HLA-CW6 ALLELE AND BIOLOGICAL TREATMENTS ARE PROTECTIVE FACTORS AGAINST LIVER FIBROSIS IN PSORIATIC ARTHRITIS PATIENTS

BackgroundNon-alcoholic fatty liver disease can be expressed from an indolent steatosis, evolve to steatohepatitis and eventually evolve to liver fibrosis. This spectrum of non-alcoholic inflammatory liver disease is increased in psoriasis and psoriatic arthritis (PsA). To date, the relationship between non-alcoholic liver fibrosis and genetics in PsA has not been studied.ObjectivesThe objective of our study is to evaluate the association between the HLA-Cw6 allele and the FIB-4 (fibrosis-4) index in patients with PsA.MethodsRetrospective longitudinal study in patients older than 18 years with PsA according to CASPAR criteria with determination of the HLA-Cw6 allele. To estimate liver fibrosis, the FIB-4 index was obtained, calculating it at the onset of PsA and at the last available visit. A descriptive analysis of the variables was carried out using mean and standard deviation (SD) for those with symmetric distribution, and median and interquartile range (IR) for the asymmetric ones. Qualitative variables were described using absolute values ​​and percentages. A bivariate analysis was carried out using parametric and non-parametric hypothesis contrast tests to determine the association between the main variable (current FIB-4) and the secondary variables. Bivariate correlations were analyzed using Pearson’s coefficient. A multivariate model was developed to assess the association between HLA-Cw6 and liver fibrosis adjusted for potential confounding factors, and results were presented as Odds Ratio (OR) with 95% confidence interval (CI) and level of statistical significance p-value=0.05. The statistical program SPSS version 20 was used. The study was approved by the local committee.Results209 patients with PsA were included (56.9% men, mean age 42.72±14.24 years), 84.7% with psoriasis, and median (IR) ESR (mm/h) of 16.9(9-28) and CRP (mg/l) 5.0(2.52-12.25). 74.3% of patients were HLA-Cw6 negative. 79.4% of patients were receiving treatment with MTX, and 59.8% biological therapy. Regarding comorbidities, 29.6% had hypertension, 24% dyslipidemia, 10.1% diabetes, and 4.2% acute myocardial infarction. FIB-4 could be calculated in 154 patients at the onset of PsA, with a mean of 1.53±9.05 points, being 58.9% of patients at FIB-4 F0-1 (non advanced fibrosis, <1, 30 points). At the last available visit, FIB-4 could be calculated in 180 patients, mean of 1.35±0.85 points, 86.4% of the patients at FIB-4 F0-1. Table 1 shows bivariate analysis and Table 2 the multivariate one.Table 1.Bivariate analysis of the main variable (current FIB-4) categorized into normal (result F0-1, non advanced fibrosis, <1.30 points) and altered (result F2-3-4, intermediate zone and significant fibrosis, >1.3 points).1Median (IR) 2Mean±SD. * p-value < 0.05. AMI acute myocardial infarction.Normal current FIB-4 (N = 106)Altered current FIB-4 (N = 74)p valueHLA-Cw6 (%)18.546.740.024 *ESR (mm/h)116 (9-32)10 (6-19)0.362CRP (mg/l)15.31 (2.41-12.97)3.30 (2.11-9.00)0.348PsA age onset (years)237.33±11.7151.53±12.330.630Male sex (%)60.439.60.627Biologic (%)64.335.70.059Methotrexate (%)56.843.30.211Leflunomide (%)60400.915Psoriasis (%)58.941.10.648Hypertension (%)42.257.80.002 *Diabetes (%)40600.079AMI (%)16.783.30.023 *Dyslipidemia (%)45.954.10.030 *Table 2.Multivariate analysis. * p-value < 0.05.VariableOR (IC 95%)p valueHLA-Cw60.210 (0.062-0.707)0.012 *Male sex1.553 (0.624-3.864)0.344Hypertension2.973 (1.125-7.858)0.028 *Diabetes1.478 (0.395-5.530)0.561Dyslipidemia1.429 (0.541-3.773)0.471Methotrexate1.113 (0.357-3.466)0.854ESR at onset (mm/h)0.993 (0.967-1.019)0.605AMI6.302 (0.495-80.246)0.156Biologic0.397 (0.166-0.949)0.038 *ConclusionIn our study, having the HLA-Cw6 allele and receiving biological treatment behaved as a protective factor for liver fibrosis in PsA, while arterial hypertension was an independent risk factor. The presence of psoriasis was not related to hepatic fibrosis measured by FIB-4.Disclosure of InterestsNone declared