Beyond the Skin Plaques: Psoriasis and Its Cardiovascular Comorbidities

Abstract

Psoriasis, a widely prevalent chronic disease of the skin and joints, has long been associated with far-reaching systemic ramifications and decreased quality of life. However, psoriasis is largely underdiagnosed and insufficiently treated. Classical risk factors predisposing to cardiovascular diseases, such as hypertension, diabetes, metabolic syndrome, and dyslipidemia, have been noted in patients with mild and severe psoriasis. Furthermore, the magnitude of the cardiovascular comorbidity and the need to screen for risk factors has often been ignored while considering the management options for psoriasis. This article has reviewed the cardiovascular implications of psoriasis from the shared pathogenesis behind these two diseases to the increased incidence of cardiovascular events, such as myocardial infarction, stroke, and other causes of vascular mortality. Additionally, the therapeutic targets of common inflammatory pathways, such as those involving tumor necrosis factor α (TNF-α), interleukin-12/interleukin-23 (IL-12/IL-23), and helper T cells 17 (Th17), have been discussed with an emphasis on their efficacy in controlling psoriasis and its cardiovascular consequences.

Keywords: anti-il12/23; anti-tumor-necrosis factor-alpha; cardiovascular disease; cardiovascular risk; psoriasis; systemic inflammation.

Figure 1. Summary of chronic inflammation in psoriasis leading to an increased risk of cardiovascular disease

Th1 cells, Helper T cells one; TNF-a, tumor necrosis factor-a; IFN, interferon; Th17 cells, helper T cells 17; IL-17, interleukin-17; Treg cells, regulatory T cells.

Figure 2. Summary of the different drugs against psoriasis and their mechanisms of action

IL-23, Interleukin 23; Th17 cell, helper T cell 17; IL-17, interleukin 17; TNFα, tumor necrosis factor α; IL-12, interleukin 12; Th1 cells, helper T cells one.