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The relationship between duration of psoriasis, vascular inflammation, and cardiovascular events - 14/09/17

Doi : 10.1016/j.jaad.2017.06.028 
Alexander Egeberg, MD, PhD a, , Lone Skov, MD, PhD, DMSc a, Aditya A. Joshi, MD b, Lotus Mallbris, MD, PhD c, Gunnar H. Gislason, MD, PhD d, e, f, Jashin J. Wu, MD g, Justin Rodante, PA-C b, Joseph B. Lerman, MD b, Mark A. Ahlman, MD b, Joel M. Gelfand, MD, MSCE h, Nehal N. Mehta, MD, MSCE b,
a Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark 
d Department of Cardiology, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark 
b National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 
c Unit of Dermatology and Venerology, Karolinska Institutet, Stockholm, Sweden 
e Danish Heart Foundation, Copenhagen, Denmark 
f National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark 
g Kaiser Permanente Los Angeles Medical Center, Los Angeles, California 
h Department of Dermatology, Department of Biostatistics and Epidemiology, and Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, Pennsylvania 

Correspondence to: Alexander Egeberg, MD, PhD, Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University of Copenhagen, Kildegsity of 28, Hellerup 2900, Denmark.Department of Dermatology and AllergyHerlev and Gentofte HospitalUniversity of CopenhagenKildegsity of 28Hellerup2900Denmark∗∗Nehal N. Mehta, MD, MSCE, Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung and Blood Institute, 10 Center Dr, Bethesda, MD 20892.Section of Inflammation and Cardiometabolic DiseasesNational Heart, Lung and Blood Institute10 Center DrBethesdaMD20892

Abstract

Background

Psoriasis is associated with risk of cardiovascular (CV) disease (CVD) and a major adverse CV event (MACE). Whether psoriasis duration affects risk of vascular inflammation and MACEs has not been well characterized.

Objectives

We utilized two resources to understand the effect of psoriasis duration on vascular disease and CV events: (1) a human imaging study and (2) a population-based study of CVD events.

Methods

First, patients with psoriasis (N = 190) underwent fludeoxyglucose F 18 positron emission tomography/computed tomography (duration effect reported as a β-coefficient). Second, MACE risk was examined by using nationwide registries (adjusted hazard ratios in patients with psoriasis (n = 87,161) versus the general population (n = 4,234,793).

Results

In the human imaging study, patients were young, of low CV risk by traditional risk scores, and had a high prevalence of cardiometabolic diseases. Vascular inflammation by fludeoxyglucose F 18 positron emission tomography/computed tomography was significantly associated with disease duration (β = 0.171, P = .002). In the population-based study, psoriasis duration had strong relationship with MACE risk (1.0% per additional year of psoriasis duration [hazard ratio, 1.010; 95% confidence interval, 1.007-1.013]).

Limitations

These studies utilized observational data.

Conclusion

We found detrimental effects of psoriasis duration on vascular inflammation and MACE, suggesting that cumulative duration of exposure to low-grade chronic inflammation may accelerate vascular disease development and MACEs. Providers should consider inquiring about duration of disease to counsel for heightened CVD risk in psoriasis.

Le texte complet de cet article est disponible en PDF.

Key words : cardiovascular disease, 18-FDG PET/CT, inflammation, psoriasis

Abbreviations used : CV, CVD, CI, 18-FDG, 18-FDG PET/CT, HR, MACE, MI, NIH, PUVA, SD, TBR, UVB


Plan


 The work at the National Institutes of Health cohort was supported by the National Heart, Lung and Blood Institute Intramural Research Program (HL006193-02). Dr Gelfand's role in this study was supported by National Institute of Arthritis and Musculoskeletal and Skin Diseases grant K24-AR064310.
 Disclosure: Dr Egeberg has received research funding from Pfizer and Eli Lilly and honoraria as consultant and/or speaker from Pfizer, Eli Lilly, Novartis, Galderma, and Janssen Pharmaceuticals. Dr Skov has been a paid speaker for Pfizer, AbbVie, Eli Lilly, Novartis, and LEO Pharma and has been a consultant or served on advisory boards with Pfizer, AbbVie, Janssen Cilag, Novartis, Eli Lilly, LEO Pharma, and Sanofi; she has served as an investigator for Pfizer, AbbVie, Eli Lilly, Novartis, Amgen, Regeneron, and LEO Pharma and received research and educational grants from Pfizer, AbbVie, Novartis, Sanofi, Janssen Cilag, and Leo Pharma. Dr Mallbris is currently employed by Eli Lilly. Dr Gislason is supported by an unrestricted research scholarship from the Novo Nordisk Foundation and reports research grants from Pfizer, Bristol-Myers Squibb, AstraZeneca, Bayer, and Boehringer Ingelheim. Dr Wu has received research funding from AbbVie, Amgen, AstraZeneca, Boehringer Ingelheim, Coherus Biosciences, Dermira, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Regeneron, Sandoz, and Sun Pharmaceutical Industries; he is a consultant for AbbVie, Amgen, Celgene, Dermira, Eli Lilly, Pfizer, Regeneron, and Sun Pharmaceutical Industries. In the previous 12 months Dr Gelfand has served as a consultant for and received honoraria from Coherus (data safety and monitoring board), Dermira, Janssen Biologics, Merck (data safety and monitoring board), Novartis Corp, Regeneron, Sanofi and Pfizer Inc; he receives research grants (to the Trustees of the University of Pennsylvania) from Abbvie, Janssen, Novartis Corp, Regeneron, Sanofi, Celgene, and Pfizer Inc; and he has received payment for CME work related to psoriasis that was supported indirectly by Lilly and Abbvie. Dr Gelfand is a co–patent holder of resiquimod for treatment of cutaneous T-cell lymphoma. Dr Mehta is a full-time US government employee and receives research grants to the NHLBI from AbbVie, Janssen, Novartis and Celgene. No other potential conflicts of interest were declared by the authors.
 Dr Egeberg (Danish cohort) and Dr Mehta (National Institutes of Health cohort) had full access to all of the data in the study and take responsibility for integrity of the data and accuracy of the data analysis. Drs Egeberg, Skov, Mallbris, Gislason, Gelfand, and Mehta are responsible for the study concept and design. Drs Joshi, Ahlman, Rodante, Lerman, Gelfand, and Mehta (National Institutes of Health cohort) and Drs Egeberg and Gislason (Danish cohort) are responsible for acquisition, analysis, and interpretation of data. Drs Egeberg and Mehta are responsible for drafting of the manuscript. All authors the are responsible for critical revision of the manuscript for important intellectual content. Drs Egeberg, Gislason and Joshi are responsible for statistical analysis. Dr Mehta obtained funding. Drs Egeberg, Skov, Gislason, and Mehta are responsible for administrative, technical, or material support, and Drs Egeberg and Mehta are responsible for study supervision.
 Reprints not available from the authors.


© 2017  American Academy of Dermatology, Inc. Tous droits réservés.
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Vol 77 - N° 4

P. 650 - octobre 2017 Retour au numéro
Article précédent Article précédent
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