Psoriasis has both cutaneous and systemic manifestations. Psoriatic pathogenesis is driven by chronic, immune-mediated inflammation.1, 2 Multiple cormorbidities of psoriasis, such as obesity, diabetes, hypertension, and dyslipidemia predispose to cardiovascular disease. Furthermore, psoriasis alone may represent an independent cardiovascular risk factor.3 Biologic therapies specifically targeting inflammatory pathways have emerged in the management of psoriasis. Given the role of chronic inflammation in both psoriasis and cardiovascular disease, the impact of these therapeutic agents on cardiovascular risk has been of research interest. To date, the data suggest an overall reduction in risk for cardiovascular events with tumor necrosis factor–alpha inhibitors and a neutral effect for ustekinumab, an IL-12/23 inhibitor.1, 4, 5 Fewer data exist to corroborate the relationship between ustekinumab and cardiovascular risk, and concern still exists for an increased susceptibility to major adverse cardiovascular events.1, 6, 7, 8 There are limited data guiding the combination of biologic agents in the management of psoriasis and psoriatic arthritis.
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Babalola et al. (2014) studied this question.
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