Introduction
Auto-inflammatory conditions like inflammatory bowel disease (IBD) and rheumatoid arthritis (RA) have a higher prevalence of liver fibrosis and cardiovascular risk(CVR), compared to the general population. This is relevant, given the potential metabolic and cardiovascular adverse effects of some drug classes.
Aims & Methods
Cross-sectional study of IBD and RA patients. Pregnancy or known cause of chronic liver disease were excluded. All patients underwent transient elastography, clinical and laboratorial assessment. International Physical Activity Questionnaire(IPAQ) classified activity as low, moderate, or high. Presence of steatosis and fibrosis was defined as Controlled Attenuated Parameter(CAP) measurement of >248dB/m and Liver Stiffness Measurement(LSM) >8kPa, respectively. For CVR, SCORE2 was calculated according to European Society of Cardiology (if>40 years).
Results
130 patients were enrolled (79 with IBD and 51 with RA). Most RA patients (80%) have received treatment with methotrexate. Demographics and CVR factors are presented in table 1. RA patients were significantly older and had higher prevalence of CVR factors. Nonetheless, no differences in the median SCORE2 were found [4 (IQR 3-10) vs 8 (IQR 6-11), p=0.06]. 16% of IBD and 57% of RA patients had liver fibrosis(p<0.01); No differences were found in liver fibrosis between RA patients on methotrexate (70% vs 54%; p=0.35); 46% of IBD and 73% of RA patients had liver steatosis (p=0.006). RA had a higher risk of fibrosis (OR=5.16 (95%CI 1.8-14.7),p=0.004), even after adjustment for age, gender, body mass index, physical activity and CVR factors.
| | IBD | RA | p |
| Male,% | 51% | 45% | 0.54 |
| Age, median,IQR | 40, 30-54 | 64, 54-69 | <0.001 |
| Diabetes mellitus,% | 5% | 17% | 0.027 |
| Dyslipidemia,% | 11% | 39% | <0.001 |
| thromboembolic diseases,% | 6% | 10% | 0.48 |
| Smoker/Previous smoker,% | 38% | 24% | 0.46 |
| Low IPAQ,(%) | 87% | 71% | 0.93 |
Conclusion
In our cohort, more than half of the RA patients had undiagnosed liver fibrosis and RA appears to be to be an independent risk factor for this condition. Further research is warranted to elucidate the underlying pathophysiology and identify actionable risk factors for the development of these condition.