BackgroundNon-alcoholic fatty liver disease (NAFLD), the most common cause of liver disease, has a prevalence of about 25% in the general population. It increases mortality and comorbidity in patients with immune-mediated inflammatory diseases.ObjectivesThe main objective is to estimate the prevalence of NAFLD in three of the most common rheumatologic pathologies: rheumatoid arthritis (RA), axial spondyloarthritis (SpA-ax) and psoriatic arthritis (PsA). As a secondary objective, the possibility of finding associated risk factors in this group of subjects that may imply a higher risk of developing NAFLD is proposed.MethodsWe conducted a prospective single center observational study which included patients diagnosed with RA, EspA-ax, and PsA attended in the Rheumatology department of a tertiary hospital from January to April 2021. Anthropometric parameters, history related to cardiovascular risk factors and disease activity at the time of the visit were collected. Additionally, blood tests and transitional elastography were performed in all patients and the presence of NAFLD was assessed by the fatty liver index (FLI) scale. Different variables were considered to study their association with NAFLD.Results90 patients were included: 28 diagnosed with RA, 36 with EspA-ax and 26 with PAs. 41.1% were male (age range: 27-79 years). Patients with previous liver disease were excluded from the study. 22 (27.2%) patients had NAFLD measured by FLI ≥ 60. No significant differences in prevalence of hepatic steatosis were found between the 3 groups, although values were higher in patients with PsA.The variables that were significantly associated with the development of NAFLD in our cohort were: body mass index (BMI), abdominal perimeter, blood glucose level, HOMA-IR (Homeostatic Model Assessment for Insulin Resistance), HDL, TG, GGT, ferritin and uric acid levels. The rest of the variables studied did not show statistically significant differences (Table 1).Table 1.NO STEATOSIS (FLI<60)n=59STEATOSIS (FLI>60)n=22MeanStandard deviationMeanStandard deviationpBMI24,523,0030,292,77< 0,001Abdominal perimeter86,3410,01106,828,55< 0,001Age52,9312,8757,598,240,1185Glucose78,648,3790,6419,690,0002Insulin8,8310,1212,406,660,1302HOMA1,752,022,761,700,0500HbA1c5,350,455,690,640,0096Total cholesterol190,9829,46201,4138,530,1977HDL64,8817,6655,5911,550,0249LDL110,4428,45120,0036,210,2163TG81,1232,42128,5055,52< 0,001GPT25,8330,7337,1819,820,1116GOT27,2023,4926,8210,690,9413GGT20,8017,6649,9538,46< 0,001Creatinin0,750,190,840,180,0583Uric acid4,781,305,911,140,0007Ferritina121,75111,30208,00140,170,0050PCR2,894,552,672,330,8307ConclusionHepatic steatosis was present in 27.2% of patients vs 25% estimated prevalence in the general population. Identification of risk factors involved would allow better control of the comorbidities associated with NAFLD.The fact that the prevalence found in our sample population is so close to that of the general population, may be related to a good inflammatory control of the underlying disease.Further prospective studies with larger sample sizes are needed to find additional predictive factors for the development of NAFLD in this group of diseases.References[1]Bedogni, G., Bellentani, S., Miglioli, L., Masutti, F., Passalacqua, M., Castiglione, A. y Tiribelli, C. (2006). The Fatty Liver Index: a simple and accurate predictor of hepatic steatosis in the general population. BMC Gastroenterology, 6: 33.[2]Brenner, C., Galluzzi, L., Kepp, O. y Kroemer, G. (2013). Decoding cell death signals in liver inflammation. Journal of Hepatology, 59(3): 583-594.[3]Byrne, C.D. y Targher, G. (2015). NAFLD: a multisystem disease. Journal of Hepatology, 62(1 Suppl): 47[4]Miele, L., Vallone, S., Cefalo, C., La Torre, G., Di Stasi, C., Vecchio, F.M., et al. (2009). Prevalence, characteristics and severity of non-alcoholic fatty liver disease in patients with chronic plaque psoriasis. Journal of Hepatology, 51(4): 778-786.Disclosure of InterestsNone declared
