Management of psoriasis as a systemic disease: what is the evidence?

Abstract

Background: Psoriasis is a chronic, systemic immune-mediated disease characterized by development of erythematous, indurated, scaly, pruritic and often painful skin plaques. Psoriasis pathogenesis is driven by proinflammatory cytokines and psoriasis is associated with increased risk for comorbidities, including, but not limited to, psoriatic arthritis, cardiovascular disease, diabetes mellitus, obesity, inflammatory bowel disease and nonalcoholic fatty liver disease compared with the general population.

Objectives: To explore the pathophysiological relationship between psoriasis and its common comorbidities and discuss the need for new treatment paradigms that include strategies to reduce systemic inflammation in patients with moderate-to-severe psoriasis.

Methods: This narrative review summarizes the published evidence related to the ability of biological therapies to ameliorate the consequences of systemic inflammation in patients with psoriasis.

Results: Current evidence suggests that preventing damage associated with inflammation, and preventing development of future inflammatory damage and comorbidities, may be a potentially achievable treatment goal for many patients with moderate-to-severe plaque psoriasis when biological therapies are utilized early in the disease. Encouraging data from recent studies suggest that the loftier goal of reversing existing inflammatory damage and improving signs and symptoms of inflammatory comorbidities could also possibly be attainable.

Conclusions: Results from ongoing prospective studies regarding the effects of biologics on markers of systemic inflammation in patients with psoriasis will strengthen the clinical evidence base that can be used to inform treatment decisions for patients with moderate-to-severe psoriasis. What's already known about this topic? Psoriasis is a systemic inflammatory disease and treatments are needed to optimize patient outcomes. What does this study add? This review discusses new psoriasis treatment paradigms that may potentially reduce effects of systemic inflammation. Evidence demonstrating that biological treatment may prevent or reverse inflammatory damage associated with psoriasis comorbidities is reviewed.

Figure 1

Psoriasis. Systemic inflammation. DDC, dermal dendritic cell; IFN, interferon; IL, interleukin; KC, keratinocyte; KGF, keratinocyte growth factor; LC, lymphocyte; PDC, plasmacytoid dendritic cell; Tc, cytotoxic T cell; Th, T helper cell; TNF, tumour necrosis factor; VEGF, vascular endothelial growth factor; VLA, very late antigen. Adapted from Di Cesare et al.,76 with permission from Elsevier.

Figure 2

Psoriasis. Comorbidities and key inflammatory cytokines. IFN, interferon; IL, interleukin; TNF, tumour necrosis factor.