关键词: ACLF, acute-on-chronic liver failure AIH, autoimmune hepatitis ALIC, anterior limb of internal capsule APASL, Asian pacific association for study of liver diseases AUROC, area under receiver operating characteristic BBB, blood–brain barrier BG, basal ganglia CANONIC, chronic liver failure (CLIF) acute-on-chronic liver failure in cirrhosis CI, confidence interval CLIF-SOFA, chronic liver failure-sequential organ failure assessment CTP, Child–Turcott–Pugh DTI, diffusion tensor imaging FA, fractional anisotropy FLAIR, fluid attenuation inversion recovery FWM, frontal white matter HBV, hepatitis B virus HE, hepatic encephalopathy IC, internal capsule IL-1 beta, interleukin 1 beta IL-6, interleukin 6 MD, mean diffusivity MELD, model for end-stage liver disease MRI, magnetic resonance imaging MTR, magnetization transfer ratio PLIC, posterior limb of internal capsule PWM, parietal white matter ROI, regions of interest SIRS, systemic inflammatory response syndrome T1W, T1 weighted T2W, T2 weighted TE, echo-time TNF-alpha, tumor necrosis factor-alpha TR, repetition time acute-on-chronic liver failure cerebral edema diffusion tensor imaging magnetic resonance imaging

来  源:   DOI:10.1016/j.jceh.2017.04.001   PDF(Sci-hub)

Abstract:
OBJECTIVE: The nature of cerebral edema in acute-on-chronic liver failure (ACLF) is not well studied. We aimed to characterize cerebral edema in ACLF using magnetization transfer ratio (MTR) and diffusion tensor imaging (DTI).
METHODS: Forty-six patients with cirrhosis and acute decompensation were included. Patients were divided into groups A (no cerebral failure, n = 39) and B (cerebral failure, n = 7). Group A was subdivided into no-ACLF (n = 11), grade 1 (n = 10), grade 2 (n = 9) and grade 3 (n = 9) ACLF as per CANONIC study. MRI brain and plasma TNF-alpha, IL-1beta and IL-6 were measured at baseline and 7-10 days after admission. Ten age- and sex-matched healthy controls were also included.
RESULTS: Mean diffusivity (MD) values, an MRI marker of water content, progressively increased from controls to no-ACLF to ACLF grade 1, 2 and 3 in group A in frontal white matter (FWM) and basal ganglia (P < 0.0001). MD values improved only in survivors on follow-up. MD values correlated with IL-6 levels at baseline. On multivariate analysis MELD score ≥28 and MD values (>8 × 10-9 M2/s) in FWM were independent predictors of 90-day mortality. There was no significant difference in clinical and MRI parameters between group A and B.
CONCLUSIONS: Cerebral edema increases with severity of ACLF. Correlation between MD values and IL-6 levels suggests pathogenic role of inflammation in cerebral edema. Patients with grade 3 ACLF have cerebral edema irrespective of presence of clinically evident cerebral failure. MELD score and cerebral edema have prognostic significance in ACLF.
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