Atherosclerosis in psoriatic arthritis

doi:10.1016/j.autrev.2011.05.022

Autoimmunity Reviews

Volume 10, Issue 12, October 2011, Pages 773-778

https://doi.org/10.1016/j.autrev.2011.05.022 Get rights and content

Abstract

The atherosclerotic process is accelerated in several autoimmune rheumatic diseases. Effector cells of innate and adaptive immunity along with pro-inflammatory cytokines and other immune mediators are found in atherosclerotic lesions, where they play an important role in induction, progression and rupture of plaques.

Psoriatic arthritis (PsA) is a chronic inflammatory disease, characterized by arthritis, enthesitis, dactilytis, osteitis, and axial involvement, along with skin manifestations. PsA is frequently associated with obesity, diabetes, dyslipidemia, hypertension, accelerated atherosclerosis and with increased cardiovascular morbidity and mortality. Disease-specific and traditional risk factors seem to account for the atherosclerotic burden in PsA patients. Some immunological factors which are involved in PsA can also contribute to atherosclerosis including C reactive protein (CRP), TNF-α, IFN-γ, IL-1, Il 6, IL23, and Th17.

Introduction

Atherosclerosis is accelerated in many autoimmune rheumatic diseases [1], [2], [3], [4], [5], [6], and the relative risk of coronary artery disease is 1.6 in patients with ankylosing spondylitis and psoriatic arthritis (PsA), 3.0 in individuals with rheumatoid arthritis (RA), and 6.0 in subjects with systemic lupus erythematosus (SLE) [7], [8]. However, the reason why atherosclerosis is accelerated in immune-inflammatory diseases has not been completely elucidated.

One of the most recent advances in understanding the pathogenesis of atherosclerosis is the recognition of the inflammatory nature of atherosclerotic lesions. Inflammatory mechanisms have been demonstrated in all stages of atherogenesis including induction, progression, and rupture of plaques.

Section snippets

Pathogenesis of atherosclerosis

The first step in atherogenesis is endothelial cell activation, a process which involves both traditional and non-traditional risk factors. Once activated, endothelial cells exhibit a pro-inflammatory phenotype characterized by an increased expression of adhesion molecules, which in turn promote the rolling and sticking of monocytes to the endothelial cell membrane [9], [10], [11]. The endothelial wall becomes more permeable allowing low-density lipoproteins (LDLs) to pass from the circulation

Immuno-inflammatory players in atherogenesis

Various molecules, as well as inflammatory and immune cells, have been shown to play an important role in the amplification loop of the inflammatory process promoting the activation of endothelial cells, smooth muscle cells, and macrophages [12].

Psoriatic arthritis: an immuno-inflammatory disease

PsA is defined as an axial and/or peripheral inflammatory arthritis associated with psoriasis. It is recognized as a disease entity distinct from RA and characterized by distal inter-phalangeal joint involvement, asymmetric distribution of arthritis, dactylitis, enthesitis, spinal involvement, and frequent association with HLA-B27. Interestingly, it has recently been suggested that PsA could be a multisystem disease involving even coronary arteries and the heart [41]. The pathogenesis of PsA is

Atherosclerosis and psoriatic arthritis

The risk of atherosclerosis in PsA patients could be increased by the chronic inflammatory state, due to an imbalanced secretion of pro-and anti-inflammatory cytokines.

Both PsA and atherosclerosis are mainly mediated by Th1 cells [9]. In fact, both diseases have a common pattern of T cell activation, including an increased percentage of cells expressing a Th1 cytokine profile (TNF-α, IL-1β, IL-10 and IFN) [9], [43].

The perturbation of angiogenesis appears to be an early pathogenetic event in

Conclusions

While rheumatic diseases have generally been regarded as non-fatal, the natural history of most of them is characterized by premature death due to cardiovascular disease. Even in patients with PsA, inflammatory mediators have been found in atherosclerotic plaques. This suggests that chronic inflammation acts independently and/or synergistically with the traditional risk factors in the pathogenesis of atherosclerosis. Moreover, with respect to other inflammatory rheumatic diseases, PsA patients

Take-home messages

•
PsA, is associated with an increased prevalence of cardiovascular events due to accelerated atherosclerosis.
•
In PsA atherosclerosis seems to depend on traditional and non-traditional risk factors, including immune-inflammatory biomarkers.
•
Preclinical stages of atherosclerosis can be detected with non-invasive methods, such as carotid ultrasound.

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