Erschienen in:
29.07.2019 | Original Communication
Antibodies against neural antigens in patients with acute stroke: joint results of three independent cohort studies
verfasst von:
Georg Royl, Tsafack Judicael Fokou, Rittika Chunder, Rakad Isa, Thomas F. Münte, Klaus-Peter Wandinger, Markus Schwaninger, Oliver Herrmann, José Manuel Valdueza, Jan Brocke, Martin Willkomm, Dietrich Willemsen, Gerd U. Auffarth, Swantje Mindorf, Britta Brix, Angel Chamorro, Anna Planas, Xabier Urra
Erschienen in:
Journal of Neurology
|
Ausgabe 11/2019
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Abstract
Background and purpose
Ischemic stroke (IS) and hemorrhagic stroke (HemS) typically lead to a breakdown of the blood–brain barrier with neural antigen presentation. This presentation could potentially generate destructive auto-immune responses. Pre-existing antineuronal and antiglial antibodies (AA), predominantly NMDA receptor antibodies, have been reported in patients with stroke. This article summarizes three independent prospective studies, the Lübeck cohort (LC), Barcelona cohort (BC), and Heidelberg cohort (HC), exploring the frequency and clinical relevance of AA in patients with acute stroke (AS).
Methods
In all cohorts together, 344 consecutive patients admitted with AS (322 × IS, 22 × HemS) were screened for AA in serum at admission. Clinical outcome parameters as well as a second AA screening were available at 30 days in the LC or at 90 days in the BC. A control group was included in the BC (20 subjects free from neurological disease) and the HC (78 neurological and ophthalmological patients without evidence for stroke).
Results
The rate of positivity for AA was similar in control subjects and AS patients (13%, 95% CI [7%, 22%] vs. 13%, 95% CI [10%, 17%]; p = 0.46) with no significant difference between cohorts (LC 25/171, BC 12/75, HC 9/98). No patient had developed new AA after 30 days, whereas 2 out of 60 patients had developed new AA after 90 days. AA positive patients did not exhibit significant differences to AA negative patients in stroke subtype (LC, BC), initial stroke severity (BC, LC, HC), infarct volume (BC), and functional status at admission (BC, LC, HC) and follow-up (BC, LC).
Conclusions
AS does not induce AA to a relevant degree. Pre-existing AA can be found in the serum of stroke patients, but they do not have a significant association with clinical features and outcomes.