BACKGROUND AND PURPOSE: immunodepression after stroke is associated with complications like high infection rate, but its role in aneurysmal subarachnoid hemorrhage (aSAH) is unclear. This pilot study aimed to assess the presence of immunodepression and its association with infections after aSAH. METHODS: sixteen aSAH patients were enrolled in a prospective study on immune function in a single institution. Detailed immune monitoring (peripheral blood leukocyte subsets, monocyte human leukocyte antigen-DR expression, ex vivo lipopolysaccharide-induced monocytic, Concanavalin A-induced lymphocytic cytokine secretion) was performed until day 10 after aSAH. Occurrence of infection was assessed within 14 days after aSAH. RESULTS: sixteen consecutive aSAH patients (53.1 ± 10.2 years; mean ± SD) met the inclusion criteria, classified as asymptomatic (World Federation of Neurological Surgeons; median, 1; quartile, 1-1; n=7) and symptomatic (median, 4; quartile, 3-5; n=9), all presenting with acute neurological deficits, and 5 of these had additional delayed cerebral ischemia. T-lymphopenia, impaired ex vivo lymphocytic/monocytic cytokine secretion, and decreased monocyte human leukocyte antigen-DR expression occurred over all World Federation of Neurological Surgeons grades but persisted beyond day 3 only in symptomatic patients. Pneumonia (67%; P=0.011) was more frequent in symptomatic patients. Already at day 1, patients with pneumonia showed significantly lower T-cell counts and mitogen-induced interferon-γ production compared to patients without infections. CONCLUSIONS: a pronounced SAH-induced immunodepression was observed early after aSAH but persisted only in symptomatic patients. Immunodepression was associated with a high incidence of pneumonia. Early diagnosis of immunodepression might allow targeted treatment to prevent infectious complications after aSAH.
BACKGROUND AND PURPOSE: immunodepression after stroke is associated with complications like high infection rate, but its role in aneurysmal subarachnoid hemorrhage (aSAH) is unclear. This pilot study aimed to assess the presence of immunodepression and its association with infections after aSAH. METHODS: sixteen aSAH patients were enrolled in a prospective study on immune function in a single institution. Detailed immune monitoring (peripheral blood leukocyte subsets, monocyte human leukocyte antigen-DR expression, ex vivo lipopolysaccharide-induced monocytic, Concanavalin A-induced lymphocytic cytokine secretion) was performed until day 10 after aSAH. Occurrence of infection was assessed within 14 days after aSAH. RESULTS: sixteen consecutive aSAH patients (53.1 ± 10.2 years; mean ± SD) met the inclusion criteria, classified as asymptomatic (World Federation of Neurological Surgeons; median, 1; quartile, 1-1; n=7) and symptomatic (median, 4; quartile, 3-5; n=9), all presenting with acute neurological deficits, and 5 of these had additional delayed cerebral ischemia. T-lymphopenia, impaired ex vivo lymphocytic/monocytic cytokine secretion, and decreased monocyte human leukocyte antigen-DR expression occurred over all World Federation of Neurological Surgeons grades but persisted beyond day 3 only in symptomatic patients. Pneumonia (67%; P=0.011) was more frequent in symptomatic patients. Already at day 1, patients with pneumonia showed significantly lower T-cell counts and mitogen-induced interferon-γ production compared to patients without infections. CONCLUSIONS: a pronounced SAH-induced immunodepression was observed early after aSAH but persisted only in symptomatic patients. Immunodepression was associated with a high incidence of pneumonia. Early diagnosis of immunodepression might allow targeted treatment to prevent infectious complications after aSAH.
Authors: Heinrich P Mattle; Michael Brainin; Angel Chamorro; Hans Christoph Diener; Werner Hacke; Didier Leys; Bo Norrving; Nick Ward Journal: Stroke Date: 2012-07-26 Impact factor: 7.914
Authors: Joanna Pera; Michal Korostynski; Slawomir Golda; Marcin Piechota; Jaroslaw Dzbek; Tadeusz Krzyszkowski; Tomasz Dziedzic; Marek Moskala; Ryszard Przewlocki; Andrzej Szczudlik; Agnieszka Slowik Journal: J Cereb Blood Flow Metab Date: 2013-03-20 Impact factor: 6.200
Authors: Jens P Dreier; Martin Fabricius; Cenk Ayata; Oliver W Sakowitz; C William Shuttleworth; Christian Dohmen; Rudolf Graf; Peter Vajkoczy; Raimund Helbok; Michiyasu Suzuki; Alois J Schiefecker; Sebastian Major; Maren Kl Winkler; Eun-Jeung Kang; Denny Milakara; Ana I Oliveira-Ferreira; Clemens Reiffurth; Gajanan S Revankar; Kazutaka Sugimoto; Nora F Dengler; Nils Hecht; Brandon Foreman; Bart Feyen; Daniel Kondziella; Christian K Friberg; Henning Piilgaard; Eric S Rosenthal; M Brandon Westover; Anna Maslarova; Edgar Santos; Daniel Hertle; Renán Sánchez-Porras; Sharon L Jewell; Baptiste Balança; Johannes Platz; Jason M Hinzman; Janos Lückl; Karl Schoknecht; Michael Schöll; Christoph Drenckhahn; Delphine Feuerstein; Nina Eriksen; Viktor Horst; Julia S Bretz; Paul Jahnke; Michael Scheel; Georg Bohner; Egill Rostrup; Bente Pakkenberg; Uwe Heinemann; Jan Claassen; Andrew P Carlson; Christina M Kowoll; Svetlana Lublinsky; Yoash Chassidim; Ilan Shelef; Alon Friedman; Gerrit Brinker; Michael Reiner; Sergei A Kirov; R David Andrew; Eszter Farkas; Erdem Güresir; Hartmut Vatter; Lee S Chung; K C Brennan; Thomas Lieutaud; Stephane Marinesco; Andrew Ir Maas; Juan Sahuquillo; Markus A Dahlem; Frank Richter; Oscar Herreras; Martyn G Boutelle; David O Okonkwo; M Ross Bullock; Otto W Witte; Peter Martus; Arn Mjm van den Maagdenberg; Michel D Ferrari; Rick M Dijkhuizen; Lori A Shutter; Norberto Andaluz; André P Schulte; Brian MacVicar; Tomas Watanabe; Johannes Woitzik; Martin Lauritzen; Anthony J Strong; Jed A Hartings Journal: J Cereb Blood Flow Metab Date: 2016-01-01 Impact factor: 6.200