ORLANDO – Vascular inflammation was no different in patients with moderate to severe psoriasis after 16 weeks of treatment with adalimumab than in untreated controls, according to a study that evaluated the impact of blocking tumor necrosis factor–alpha on vascular inflammation.
Further, there was a modest increase in vascular inflammation in carotid arteries after 52 weeks of treatment with the tumor necrosis factor (TNF) alpha-antagonist adalimumab,, MD, president of Innovaderm Research, Montreal, reported in a late-breaking session at the annual meeting of the American Academy of Dermatology.
At 16 weeks, there were no significant differences in vascular inflammation between the treatment and control arms, based on the change from baseline in the vessel wall target to background ratio from the ascending aorta (the primary endpoint). In the carotid arteries at 16 weeks, differences in vascular inflammation between the adalimumab group and control group were also not significant.
At 52 weeks, there was no significant change in target to background ratio from the ascending aorta between baseline and the start of adalimumab, although in the carotid arteries, there was a modest increase in vascular inflammation.
Several previous studies have suggested that reducing inflammation in psoriasis can also reduce the risk of some cardiovascular events. As to why this study did not demonstrate a correlation between vascular inflammation and treatment, Dr. Bissonnette said during the question and answer portion of the presentation that “either the dose of adalimumab that is used for psoriasis has no impact on vascular inflammation or it may be possible that levels of interleukin-6, a key cytokine correlated with vascular inflammation, were very low in our study.”
Interleukin-6 typically is increased in patients with psoriatic arthritis, he explained, noting that in this study, only 7.5% of patients in the treatment group and about 10% of those in the control group had a history of psoriatic arthritis.
Additionally, at baseline, high-sensitivity C-reactive protein levels were significantly higher in controls: 5.32, compared with 2.72 in the treatment arm (P = .003).
Another possible reason for the results could be the molecule size of adalimumab, session comoderatornoted in an interview. “The drug may not penetrate the aorta. These are large molecules. It also might be that [TNF–alpha] is not the main driver of aortic inflammation in people with psoriasis. Increasingly, we think of people with psoriasis as an IL-23 and IL-17 disease, so maybe that is part of it,” said Dr. Gelfand, professor of dermatology and epidemiology at the University of Pennsylvania, Philadelphia. He also directs the psoriasis and phototherapy treatment center at the university.
In addition to being presented at the meeting, the results were published in the Journal of Investigative Derma
Adalimumab is marketed asby Abbvie; a biosimilar version, (Amjevita), was approved in the United States in 2016.
Dr. Bissonnette’s disclosures included serving as an adviser and consultant to Abbvie, which sponsored the study, as well as relationships with other companies, including Amgen, Celgene, Janssen, and Novartis. Dr. Gelfand’s disclosures included serving as a consultant and investigator for Abbvie, and serving as an investigator, speaker, and/or consultant for other companies, including Eli Lilly, Janssen, and Novartis.