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The Prevalence of Intestinal Failure-associated Liver Disease (IFALD) in Patients on Long-term Home Parenteral
Nicholas Wan1, Sharifah R Syed Mustaffa2, Andrew Holt3
1Department of Gastroenterology, Lyell McEwin Hospital, Elizabeth Vale, South Australia; South Australian Hepatology and Transplant Medicine Unit, Flinders Medical Centre, Bedford Park, South Australia; College of Medicine and Public Health, Flinders University, Bedford Park, South Australia, Australia. nicholas.wan1993@gmail.com.
Background And Aims:
Intestinal failure-associated liver disease (IFALD) is a recognized complication of long-term parenteral nutrition (PN), with reported prevalence ranging from 25-85%, reflecting heterogeneity in patient populations, diagnostic criteria, and PN practices. We aimed to estimate the prevalence of IFALD in Australian adults receiving long-term home-PN (HPN), describe its biochemical and elastographic features, and identify predictors of IFALD.
Methods:
This was a single-centre, cross-sectional observational study in an Australian tertiary centre. Adults currently receiving long-term HPN (>12 weeks) or had received HPN within the previous decade were included. Patients with malignancy or pre-existing liver disease were excluded. IFALD was defined as persistent, unexplained elevation of liver function tests after exclusion of alternative causes of liver injury. Vibration controlled transient elastography (VCTE) was performed in all patients. Univariate logistic regression was used to evaluate associations between IFALD, nutritional, and biochemical variables.
Results:
24 patients were included. The median (inter-quartile range) duration of HPN was 42.5months (15.8-62.3); and weekly calories were 6647 kilocalories (3476.3-8471.3). 15 (62.5%) patients had IFALD. Cholestasis was the predominant biochemical pattern (80%). VCTE demonstrated significant fibrosis (≥ 8 kPa) in 20% and significant steatosis in 40% of IFALD patients. Ongoing HPN was the only variable significantly associated with IFALD on univariate analysis (OR=8, p=0.03).
Conclusions:
IFALD was highly prevalent and manifested as cholestatic liver injury, with a subset demonstrating elastographic evidence of fibrosis. Ongoing HPN was the main predictor, suggesting potential reversibility with PN cessation. Larger, multicentre studies are needed to identify any clinical predictors of IFALD.
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