Skin inflammation linked to systemic inflammation, may impact cardiovascular disease
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Key takeaways:
- Systemic inflammation mediated 17% of the association between psoriasis severity and subclinical atherosclerosis.
- It also mediated 37% of the link between psoriasis severity and cardiovascular events.
Skin inflammation, such as psoriasis, was associated with systemic inflammation, whereas both psoriasis severity and systemic inflammation were linked with cardiovascular disease, according to a study.
“Multiple lines of evidence support development of cardiovascular disease (CVD) in psoriasis,” Axel Svedbom, MSc, PhD, a researcher in the division of dermatology and venereology, department of medicine, Karolinska Institute in Stockholm, and colleagues wrote.
While it is unclear why such a link exists, researchers have a few theories.
“A prevalent hypothesis is that displacement of inflammatory signals from psoriatic skin to the circulation promotes systemic inflammation, driving coronary plaque buildup and rupture, but the evidence for this is limited,” Svedbom and colleagues wrote. “Therefore, we explored whether systemic inflammation may be a mediator of the association between psoriasis skin disease severity and CVD.”
The study used data from a cross-sectional U.S. study, the Psoriasis Atherosclerosis and Cardiometabolic Disease Initiative, and a Sweden cohort study, the Stockholm Psoriasis Cohort, totaling 769 patients with psoriasis and without prior CVD.
To measure systemic inflammation in patients, researchers used a composite biomarker for systemic inflammation called the glycan biomarker of N-acetyl side chains of acute-phase proteins (GlycA).
In both cohorts, GlycA levels increased with worse psoriasis severity. The U.S. study found that a mean standardized GlycA level was linked with a noncalcified coronary burden, a measure of atherosclerosis which may be a link between skin inflammation and systemic inflammation, in both unadjusted and adjusted models.
In the Swedish study, the same levels were associated with incident cardiovascular events in both models as well. In fact, patients with third-tertile GlycA levels had higher CVD risk than patients with first-tertile GlycA levels, according to the study.
Across both studies, the authors found that GlycA significantly mediated 17% of the association between psoriasis severity and subclinical atherosclerosis and 37% of the link between psoriasis severity and cardiovascular events.
As seen through GlycA levels, the estimated direct effects of psoriasis severity on the noncalcified coronary burden in patients was 0.94 (95% CI, 0.26-1.74), whereas the indirect effects were 0.19 (95% CI, 0.02-0.47).
Psoriasis severity was found to both directly and indirectly affect cardiovascular events with odds ratios of 1.23 (95% CI, 0.7-1.92) and 1.16 (95% CI, 1.04-1.42), respectively.
“The results support the hypothesis that displacement of inflammatory signals from the skin to the circulation can contribute to the excess cardiovascular risk observed in patients with psoriasis,” the authors wrote. “Future research could explore whether controlling skin disease severity can modulate subclinical atherosclerosis and the risk of future cardiovascular events.”