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Metabolomics as a tool to predict the risk of decompensation or liver-related death in patients with compensated cirrhosis

医学 失代偿 内科学 胃肠病学 肝硬化 门脉高压 安慰剂 代谢物 门静脉压 临床终点 比例危险模型 单变量分析 随机对照试验 多元分析 病理 替代医学
作者
Oana Nicoară-Farcău,Juan José Lozano,Cristina Alonso,Julia Sidorova,Càndid Villanueva,Agustı́n Albillos,Joan Genescà,Elba Llop,J Calleja,Carles Aracil,Rafael Bañares,Rosa M. Morillas,María Poca,Beatriz Peñas,Salvador Augustín,Marcel Tanțău,Marcos Thompson,Valeria Pérez‐Campuzano,Anna Baiges,Fanny Turón,Virginia Hernández‐Gea,Juan G. Abraldeṣ,Edilmar A. Tapias,Ferràn Torres,Jaime Bosch,Juan Carlos García–Pagán
出处
期刊:Hepatology [Wiley]
卷期号:77 (6): 2052-2062 被引量:8
标识
DOI:10.1097/hep.0000000000000316
摘要

Background and Aims: Patients with compensated cirrhosis with clinically significant portal hypertension (CSPH: HVPG > 10 mm Hg) have a high risk of decompensation. HVPG is, however, an invasive procedure not available in all centers. The present study aims to assess whether metabolomics can improve the capacity of clinical models in predicting clinical outcomes in these compensated patients. Approach and Results: This is a nested study from the PREDESCI cohort (an RCT of nonselective beta-blockers vs. placebo in 201 patients with compensated cirrhosis and CSPH), including 167 patients for whom a blood sample was collected. A targeted metabolomic serum analysis, using ultra-high-performance liquid chromatography-mass spectrometry, was performed. Metabolites underwent univariate time-to-event cox regression analysis. Top-ranked metabolites were selected using Log-Rank p -value to generate a stepwise cox model. Comparison between models was done using DeLong test. Eighty-two patients with CSPH were randomized to nonselective beta-blockers and 85 to placebo. Thirty-three patients developed the main endpoint (decompensation/liver-related death). The model, including HVPG, Child-Pugh, and treatment received ( HVPG/Clinical model ), had a C-index of 0.748 (CI95% 0.664–0.827). The addition of 2 metabolites, ceramide (d18:1/22:0) and methionine (HVPG/Clinical/Metabolite model), significantly improved the model’s performance [C-index of 0.808 (CI95% 0.735–0.882); p =0.032]. The combination of these 2 metabolites together with Child-Pugh and the type of treatment received (Clinical/Metabolite model) had a C-index of 0.785 (CI95% 0.710–0.860), not significantly different from the HVPG-based models including or not metabolites. Conclusions: In patients with compensated cirrhosis and CSPH, metabolomics improves the capacity of clinical models and achieves similar predictive capacity than models including HVPG.
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