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Verfasst von:Manzhalii, Elina [VerfasserIn]   i
 Stremmel, Wolfgang [VerfasserIn]   i
Titel:Hepatic encephalopathy aggravated by systemic inflammation
Verf.angabe:Elina Manzhalii, Oleksandr Virchenko, Tetyana Falalyeyeva, Valentyna Moiseienko, Taras Nykula, Vitaliy Kondratiuk, Olexiy Savchuk, Tetyana Beregova, Wolfgang Stremmel
E-Jahr:2019
Jahr:June 06, 2019
Umfang:9 S.
Teil:volume:37
 year:2019
 number:6
 pages:509-517
 extent:9
Fussnoten:Gesehen am 14.11.2019
Titel Quelle:Enthalten in: Digestive diseases
Ort Quelle:Basel : Karger, 1983
Jahr Quelle:2019
Band/Heft Quelle:37(2019), 6, Seite 509-517
ISSN Quelle:1421-9875
Abstract:Background: The pathogenesis of hepatic encephalopathy (HE) is only partially understood. Beside ammonia accumulation in brain, a proinflammatory component has been suggested as precipitating event. Objectives: To evaluate the role of cytokines in cirrhosis for development of HE. Methods: Pro- and anti-inflammatory cytokine profiles were determined in rats with CCL4-induced cirrhosis and HE as well as in patients with cirrhosis either due to metabolic disorders or chronic hepatitis C virus (HCV) with various grades of concomitant HE and depression. Results: In the rat model and human cirrhosis a proinflammatory cytokine pattern (elevation of interferon gamma, interleukin [IL]-1β, IL-6) was registered which in humans correlated to the degree of HE and depression. The most prominent elevation of proinflammatory cytokines was observed in chronic HCV as an additional inflammatory stimulus. In all cases of cirrhosis a comparable background activation of anti-inflammatory cytokines (e.g., IL-4) was detected which was interpreted as a physiologic counterbalance mechanism. Conclusions: The degree of HE and depression correlated with a proinflammatory cytokine pattern. It suggests that beside ammonia elevation, inflammatory cytokines determine occurrence and severity of hepatic encephalopathies. Thus, it can be defined a preferential therapeutic target.
DOI:doi:10.1159/000500717
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1159/000500717
 Verlag: https://www.karger.com/Article/FullText/500717
 DOI: https://doi.org/10.1159/000500717
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1681878046
Verknüpfungen:→ Zeitschrift

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