Respiratory Syncytial Virus-like Particles Consisting of M, G and Prefusion F

Walpita, Pramila; Johns, Lisa M

doi:10.36876/smtmj.1008

Cited by 1 publication

(3 citation statements)

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“…Previous analysis of CSF anti-β-amyloid autoantibodies showed elevated titers during active CAA-ri flares, with a return to background levels when the disease entered a remission phase. 3 Our data therefore raise the possibility that even a limited course of immunosuppressive therapy can delay or prevent recurrent elevations in anti-βamyloid autoantibody production. We were unable to test this possibility directly, however, as most individuals did not have serial CSF samples, and anti-β-amyloid autoantibody measurements were not performed.…”

Section: Discussionmentioning

confidence: 76%

“…erebral amyloid angiopathy-related inflammation (CAA-ri), also referred to as inflammatory cerebral amyloid angiopathy and Aß-related angiitis, is a distinct subset of cerebral amyloid angiopathy (CAA) characterized by an autoimmune reaction to cerebrovascular β-amyloid deposits. [1][2][3][4][5][6] It differs from more common noninflammatory forms of CAA in its clinical presentation, with subacute cognitive changes and vasogenic edema rather than acute intracerebral hemorrhage. [7][8][9][10] Neuroimaging results often show multiple lobar microhemorrhages characteristic of CAA as well as patchy or confluent asymmetric white matter hyperintensities (WMHs) suggestive of subcortical edema, which may regress in response to treatment, as reported in small case studies.…”

mentioning

confidence: 99%

“…12 Clinical and imaging criteria have been described for the diagnosis of probable CAA-ri, demonstrating high sensitivity (82%) and specificity (97%) in a small validation study. 11 Disease flares are associated with elevated cerebrospinal fluid (CSF) titers of anti-β-amyloid autoantibodies, 3 but assays for the CSF autoantibodies are not commercially available and have not been validated as a diagnostic test for this disorder.…”

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confidence: 99%

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Association Between Immunosuppressive Treatment and Outcomes of Cerebral Amyloid Angiopathy–Related Inflammation

et al. 2020

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IMPORTANCE Cerebral amyloid angiopathy-related inflammation (CAA-ri), a distinct subtype of cerebral amyloid angiopathy, is characterized by an autoimmune reaction to cerebrovascular β-amyloid deposits. Outcomes and response to immunosuppressive therapy for CAA-ri are poorly understood. OBJECTIVE To identify clinical, neuroimaging, laboratory, pathologic, or treatment-related associations with outcomes after an episode of CAA-ri. DESIGN, SETTING, AND PARTICIPANTSA retrospective cohort study of prospectively identified individuals who presented from July 3, 1998, to November 27, 2017, with a median follow-up of 2.7 years (interquartile range, 1.0-5.5 years). The study included 48 consecutive patients with CAA-ri meeting diagnostic criteria who had at least 1 disease episode and subsequent outcome data. No patients refused or were excluded.EXPOSURES Prespecified candidate variables were immunosuppressive therapies, cerebrospinal fluid pleocytosis, magnetic resonance imaging findings of recent infarcts or contrast enhancement, and histopathologic evidence of vessel wall inflammation.MAIN OUTCOMES AND MEASURES Clinical improvement and worsening were defined by persistent changes in signs or symptoms, radiographic improvement by decreased subcortical foci of T2 hyperintensity or T1 enhancement, and radiographic worsening by increased subcortical T2 hyperintensity, T1 enhancement, or infarcts. Disease recurrence was defined as new-onset clinical symptoms associated with new imaging findings. RESULTSThe 48 individuals in the study included 29 women and had a mean (SD) age of 68.9 (9.9) years. Results of presenting magnetic resonance imaging revealed that 10 of 29 patients with CAA-ri (34%) had T1 contrast enhancement, 30 of 32 (94%) had subcortical T2 hyperintensity (22 of 30 [73%] asymmetric), 7 of 32 (22%) had acute or subacute punctate infarcts, and 27 of 31 (87%) had microbleeds. Immunosuppressive treatments after first episodes included corticosteroids (33 [69%]), cyclophosphamide (6 [13%]), and mycophenolate (2 [4%]); 14 patients (29%) received no treatment. Clinical improvement and radiographic improvement were each more likely in individuals treated with an immunosuppressive agent than with no treatment (clinical improvement: 32 of 34 [94%] vs 7 of 14 [50%]; odds ratio, 16.0; 95% CI, 2.72-94.1; radiographic improvement: 24 of 28 [86%] vs 4 of 14 [29%]; odds ratio, 15.0; 95% CI, 3.12-72.1). Recurrence was less likely if CAA-ri was treated with any immunosuppressant agent than not (9 of 34 [26%] vs 10 of 14 [71%]; hazard ratio, 0.19; 95% CI, 0.07-0.48). When controlling for treatment, no variables were associated with outcomes aside from an association between APOE ε4 and radiographic improvement (odds ratio, 4.49; 95% CI, 1.11-18.2). CONCLUSIONS AND RELEVANCEThese results from a relatively large series of patients with CAA-ri support the effectiveness of immunosuppressive treatment and suggest that early treatment may both improve the initial disease course and reduce the likelihood of recurrence. These results r...

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Section: Discussionmentioning

confidence: 76%