Introduction
Non-alcoholic liver disease (NAFLD) is a leading cause of liver-related morbidity and mortality having an overall prevalence of about 30%. Inflammatory bowel diseases (IBD) are caused by a dysregulated immune response in the hosts, favored by genetic susceptibility. In addition to symptoms related to the digestive tract, about 40% of patients with IBD also experience extraintestinal manifestations. Although, NAFLD has been frequently associated with IBDs, the relationship between these two pathologies remains unclear.
Aims & Methods
The aim of this study was to investigate the prevalence of NAFLD among IBD patients, as well as the factors that connect these two conditions.From January 2022 to November 2022, consecutive IBD patients were enrolled from a tertiary care center hospital in Iasi. All patients' demographic information, clinical characteristics including blood pressure, biological parameters, and anthropometric measurements were collected. Following informed consent, participants underwent a fibroscan evaluation for liver stiffness measurement (LSM) and controlled attenuation parameter (CAP).
Results
A total of 93 patients with IBD were enrolled (65,3% men, 55,6% with ulcerative colitis). 45 (48,3%) of them were diagnosed with NAFLD, with a mean CAP score of 283 ± 33.4 vs. 215 ± 23.7 in patients with IBD only. Regarding liver fibrosis, mean LSM value in the NAFLD group was 6.8 ± 1.9 kPa vs. 5.7 ± 2.3 kPa in the non-NALFD group. Subjects with NAFLD exhibited higher body mass indexes than those with IBD only (26.2 vs. 33.1, p<0.05). In addition, the prevalence of diabetes was much greater among this group (27.5% vs. 0%; p=0.0001), as was the prevalence of elevated HbA1c levels in the absence of a diabetes diagnosis (14% vs. 7.35%; p=0.23). They also had a non-significantly higher mean systolic blood pressure and greater incidences of hypertension. Age (β=0.357, p=0.034), body mass index (BMI) (β=0.185, p=0.048), disease duration (β=0.297, p=0.037), C - reactive protein (β=0.321, p=0.013), fasting plasma glucose (β=0.269, p=0.018) and triglycerides (β=0.273, p=0.021) were strongly associated at the multivariate analysis with the diagnosis of NAFLD in our cohort of patients with IBD. Advanced fibrosis (LSM > 9.7 kPa) was associated with age, BMI and the level of triglycerides. After adjusting for classic metabolic risk factors, age and gender the multivariate logistic regression analysis showed that the presence of IBD (odds ratio, 2.45; 95% confidence interval,1.17–4.391; p < 0.001). Also, in regard to age and male gender they were independent risk factors for NAFLD. Of note, the 10-year risk of myocardial infarction or death estimated by the Framingham risk scores for hard coronary heart disease was higher in the NAFLD group (2.32% vs. 4.27%, p=0.0024).
Conclusion
NAFLD is an intricate condition that has become more common in IBD patients. The connection between these two pathologies is not fully understood, although metabolic disorders, age and male gender have a notable role. Current evidence in the literature suggests a minor risk for the progression of liver fibrosis, the cardiovascular risk appears to be of more concern. Given the information presented above, patients with IBD should be assessed using a multidisciplinary approach.