amyloid beta-Peptides / Q000276:immunology / Q000378:metabolism; D000906:Antibodies / Q000134:cerebrospinal fluid; D001706:Biopsy; D001921:Brain / Q000473:pathology; D002452:Cell Count; D016657:Cerebral Amyloid Angiopathy / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000473:pathology; D016209:Interleukin-8 / Q000134:cerebrospinal fluid; D008279:Magnetic Resonance Imaging; D010446:Peptide Fragments / Q000276:immunology / Q000378:metabolism; D016133:Polymerase Chain Reaction
chemical_list: D000305:Adrenal Cortex Hormones; D016229:Amyloid beta-Peptides; D000906:Antibodies; D016209:Interleukin-8; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42)