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Psoriasis and non-alcoholic fatty liver disease (NAFLD) are both inflammatory diseases. The study objective was to estimate the risk of NAFLD, non-alcoholic steatohepatitis, and liver

fibrosis (by liver stiffness and liver biopsy) in patients with psoriasis and to determine the epidemiological, clinical, immunological (TNF-α, IL-2, IL-6, IL-12, IL-17, IL-23, and TGF-β)

characteristics, and bacterial translocation. Of the 215 psoriatic patients included, 91 presented NAFLD (prevalence: 42.3%). Compared to patients with psoriasis alone, those with NAFLD were

significantly more likely to have metabolic syndrome, diabetes, dyslipidemia, body mass index ≥ 30 kg/m2, homeostatic model assessment of insulin resistance ≥ 2.15, and greater psoriasis

area severity index. NAFLD patients also had significantly higher levels of TNF-α (p = 0.002) and TGF-β (p = 0.007) and a higher prevalence of bacterial translocation (29.7% vs. 13.7%; p = 

0.004). Liver stiffness measurement was over 7.8 kPa in 17.2% (15/87) of NAFLD patients; 13 of these underwent liver biopsy, and 5.7% (5/87) had liver fibrosis, while 1.1% (1/87) had

advanced fibrosis or non-alcoholic steatohepatitis. In conclusion the prevalence of NAFLD in patients with psoriasis is high and associated with a higher prevalence of metabolic syndrome

features, bacterial translocation and a higher pro-inflammatory state. It is worth mentioning that liver fibrosis and non-alcoholic steatohepatitis are not frequent in this population of

patients.

It is striking that the same comorbidities, especially those associated with metabolic disorders that can promote liver steatosis, have been associated with systemic inflammation in

psoriasis. Moreover, specific proinflammatory mediators have been shown to cause a chronic inflammatory state in NAFLD, psoriasis, and metabolic syndrome14,15. These similarities could

indicate a linked pathogenesis between psoriasis and NAFLD, with a potentially increased risk for advanced hepatic disease12. However, controversy remains around whether the chronic

inflammatory nature of psoriasis is a contributing factor or an independent risk factor for the development of NAFLD.

Dysregulation of immune responses in individuals who are genetically susceptible to psoriasis and have been exposed to an external environmental trigger is essential in plaque psoriasis

pathogenesis16,17,18. Various cytokines (tumor necrosis factor [TNF]-α, type I interferons [IFNs], interleukin [IL]-12, IFN-γ, IL-23, IL-17, and IL-22) mediate the interaction of

keratinocytes, dendritic cells, T cells, and other immune cells, causing an abnormal loop proliferation of keratinocytes in the psoriatic epidermis15. Cytokines are elements of immunity that

mediate the inflammatory response of the psoriasis plaque and play a mechanistic role in the development of insulin resistance and fatty liver disease. However, their role as biomarkers of

NAFLD in psoriatic patients is not well established19,20. Previous studies have suggested that NAFLD is associated with an increased pro-inflammatory state related to abnormal intestinal

permeability, endotoxemia and bacterial translocation21,22, so the NAFLD pro-inflammatory profile could be associated with psoriasis.

The aim of this study was to estimate the risk of NAFLD, NASH, and liver fibrosis in patients with psoriasis and to determine the epidemiological, clinical, immunological, and inflammatory

characteristics, along with the rate of bacterial translocation, in these patients.

An initial sample of 309 patients with moderate to severe psoriasis were registered during the recruitment period. After excluding 79 patients who presented at least one exclusion criterion,

13 who did not complete the required testing, and 2 who did not have available cytokines, we finally included 215 patients (120 men and 95 women; Supplementary Fig. S1).

Ninety-one (42.3%) included patients presented NAFLD: 62 cases were mild, and 29 were moderate to severe. Patients with and without NAFLD were similar in terms of the treatments they were

receiving for psoriasis, except for acitretin, which was more common in patients with NAFLD (11.0% vs 3.2%; p = 0.02; Supplementary Table S1).

NAFLD was associated with male sex; older age; body mass index (BMI) of 30 kg/m2 or more; homeostatic model assessment of insulin resistance (HOMA-IR) of more than 2.15; diabetes mellitus;

cardiopathy; dyslipidemia; metabolic syndrome; higher waist circumference, levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT),

LDL-cholesterol, triglycerides, erythrocyte sedimentation rate (ERS), and high-sensitivity C-reactive protein (hs-CRP); and non-viable bacterial translocation (BT). Smoking was more

prevalent in psoriatic patients without NAFLD. Patients with psoriatic arthritis did not present more NAFLD (Table 1).

Multivariable logistic regression analysis confirmed that HOMA-IR over 2.15 (p