PREDICT identifies precipitating events associated with the clinical course of acutely decompensated cirrhosis.

Abstract

INTRODUCTION

Acute decompensation (AD) of cirrhosis may present without acute-on-chronic liver failure (ACLF) (AD-No ACLF), or with ACLF phenotype (AD-ACLF) defined by organ failure(s). Precipitants may induce AD. This multicenter, prospective, observational PREDICT study (NCT03056612) analyzes and characterizes the precipitants leading to both of these AD phenotypes.

PATIENTS AND METHODS

The PREDICT study included 1273 non-electively hospitalized patients with AD (No-ACLF=1071; ACLF=202). Medical history, clinical and laboratory data were collected at enrolment and during 90-day follow up, with particular attention to the following characteristics of precipitants: induction of organ dysfunction or failure, systemic inflammation, chronology, intensity, and relationship to outcome.

RESULTS

Among various clinical events, four distinct events were precipitants consistently related to AD, including proven bacterial infections, severe alcoholic hepatitis, gastrointestinal (GI) bleeding with shock and toxic encephalopathy. Among patients with precipitants in the AD-No ACLF cohort and the AD-ACLF cohort (38% and 71%, respectively), almost all (96% and 97%, respectively) showed proven bacterial infection and severe alcoholic hepatitis, either alone or in combination with other events. In both AD phenotypes, patients with proven bacterial infections or severe alcoholic hepatitis had a similar survival. The number of precipitants was associated with significantly increased 90-day mortality, and was paralleled by increasing levels of surrogates for systemic inflammation. Importantly, adequate first-line antibiotic treatment of proven bacterial infections was associated with lower ACLF development rate and lower 90-day mortality.

CONCLUSIONS

This study identified precipitants that are significantly associated with a distinct clinical course and prognosis of patients with AD and specific preventive and therapeutic strategies targeting these events may improve outcome in decompensated cirrhosis.