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Prevalence of Steatotic Liver Disease Among US Adults with Rheumatoid Arthritis

  • Athanasios Vassilopoulos,
  • Markos Kalligeros,
  • Stephanos Vassilopoulos,
  • Fadi Shehadeh,
  • Gregorio Benitez,
  • Matthew Kaczynski,
  • Ingrid Lazaridou,
  • Kittichai Promrat,
  • Jack R Wands,
  • Eleftherios Mylonakis

摘要

Background

The prevalence of steatotic liver disease (SLD) among patients with rheumatoid arthritis (RA) remains largely unknown.

Aims

To investigate the prevalence of SLD and liver fibrosis among patients with RA.

Methods

We utilized data from the United States (US)-based National Health and Nutrition Examination Survey (NHANES) 2017–2020 cycle. After applying established sample weights, we estimated the age-adjusted prevalence of SLD and its subclassifications (CAP ≥ 285 dB/m), high-risk NASH (FAST score) and liver fibrosis (LSM) among participants with self-reported RA. Multivariable logistic regression was performed to identify independent risk factors for metabolic dysfunction associated SLD (MASLD), high-risk NASH and fibrosis, respectively, among participants with RA. We present adjusted odds ratios (aORs) and 95% confidence intervals (CIs).

Results

Age-adjusted prevalence of MASLD among US adults with RA was 34.91% (95% CI: 24.02–47.65%). We also found that the age-adjusted prevalence of high-risk NASH (FAST score > 0.35) and significant fibrosis (LSM > 8.6 kPa) was 12.97% (95% CI: 6.89–23.07%) and 10.35% (95% CI: 5.55–18.48%), respectively. BMI  30 kg/m2, (aOR 6.23; 95% CI: 1.95–19.88), diabetes (aOR 5.90; 95% CI: 1.94–17.94), and dyslipidemia (aOR 2.83; 95% CI: 1.12–7.11) were independently associated with higher odds of MASLD among participants with RA. Diabetes (aOR 19.34; 95% CI: 4.69–79.70) was also independently associated with high-risk NASH.

Conclusions

The prevalence of MASLD, high-risk NASH, and liver fibrosis among patients with RA is equal or higher than the general population. Future studies of large cohorts are needed to substantiate the role of systemic inflammation in the pathophysiology of MASLD.

Graphical Abstract