Incidence, predictors and outcomes of acute-on-chronic liver failure in outpatients with cirrhosis

Piano, Salvatore; Tonon, Marta; Vettore, Elia; Stanco, M.; Pilutti, Chiara; Romano, A.; Mareso, Sara; Gambino, Carmine; Brocca, Alessandra; Sticca, A.; Fasolato, S.; Angeli, Paolo

doi:10.1016/j.jhep.2017.07.008

Cited by 109 publications

(77 citation statements)

References 18 publications

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“…26,27 More pertinent to the findings of the present study is the recent report that a median level of 10.8 g/dl of blood hemoglobin concentration was among the independent predictors of ACLF development in stable outpatients with cirrhosis. 4 Our results showed that this is also the case in the setting of nACLF, with a cut-off value of 9.8 g/dl. There are a number of factors contributing to anemia in patients with cirrhosis, including chronic occult blood loss leading to iron depletion, malnutrition, reduced hepatic synthesis of tetrahydrofolate, hypersplenism and hemolysis.…”

Section: Discussionsupporting

confidence: 63%

“…Interestingly, the leukocyte count was not among the independent predictors of ACLF at 1-year in outpatients with stable cirrhosis. 4 The reasons for this discrepancy are not immediately identifiable. However, it sounds reasonable to consider the leukocyte count as a predictor of ACLF in the short term in a context like AD, where a burst of inflammation has already been primed, while other factors, pre-eminently related to the severity of the underlying cirrhosis, prevail in the long-term prediction in patients with a stable disease.…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, this matter is still ill-defined in patients who develop ACLF. Independent predictors for the development of this syndrome have recently been identified in outpatients with cirrhosis, 4 but scanty information is available in those admitted to hospital because of AD who subsequently develop ACLF 3 .…”

Section: Lay Summarymentioning

confidence: 99%

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Prediction of nosocomial acute-on-chronic liver failure in patients with cirrhosis admitted to hospital with acute decompensation

et al. 2019

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

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Prediction of nosocomial acute-on-chronic liver failure in patients with cirrhosis admitted to hospital with acute decompensation

et al. 2019

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“…Recent data suggest that the ACLF prevalence among outpatients is high. 10 Additionally, almost half of the CANONIC cohort developed ACLF without a precipitating event, 1 highlighting that either triggers are not completely known or in some cases SI can be so high that ACLF can develop without external triggers. Compensated and recompensated (ie, with a history of decompensation) outpatients present in similar clinical conditions in real-life clinical practice.…”

Section: Hepatologymentioning

confidence: 99%

“…However, differences in risk of ACLF development between compensated and recompensated patients have not been studied yet. 10 Although it seems consensual that SI is a hallmark of ACLF, the dynamics of SI after successfully treated AD (recompensation) has not been described and its role in ACLF development remains unclear.…”

Section: Hepatologymentioning

confidence: 99%

Differential inflammasome activation predisposes to acute-on-chronic liver failure in human and experimental cirrhosis with and without previous decompensation

Monteiro¹,

Grandt

Uschner

et al. 2020

Gut

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ObjectiveSystemic inflammation predisposes acutely decompensated (AD) cirrhosis to the development of acute-on-chronic liver failure (ACLF). Supportive treatment can improve AD patients, becoming recompensated. Little is known about the outcome of patients recompensated after AD. We hypothesise that different inflammasome activation is involved in ACLF development in compensated and recompensated patients.Design249 patients with cirrhosis, divided into compensated and recompensated (previous AD), were followed prospectively for fatal ACLF development. Two external cohorts (n=327) (recompensation, AD and ACLF) were included. Inflammasome-driving interleukins (ILs), IL-1α (caspase-4/11-dependent) and IL-1β (caspase-1-dependent), were measured. In rats, bile duct ligation-induced cirrhosis and lipopolysaccharide exposition were used to induce AD and subsequent recompensation. IL-1α and IL-1β levels and upstream/downstream gene expression were measured.ResultsPatients developing ACLF showed higher baseline levels of ILs. Recompensated patients and patients with detectable ILs had higher rates of ACLF development than compensated patients. Baseline CLIF-C (European Foundation for the study of chronic liver failure consortium) AD, albumin and IL-1α were independent predictors of ACLF development in compensated and CLIF-C AD and IL-1β in recompensated patients. Compensated rats showed higher IL-1α gene expression and recompensated rats higher IL-1β levels with higher hepatic gene expression. Higher IL-1β detection rates in recompensated patients developing ACLF and higher IL-1α and IL-1β detection rates in patients with ACLF were confirmed in the two external cohorts.ConclusionPrevious AD is an important risk factor for fatal ACLF development and possibly linked with inflammasome activation. Animal models confirmed the results showing a link between ACLF development and IL-1α in compensated cirrhosis and IL-1β in recompensated cirrhosis.

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Incidence and Mortality of Acute‐on‐Chronic Liver Failure Using Two Definitions in Patients with Compensated Cirrhosis

et al. 2019

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The term acute-on-chronic liver failure (ACLF) is intended to identify patients with chronic liver disease who develop rapid deterioration of liver function and high short-term mortality after an acute insult. The two prominent definitions (European Association for the Study of the Liver [EASL] and Asian Pacific Association for the Study of the Liver [APASL]) differ, and existing literature applies to narrow patient groups. We sought to compare ACLF incidence and mortality among a diverse cohort of patients with compensated cirrhosis, using both definitions. This was a retrospective cohort study of patients with incident compensated cirrhosis in the Veterans Health Administration from 2008 to 2016. First ACLF events were identified for each definition. Incidence rates were computed as events per 1,000 person-years, and mortality was calculated at 28 and 90 days. Among 80,383 patients with cirrhosis with 3.35 years median follow-up, 783 developed EASL and APASL ACLF, 4,296 developed EASL ACLF alone, and 574 developed APASL ACLF alone. The incidence rate of APASL ACLF was 5.7 per 1,000 person-years (95% confidence interval [CI]: 5.4-6.0), and the incidence rate of EASL ACLF was 20. 1 (95% CI: 19.5-20.6). The 28-day and 90-day mortalities for APASL ACLF were 41.9% and 56.1%, respectively, and were 37.6% and 50.4% for EASL ACLF. The median bilirubin level at diagnosis of EASL-alone ACLF was 2.0 mg/dL (interquartile range: 1.1-4.0). Patients with hepatitis C or nonalcoholic fatty liver disease had among the lowest ACLF incidence rates but had the highest short-term mortality. Conclusion: There is significant discordance in ACLF events by EASL and APASL criteria. The majority of patients with EASL-alone ACLF have preserved liver function, suggesting the need for more liver-

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Incidence, predictors and outcomes of acute-on-chronic liver failure in outpatients with cirrhosis

Cited by 109 publications

References 18 publications

Prediction of nosocomial acute-on-chronic liver failure in patients with cirrhosis admitted to hospital with acute decompensation

Prediction of nosocomial acute-on-chronic liver failure in patients with cirrhosis admitted to hospital with acute decompensation

Differential inflammasome activation predisposes to acute-on-chronic liver failure in human and experimental cirrhosis with and without previous decompensation

Incidence and Mortality of Acute‐on‐Chronic Liver Failure Using Two Definitions in Patients with Compensated Cirrhosis

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