Effects of Biologic Therapy on Cardiovascular Disease in Psoriasis

Abstract

Purpose of Review

The aim of this review is to summarize the literature on the effects of biologic treatment for psoriasis on the risk of cardiovascular (CV) disease (CVD) and adverse CV outcomes.

Recent Findings

Therapy with tumor necrosis factor-alpha (TNF-α) inhibitors has been associated with reduced risk of CV events in observational studies; however, data are conflicting. Data on interleukin (IL)-17 and IL-12/23 inhibitors are limited, and primary endpoints of studies on these drugs have not been focused on CV outcomes.

Summary

Psoriasis is a chronic inflammatory skin disease that has distinct pathogenetic overlaps with that of atherosclerosis. Patients with psoriasis, in particular moderate-to-severe disease, have an increased incidence and prevalence of CV risk factors and CVD. Biologic therapies targeted for treatment of psoriasis dampen the systemic inflammation and may therefore be effective in treating not only the cutaneous manifestations of psoriasis, but may also have beneficial or detrimental CV effects depending on the particular cytokine target and mode of action. Studies on TNF-α inhibitors have suggested that these may reduce the coronary artery calcium score, improve myocardial function, and reduce the risk of adverse CV events albeit that use of these drugs may also lead to weight gain. Studies of treatment with anti-IL-12/23 agents have yielded conflicting results, but ustekinumab, the only IL-12/23 inhibitor currently approved for psoriasis, appears to be effect neutral on CV parameters. Newer drugs such as IL-17 inhibitors have not demonstrated any notable CV safety signals based on pivotal clinical trials, but long-term data from real-life studies are lacking. As new treatment modalities emerge, there is a need for well-powered long-term observational studies to firmly establish the CV safety profile of these drugs in a real-life setting.