中文｜English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 42 Issue 7
Jul.  2026
Turn off MathJax
Article Contents
Article Navigation >  Journal of Clinical Hepatology  > 2026  >  42(7): 1623-1631

Value of C-reactive protein in predicting the progression of acute decompensation of cirrhosis to acute-on-chronic liver failure

DOI: 10.12449/JCH260719
  • 1.

    School of Public Health，Nanjing Medical University，Nanjing 211166，China

  • 2.

    Department of Hepatology，Nanjing Hospital Affiliated to Nanjing University of Chinese Medicine （Nanjing Second Hospital），Nanjing 210000，China

  • 3.

    School of Medicine，Southeast University，Nanjing 210000，China

  • 4.

    Department of Hepatology，Teaching Hospital of Nanjing Medical University School of Public Health （Nanjing Second Hospital），Nanjing 210003，China

Research funding:

Jiangsu Provincial Natural Science Foundation (BK20251727)

More Information
  • Corresponding author: Yang Yongfeng， yyf1997@163.com （ORCID： 0000-0002-3214-0038）
  • Received Date: 2025-12-29
  • Accepted Date: 2026-03-19
  • Published Date: 2026-07-25
    Abstract
  •   Objective  To investigate the efficacy of C-reactive protein （CRP） in predicting the progression to acute-on-chronic liver failure （ACLF） within 90 days after disease onset in patients with acute decompensation （AD） of cirrhosis， and to provide a reference for the early identification of high-risk populations in clinical practice.  Methods  A retrospective study was conducted among 906 patients with liver cirrhosis who were hospitalized due to AD in Nanjing Second Hospital from January 1， 2015 to October 31， 2024， and demographic features， AD type， and laboratory markers were collected on admission. The primary endpoint was progression to ACLF within 90 days after admission， and according to the presence or absence of ACLF， the patients were divided into non-ACLF group with 676 patients and ACLF group with 230 patients. The independent-samples t test was used for comparison of normally distributed continuous data between groups， and the Wilcoxon rank-sum test was used for comparison of non-normally distributed continuous data between groups； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. The univariate and multivariate Cox proportional-hazards regression models were used to identify independent predictive factors for ACLF. The receiver operating characteristic （ROC） curve was used to assess the predictive performance of CRP and existing scoring systems （Model for End-Stage Liver Disease ［MELD］， Child-Turcotte-Pugh ［CTP］ score， and Chronic Liver Failure Consortium Acute Decompensation ［CLIF-C AD］ score）， and the restricted cubic spline analysis was used to investigate the nonlinear relationship between CRP and the risk of ACLF. Youden index was used to determine the optimal predictive cut-off value for CRP， and the Kaplan-Meier survival curve was plotted for risk stratification， while the log-rank test was used for survival analysis.  Results  Among the 906 AD patients， the incidence rate of ACLF was 25.39% within 90 days. The incidence rate of ACLF within 90 days was 45.1% in the 264 patients with bacterial infection and 17.3% in the 642 patients without bacterial infection （χ²=74.791， P<0.001）. Among the 906 patients， 312 patients （34.44%） had acute-on-chronic pre-liver failure （pre-ACLF）， with a significantly higher proportion of patients who progressed to ACLF than those in the non-pre-ACLF group ［60.58% （189/312） vs 6.90% （41/594）， χ²=310.234， P<0.001］. Among the 230 patients with ACLF， there were 102 patients with stable ACLF （44.35%） and 128 patients with unstable ACLF （55.65%）， with a significant difference in CRP between the two groups of patients （U=5 234.500， P<0.001）. The restricted cubic spline analysis showed a significant nonlinear relationship between CRP and the risk of ACLF （P<0.001）. The optimal cut-off value of CRP was determined as 10.16 mg/L based on the Youden index， with a sensitivity of 70.4% and a specificity of 64.5%. The Kaplan-Meier curve analysis showed that the high-risk group with CRP≥10.16 mg/L had a significantly higher event-free survival rate of ACLF within 90 days compared with the low-risk group （P<0.001）. The multivariate Cox regression analysis showed that AD type-hepatic encephalopathy （hazard ratio ［HR］=4.199， 95% confidence interval ［CI］： 3.056 — 5.770， P<0.001）， AD type-bacterial infection （HR=1.826， 95%CI： 1.356 — 2.459， P<0.001）， CRP （≥10.16 mg/L） （HR=2.356， 95%CI： 1.825 — 3.047， P<0.001）， white blood cell count （HR=1.021， 95%CI： 1.002 — 1.041， P=0.035）， hemoglobin （HR=0.994， 95%CI： 0.989 — 0.999， P=0.025）， international normalized ratio （HR=1.657， 95%CI： 1.372 — 2.001， P<0.001）， total bilirubin （HR=1.003， 95%CI： 1.002 — 1.004， P<0.001）， albumin （HR=0.956， 95%CI： 0.926 — 0.986， P=0.004）， creatinine （HR=1.005， 95%CI： 1.004 — 1.006， P<0.001）， serum sodium （HR=0.976， 95%CI： 0.956 — 0.997， P=0.025）， and lactate dehydrogenase （HR=1.001， 95%CI： 1.001 — 1.002， P<0.001） were all independent predictive factors for progression to ACLF within 90 days. The ROC curve analysis showed that CRP alone had an area under the ROC curve （AUC） of 0.724 （95%CI： 0.685 — 0.763） in predicting ACLF， and CRP+MELD score had the best predictive performance （AUC=0.870， 95%CI： 0.843 — 0.898）， while CRP+CTP score and CRP+CLIF-C AD score had an AUC of 0.852 （95%CI： 0.823 — 0.881） and 0.845 （95%CI： 0.812 — 0.877）， respectively. There was a significant increase in model performance after integration （P<0.05）.  Conclusion  Serum CRP level on admission is an independent predictive factor for progression to ACLF within 90 days in patients with AD of cirrhosis， and a CRP level of ≥10.16 mg/L can be used as a simple threshold for identifying high-risk patients. Incorporating CRP into existing assessment systems may enhance the early identification of patients at a high risk for ACLF， which provides a reference for clinical intervention.

     

    • FullText(HTML)
  • loading
    • References(29)
  • [1]
    Tsochatzis E A, Bosch J, Burroughs A K. Liver cirrhosis[J]. Lancet, 2014, 383( 9930): 1749- 1761. DOI: 10.1016/S0140-6736(14)60121-5.
    [2]
    Goh X E, Goh M X, Chen V L, et al. Prevalence and clinical outcomes of recompensation in decompensated cirrhosis: A systematic review and meta-analysis[J]. Clin Gastroenterol Hepatol, 2026, 24( 4): 911- 922. DOI: 10.1016/j.cgh.2025.08.010.
    [3]
    Wang S P, Guo G Y, Wang H, et al. Improved discrimination and predictive ability of novel prognostic scores for long-term mortality in hospitalized patients with cirrhosis[J]. J Clin Transl Hepatol, 2025, 13( 6): 484- 492. DOI: 10.14218/JCTH.2025.00004.
    [4]
    Moreau R, Tonon M, Krag A, et al. EASL clinical practice guidelines on acute-on-chronic liver failure[J]. J Hepatol, 2023, 79( 2): 461- 491. DOI: 10.1016/j.jhep.2023.04.021.
    [5]
    D’Amico G, Bernardi M, Angeli P. Towards a new definition of decompensated cirrhosis[J]. J Hepatol, 2022, 76( 1): 202- 207. DOI: 10.1016/j.jhep.2021.06.018.
    [6]
    Zanetto A, Pelizzaro F, Campello E, et al. Severity of systemic inflammation is the main predictor of ACLF and bleeding in individuals with acutely decompensated cirrhosis[J]. J Hepatol, 2023, 78( 2): 301- 311. DOI: 10.1016/j.jhep.2022.09.005.
    [7]
    Wong F, Reddy K R, Tandon P, et al. The prediction of in-hospital mortality in decompensated cirrhosis with acute-on-chronic liver failure[J]. Liver Transpl, 2022, 28( 4): 560- 570. DOI: 10.1002/lt.26311.
    [8]
    Trebicka J, Fernandez J, Papp M, et al. The PREDICT study uncovers three clinical courses of acutely decompensated cirrhosis that have distinct pathophysiology[J]. J Hepatol, 2020, 73( 4): 842- 854. DOI: 10.1016/j.jhep.2020.06.013.
    [9]
    Valainathan S R, Xie Q, Arroyo V, et al. Prognosis algorithms for acute decompensation of cirrhosis and ACLF[J]. Liver Int, 2025, 45( 3): e15927. DOI: 10.1111/liv.15927.
    [10]
    Kim J W, Kim J H, Choe W H, et al. MELD-GRAIL-Na is a better predictor of mortality than MELD in Korean patients with cirrhosis[J]. Medicina(Kaunas), 2023, 59( 3): 592. DOI: 10.3390/medicina59030592.
    [11]
    Piano S, Mahmud N, Caraceni P, et al. Mechanisms and treatment approaches for ACLF[J]. Liver Int, 2025, 45( 3): e15733. DOI: 10.1111/liv.15733.
    [12]
    Li J, Liang X, Jiang J, et al. PBMC transcriptomics identifies immune-metabolism disorder during the development of HBV-ACLF[J]. Gut, 2022, 71( 1): 163- 175. DOI: 10.1136/gutjnl-2020-323395.
    [13]
    Arroyo V, Angeli P, Moreau R, et al. The systemic inflammation hypothesis: Towards a new paradigm of acute decompensation and multiorgan failure in cirrhosis[J]. J Hepatol, 2021, 74( 3): 670- 685. DOI: 10.1016/j.jhep.2020.11.048.
    [14]
    Costa D, Simbrunner B, Jachs M, et al. Systemic inflammation increases across distinct stages of advanced chronic liver disease and correlates with decompensation and mortality[J]. J Hepatol, 2021, 74( 4): 819- 828. DOI: 10.1016/j.jhep.2020.10.004.
    [15]
    Jachs M, Hartl L, Schaufler D, et al. Amelioration of systemic inflammation in advanced chronic liver disease upon beta-blocker therapy translates into improved clinical outcomes[J]. Gut, 2021, 70( 9): 1758- 1767. DOI: 10.1136/gutjnl-2020-322712.
    [16]
    Solé C, Solà E, Morales-Ruiz M, et al. Characterization of inflammatory response in acute-on-chronic liver failure and relationship with prognosis[J]. Sci Rep, 2016, 6: 32341. DOI: 10.1038/srep32341.
    [17]
    Pompili E, Baldassarre M, Bedogni G, et al. Predictors of clinical trajectories of patients with acutely decompensated cirrhosis. An external validation of the PREDICT study[J]. Liver Int, 2024, 44( 1): 72- 82. DOI: 10.1111/liv.15734.
    [18]
    Rizo-Téllez S A, Sekheri M, Filep J G. C-reactive protein: A target for therapy to reduce inflammation[J]. Front Immunol, 2023, 14: 1237729. DOI: 10.3389/fimmu.2023.1237729.
    [19]
    Zhou H H, Tang Y L, Xu T H, et al. C-reactive protein: Structure, function, regulation, and role in clinical diseases[J]. Front Immunol, 2024, 15: 1425168. DOI: 10.3389/fimmu.2024.1425168.
    [20]
    Balcar L, Semmler G, Pomej K, et al. Patterns of acute decompensation in hospitalized patients with cirrhosis and course of acute-on-chronic liver failure[J]. United European Gastroenterol J, 2021, 9( 4): 427- 437. DOI: 10.1002/ueg2.12089.
    [21]
    Engelmann C, Clària J, Szabo G, et al. Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction[J]. J Hepatol, 2021, 75( Suppl 1): S49- S66. DOI: 10.1016/j.jhep.2021.01.002.
    [22]
    Taru V, Szabo G, Mehal W, et al. Inflammasomes in chronic liver disease: Hepatic injury, fibrosis progression and systemic inflammation[J]. J Hepatol, 2024, 81( 5): 895- 910. DOI: 10.1016/j.jhep.2024.06.016.
    [23]
    Albillos A, Martin-Mateos R, Van der Merwe S, et al. Cirrhosis-associated immune dysfunction[J]. Nat Rev Gastroenterol Hepatol, 2022, 19( 2): 112- 134. DOI: 10.1038/s41575-021-00520-7.
    [24]
    Moreau R, Jalan R, Gines P, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis[J]. Gastroenterology, 2013, 144( 7): 1426- 1437.e9. DOI: 10.1053/j.gastro.2013.02.042.
    [25]
    Barosa R, Roque Ramos L, Patita M, et al. CLIF-C ACLF score is a better mortality predictor than MELD, MELD-Na and CTP in patients with Acute on Chronic Liver Failure admitted to the ward[J]. Rev Esp Enferm Dig, 2017, 109: 399- 405. DOI: 10.17235/reed.2017.4701/2016.
    [26]
    Hernaez R, Liu Y, Kramer J R, et al. Model for end-stage liver disease-sodium underestimates 90-day mortality risk in patients with acute-on-chronic liver failure[J]. J Hepatol, 2020, 73( 6): 1425- 1433. DOI: 10.1016/j.jhep.2020.06.005.
    [27]
    Viveiros A, Finkenstedt A, Schaefer B, et al. Transferrin as a predictor of survival in cirrhosis[J]. Liver Transplant, 2018, 24( 3): 343- 351. DOI: 10.1002/lt.24981.
    [28]
    Turco L, Garcia-Tsao G, Magnani I, et al. Cardiopulmonary hemodynamics and C-reactive protein as prognostic indicators in compensated and decompensated cirrhosis[J]. J Hepatol, 2018, 68( 5): 949- 958. DOI: 10.1016/j.jhep.2017.12.027.
    [29]
    di Martino V, Coutris C, Cervoni J P, et al. Prognostic value of C-reactive protein levels in patients with cirrhosis[J]. Liver Transpl, 2015, 21( 6): 753- 760. DOI: 10.1002/lt.24088.
    • Relative Articles
    • Supplements(0)
    • Cited By
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(4)  / Tables(2)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (64) PDF downloads(15) Cited by()
    Proportional views
    Related
        

    The first journal specializing in hepatobiliary and pancreatic diseases in China

    Supervisor：Ministry of Education of the People's Republic of China

    Sponsor：Jilin University

    Academic Support: Chinese Society of Hepatology，Chinese Medical Association

    Address: 461 Xinjiang Road, Changchun

    Submit：0431-88782044

    Peer review：0431-88783542

    Email：lcgdb@vip.163.com

    About Journal

    Submission Guideline

    Journal Online

    Hepatobiliary College

    Guidelines

    YesterdayIP[]YesterdayPV[]TodayIP[]TodayPV[]Online[]

    Website Design © 2020 Editorial Board of Journal of Clinical Hepatology 吉ICP备10000617号-1 Supported by: Beijing Renhe Information Technology Co. Ltd  

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return