Is non‐alcoholic steatohepatitis a predisposing factor to porphyria cutanea tarda?

Porphyria cutanea tarda (PCT) is a disease caused by a deficiency of the fifth enzyme of the heme biosynthetic pathway in the liver that manifests in the skin as blistering and fragility of predominantly sun‐exposed skin. It occurs in individuals with environmental and/or genetic risk factors such as estrogen use, hepatitis C infection and hemochromatosis gene mutations. This report highlights a case of PCT which manifested in an individual with non‐alcoholic fatty liver disease (non‐alcoholic steatohepatitis; NASH). We propose that NASH may have been a contributing factor for the development of PCT in our patient.     

Initial outcomes of a dedicated multidisciplinary non-alcoholic fatty liver disease clinic: a retrospective cohort study

Background

Non-alcoholic fatty liver disease (NAFLD) is a major healthcare burden. Real-world outcomes in dedicated tertiary care settings in Australia remain unknown.

Aim

To evaluate the initial outcomes of patients referred to a dedicated multidisciplinary tertiary care NAFLD clinic.

Methods

Retrospective review of all adult patients with NAFLD who attended a dedicated tertiary care NAFLD clinic between January 2018 and February 2020 and who had two clinic visits and FibroScans at least 12 months apart. Demographic and health-related clinical and laboratory data were extracted from electronic medical records. Key outcome measures were serum liver chemistries, liver stiffness measurement (LSM) and weight control at 12 months.

Results

A total of 137 patients with NAFLD were included. Median (interquartile range (IQR)) follow-up time was 392 days (343–497 days). One hundred and eleven patients (81%) achieved weight control (i.e. weight loss or stability). Markers of liver disease activity were significantly improved, including median (IQR) serum alanine aminotransferase (48 (33–76) vs 41 (26–60) U/L, P = 0.009) and aspartate aminotransferase (35 (26–54) vs 32 (25–53) U/L, P = 0.020). Median (IQR) LSM across the whole cohort was significantly improved (8.4 (5.3–11.8) vs 7.0 (4.9–10.1) kPa, P = 0.001). No significant reduction was observed in mean body weight or the frequency of metabolic risk factors.

Conclusions

This study highlights a new model of care for patients with NAFLD and demonstrates promising initial outcomes in relation to significant reductions in markers of liver disease severity. Although most patients achieved weight control, further refinements are needed to achieve significant weight reduction including more frequent and structured dietetic and/or pharmacotherapeutic interventions.     

Metabolic dysfunction outperforms ultrasonographic steatosis to stratify hepatocellular carcinoma risk in patients with advanced hepatitis C cured with direct-acting antivirals

Background and Aims

Metabolic dysfunction (MD)-associated fatty liver disease has been proposed to identify individuals at risk of liver events irrespectively of the contemporary presence of other liver diseases. The aim of this study was to examine the impact of MD in patients cured of chronic hepatis C (CHC).

Patients and Methods

We analysed data from a real-life cohort of 2611 Italian patients cured of CHC with direct antiviral agents and advanced liver fibrosis, without HBV/HIV, transplantation and negative for hepatocellular carcinoma (HCC) history (age 61.4 ± 11.8 years, 63.9% males, median follow-up 34, 24–40 months). Information about ultrasonographic steatosis (US) after sustained virological response was available in 1978.

Results

MD affected 58% of patients, diagnosed due to the presence of diabetes (MD-diabetes, 19%), overweight without diabetes (MD-overweight, 37%) or multiple metabolic abnormalities without overweight and diabetes (MD-metabolic, 2%). MD was more frequent than and not coincident with US (32% MD-only, 23% MD-US and 13% US-only). MD was associated with higher liver stiffness (p < 0.05), particularly in patients with MD-diabetes and MD-only subgroups, comprising older individuals with more advanced metabolic and liver disease (p < 0.05). At Cox proportional hazard multivariable analysis, MD was associated with increased risk of HCC (HR 1.97, 95% CI 1.27–3.04; p = 0.0023). Further classification according to diagnostic criteria improved risk stratification (p < 0.0001), with the highest risk observed in patients with MD-diabetes. Patients with MD-only appeared at highest risk since the sustained virological response achievement (p = 0.008), with a later catch-up of those with combined MD-US, whereas US-only was not associated with HCC.

Conclusions

MD is more prevalent than US in patients cured of CHC with advanced fibrosis and identifies more accurately individuals at risk of developing HCC.