Abstract
Patients with psoriasis are at an increased risk for nonalcoholic fatty liver disease (NAFLD) compared to the general population. However, the pathophysiology underlying this comorbidity and elucidation of effective treatment strategies are unclear. This review provides insights into the possible role of chronic, low-grade inflammation in the pathogenesis of NAFLD in patients with psoriasis. Both conditions are associated with increased levels of pro-inflammatory adipokines (such as tumor necrosis factor-α and interleukin-6), and hepatokines, and decreased levels of adiponectin, an anti-inflammatory adipokine. This imbalance in inflammatory mediators could result in insulin resistance and, thereby, facilitate the occurrence and progression of NAFLD in a multistep manner. All patients with psoriasis should, therefore, be considered candidates for NAFLD screening and managed accordingly. Given the common etiology of inflammation between these conditions, it is hypothesized that biologic therapies for psoriasis may attenuate the systemic inflammatory process and progression of NAFLD in patients with psoriasis.
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