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ADMA Levels and Arginine/ADMA Ratios Reflect Severity of Disease and Extent of Inflammation After Subarachnoid Hemorrhage
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2014 (Engelska)Ingår i: Neurocritical Care, ISSN 1541-6933, E-ISSN 1556-0961, Vol. 21, nr 1, s. 91-101Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Subarachnoid hemorrhage (SAH) is characterized by an inflammatory response that might induce endothelial dysfunction. The aim of this study was to evaluate if ADMA and arginine/ADMA ratios after SAH (indicators of endothelial dysfunction) are related to clinical parameters, inflammatory response, and outcome. Prospective observational study. ADMA, arginine, C-reactive protein (CRP), and cytokines were obtained 0-240 h (h) after SAH. Definition of severe clinical condition was Hunt&Hess (H&H) 3-5 and less severe clinical condition H&H 1-2. Impaired cerebral circulation was assessed by clinical examination, transcranial doppler, CT-scan, and angiography. Glasgow outcome scale (GOS) evaluated the outcome. Compared to admission, 0-48 h after SAH, the following was observed 49-240 h after SAH; (a) ADMA was significantly increased at 97-240 h (highest 217-240 h), (b) CRP was significantly increased at 49-240 h (highest 73-96 h), (c) interleukin-6 (IL-6) was significantly lower at 97-240 h (highest 49-96 h), p < 0.05. ADMA, CRP, and IL-6 were significantly lower and peak arginine/ADMA ratio was significantly higher in patients with H&H 1-2 compared to patients with H&H 3-5, p < 0.05. The peak ADMA or the nadir arginine/ADMA ratio did not differ significantly between patients with (55 %) or without (45 %) signs of impaired cerebral circulation. The peak ADMA or the nadir arginine/ADMA ratio did not differ significantly between patients with GOS 1-3 and patients with GOS 4-5. ADMA increased significantly after SAH, and the increase in ADMA started after the pro-inflammatory markers (CRP and IL-6) had peaked. This might indicate that endothelial dysfunction, with ADMA as a marker, is induced by a systemic inflammation.

Ort, förlag, år, upplaga, sidor
2014. Vol. 21, nr 1, s. 91-101
Nyckelord [en]
Subarachnoid hemorrhage, ADMA, Arginine, Inflammation, Interleukin-1beta, Interleukin-6, Interleukin-8, Interleukin-10, Tumor necrosis factor-alpha
Nationell ämneskategori
Klinisk medicin Medicinska och farmaceutiska grundvetenskaper
Identifikatorer
URN: urn:nbn:se:uu:diva-230076DOI: 10.1007/s12028-013-9945-8ISI: 000339350500014PubMedID: 24408146OAI: oai:DiVA.org:uu-230076DiVA, id: diva2:743214
Tillgänglig från: 2014-09-03 Skapad: 2014-08-19 Senast uppdaterad: 2018-01-11Bibliografiskt granskad

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