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Adalimumab reduces inflammation markers in patients with psoriasis
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Patients with psoriasis who were treated with adalimumab had a reduction in key markers of inflammation such as glycoprotein acetylation compared with those treated with phototherapy, according to a study published in Circulation: Cardiovascular Imaging.
“[Tumor necrosis factor, interleukin-6, C-reactive protein and glycoprotein acetylation] are known to predict future cardiovascular events, and thus reducing these markers of inflammation suggests a cardioprotective effect,” Joel M. Gelfand, MD, MSCE, professor of dermatology and epidemiology, vice chair of clinical research, medical director of the dermatology clinical studies unit, director of the psoriasis and phototherapy treatment center and senior scholar at the Center for Clinical Epidemiology and Biostatistics at University of Pennsylvania Perelman School of Medicine, told Cardiology Today. “However, we did not see any changes in aortic vascular inflammation, and longer-term treatment was associated with mild impairments in HDL.”
Psoriasis treatments
Nehal N. Mehta, MD, MSCE, FAHA, chief of the laboratory of inflammation and cardiometabolic diseases at the NHLBI, and colleagues analyzed data from 97 patients with psoriasis who were assigned subcutaneous injections of adalimumab (Humira, AbbVie; n = 33; mean age, 44 years; 27% women), placebo injections (n = 31; mean age, 44 years; 35% women) or narrowband ultraviolet B phototherapy (n = 33; mean age, 42 years; 30% women). Patients had psoriasis for at least 6 months or moderate to severe psoriasis for at least 2 months. Exclusion criteria included those who received certain treatments for psoriasis before baseline.
An open-label extension started at week 12 for eligible patients. Patients assigned phototherapy were treated with adalimumab for 52 weeks, and those assigned adalimumab continued the same treatment for 40 weeks.
The primary outcome was change in vascular inflammation.
At 12 weeks, vascular inflammation did not change in patients assigned adalimumab compared with placebo (0.64%; 95% CI, –5.84 to 7.12) or the phototherapy group (–1.6%; 95% CI, –6.78 to 3.59). Vascular inflammation remained unchanged at 52 weeks compared with baseline in patients assigned adalimumab (0.02%; 95% CI, –2.85 to 2.9).
Inflammation markers
Patients assigned adalimumab had a reduction in inflammation, as shown by tumor necrosis factor-alpha, CRP, glycoprotein acetylation and interleukin-6. The phototherapy group only had reductions in interleukin-6 and CRP.
Those assigned adalimumab also had a reduction in glycoprotein acetylation and tumor necrosis factor at 12 and 52 weeks.
Insulin, leptin and adiponectin did not change in both treatment groups. Patients assigned phototherapy had an increase of HDL particle concentration at 12 weeks.
At 52 weeks, HDL particle concentration and cholesterol efflux were reduced in the adalimumab group.
“The cardiovascular effects of treatments for psoriasis are still being determined,” Gelfand said in an interview. “In the meantime, it is important that patients with psoriasis, especially when disease is more severe, undergo screenings for traditional CV risk factors (cholesterol, diabetes, blood pressure) and have these risk factors optimally managed.”
In a related editorial, Marwa Daghem, MBChB, clinical research fellow at the Centre for Cardiovascular Science at University of Edinburgh in Scotland, and David Newby, MD, PhD, professor of cardiology at the Centre for Cardiovascular Science, wrote: “The current trial is a major step forward in exploring how to assess the cardiovascular consequences of anti-inflammatory interventions in patients with psoriasis and this study has wider ramifications for other proinflammatory conditions associated with high cardiovascular risk. Further research is need to better elucidate the complex nature of the pathophysiological mechanisms underpinning inflammation, psoriasis and cardiovascular disease.” – by Darlene Dobkowski
For more information:
Joel M. Gelfand, MD, MSCE, can be reached at Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Blvd., Perelman Center for Advanced Medicine, 7th Floor, South Tower, Office No. 730, Philadelphia, PA 19104; email: joel.gelfand@uphs.upenn.edu.
Disclosures: Mehta reports he is a full-time U.S. government employee and receives research grants to the NHLBI from AbbVie, Celgene, Janssen and Novartis. Gelfand reports he consults for Coherus, Dermira, Janssen Biologics, Merck, Novartis, Regeneron, Dr. Reddy’s Laboratories, Sanofi and Pfizer; receives research grants from AbbVie, Celgene, Janssen, Novartis, Pfizer, Regeneron and Sanofi; received payment for CME work that was supported indirectly by AbbVie and Eli Lilly and is a co-patent holder of resiquimod for the treatment of cutaneous T-cell lymphoma. Daghem and Newby report no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
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