Abstract
Background and Aims
Frailty is associated with morbidity and mortality in advanced cirrhosis. However, the information on the association between frailty and outcome in compensated cirrhosis is scarce. We aimed to explore the prognostic impact of frailty in compensated cirrhosis.
Methods
Compensated cirrhotic patients were prospectively enrolled. Frailty was defined by the Liver Frailty Index (LFI). Development of new hepatic decompensation (worsening ascites, portal hypertension-related bleeding, hepatic encephalopathy, or acute kidney injury), unplanned hospitalization, and decompensation-free survival were recorded. Quality of life (QoL) was assessed by SF-36 questionnaire.
Results
152 patients were included (MELD 9.2 ± 3.4, Child-Pugh A/B 84.9%/15.1%), and 24.3% were frail. By multivariable logistic regression analysis, age > 65 years, MELD score > 10, and Child-Pugh B were associated with frailty. Compared to the robust group, pre-frail and frail patients had significantly higher cumulative 1-year probabilities of developing decompensation (0% vs. 8.5% vs. 18.4%, p = .009), and unplanned hospitalization (0% vs. 13.5% vs. 34.2%, p < .001), and lower 1-year decompensation-free survival (100% vs. 90.8% vs. 80.4%, p = .014). Two models of multivariable Cox regression analysis were done adjusted with MELD-Na and Child-Pugh B, frailty was associated with developing decompensation (HR 3.01, p = .04; and 2.98, p = .04, respectively) and unplanned hospitalization (HR 2.46, p = .02; and 2.39, p = .03, respectively), but not the decompensation-free survival. By multivariable linear regression analysis, Child-Pugh B and frailty significantly decreased both physical and mental component scores of the SF-36 questionnaire.
Conclusion
Frailty is prevalent in compensated cirrhosis. The LFI provides additional prognostic values to recognized risk scores regarding the development of decompensation, hospitalization, and impaired QoL.
Correction Statement
This article has been corrected with minor changes. These changes do not impact the academic content of the article.
Acknowledgement
This work was partially supported by the Gastrointestinal Association of Thailand and the Center of Excellence in Digestive Diseases, Thammasat University.
Author contributions
(I) Conception and design: S Siramolpiwat; (II) Administrative support: S Siramolpiwat; (III) Provision of study materials or patients: All authors; (IV) Collection and assembly of data: K Kiattikunrat, R Soontararatpong and S Siramolpiwat; (V) Data analysis and interpretation: K Kiattikunrat and S Siramolpiwat; (VI) Manuscript writing: K Kiattikunrat and S Siramolpiwat; (VII) Manuscript editing: S Siramolpiwat; (VIII) Final approval of manuscript: All authors.
Disclosure statement
Sith Siramolpiwat has acted as a speaker for Ferring Pharmaceuticals and Takeda. The remaining authors have no conflicts of interest to declare.