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BACKGROUND AND AIMS: Intestinal inflammation assessed by fecal calprotectin (F-CAL) in advanced chronic liver disease (ACLD) may represent an early sign of intestinal barrier dysfunction. We aimed to explore the usefulness of F-CAL testing in ACLD in the prediction of adverse outcomes (AO, death, or LT) and refinement of prognostic stratification. PATIENTS AND METHODS: We explored the RH7 cirrhosis registry comprising consecutive hospitalized patients and a control group with data on disease phenotype, demographics, anthropometrics, prognostic indices, and medication. The F-CAL was evaluated on admission and reported in multiples of the upper limit of normal or terciles. Predictive power was tested in the Cox model for AO over 180 days. Additional risk refinement by F-CAL was tested for both groups. RESULTS: We enrolled 263 cases in the study group with a median age of 57.2 years, M/F ratio 167/96, with alcohol, metabolic dysfunction-associated steatotic liver disease, MetALD, and viral etiologies in 72.2%, 9.1, 8.0, 3.4%. The median F-CAL was 3.92 × ULN. The control group comprised 108 cases. The adjusted Cox model confirmed F-CAL (hazard ratio [HR] = 1.05, p < 0.001) and F-CAL terciles (HR = 1.413, p = 0.009) as independent predictors of AO. F-CAL terciles had higher predictive accuracy in CLIF-C-AD<50 (HR = 2.49, p = 0.013) and Child stages A and B (HR = 1.706, p = 0.025), in whom high F-CAL (cut-off >11 × ULN) could identify patients having 2-3 times higher risk of AO. This approach has been validated in the control group. CONCLUSION: Among hospitalized patients with ACLD, F-CAL values were independently proportional to the risk of AO, particularly in early disease stages when high F-CAL values could refine prognostic stratification.
RESUMEN
AIM OF THE STUDY: We set out to determine the applicability of acute-on-chronic liver failure (ACLF) diagnostic criteria and characteristics of thus defined ACLF sub-cohorts in a real-life clinical context. MATERIAL AND METHODS: Retrospective charts' analysis of consecutive patients hospitalized with decompensated liver disease. Inclusion criteria: acute decompensation, informed consent. Exclusion criteria: malignancy. Diagnostic tools: 1st phase - CLIF-SOFA score calculated manually; 2nd phase - CLIF-C ACLF score calculated at www.efclif.com. RESULTS: Of 432 hospitalized patients aged 52 years, 41% were female, with MELD 20, 32% patients had acute decompensation (AD); main triggers were alcoholic hepatitis (38%), infections (26%), and variceal bleeding (23%). Of patients with AD, ACLF grades 0-3 was present in 64%, 19%, 13%, and 4%, respectively. In hospital mortality according to final AD/ACLF grade in ACLF 0-3 was 7.5%, 42%, 47%, and 80%, respectively (p < 0.0001). CONCLUSIONS: Diagnosing ACLF is nowadays easy; it helps to stratify patients at admission, and refine risk stratification at day 7. The main trigger of AD/ACLF in this region is alcohol. Currently, there are no ACLF-specific treatments; however, timely intensive supportive care can influence the prognosis. Even though still elusive and controversial, the ACLF concept can help systematize management of patients admitted with acute decompensation of advanced chronic liver disease.