Haley B Naik1, Balaji Natarajan1, Elena Stansky1, Mark A Ahlman1, Heather Teague1, Taufiq Salahuddin1, Qimin Ng1, Aditya A Joshi1, Parasuram Krishnamoorthy1, Jenny Dave1, Shawn M Rose1, Julia Doveikis1, Martin P Playford1, Ronald B Prussick1, Alison Ehrlich1, Mariana J Kaplan1, Benjamin N Lockshin1, Joel M Gelfand1, Nehal N Mehta2. 1. From the Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute (H.B.N., B.N., E.S., H.T., T.S., Q.N., A.A.J., J.D., S.M.R., J.D., M.P.P., N.N.M.), Dermatology Branch, Center for Cancer Research, National Cancer Institute (H.B.N.), Molecular Biomedical Imaging Laboratory (M.A.A.), and Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (M.J.K.), National Institutes of Health, Bethesda, MD; Englewood Hospital, NJ (P.K.); The Washington Dermatology Center, Rockville, MD (R.B.P.); Department of Dermatology, George Washington Hospital, Washington DC (R.B.P., A.E.); DermAssociates, Silver Spring, MD (B.N.L.); and Department of Dermatology, Department of Biostatistics and Epidemiology, and Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia (J.M.G.). 2. From the Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute (H.B.N., B.N., E.S., H.T., T.S., Q.N., A.A.J., J.D., S.M.R., J.D., M.P.P., N.N.M.), Dermatology Branch, Center for Cancer Research, National Cancer Institute (H.B.N.), Molecular Biomedical Imaging Laboratory (M.A.A.), and Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (M.J.K.), National Institutes of Health, Bethesda, MD; Englewood Hospital, NJ (P.K.); The Washington Dermatology Center, Rockville, MD (R.B.P.); Department of Dermatology, George Washington Hospital, Washington DC (R.B.P., A.E.); DermAssociates, Silver Spring, MD (B.N.L.); and Department of Dermatology, Department of Biostatistics and Epidemiology, and Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia (J.M.G.). nehal.mehta@nih.gov.
Abstract
OBJECTIVE: To understand whether directly measured psoriasis severity is associated with vascular inflammation assessed by (18)F-fluorodeoxyglucose positron emission tomography computed tomography. APPROACH: In-depth cardiovascular and metabolic phenotyping was performed in adult psoriasis patients (n=60) and controls (n=20). Psoriasis severity was measured using psoriasis area severity index. Vascular inflammation was measured using average aortic target-to-background ratio using (18)F-fluorodeoxyglucose positron emission tomography computed tomography. RESULTS: Both the psoriasis patients (28 men and 32 women, mean age 47 years) and controls (13 men and 7 women, mean age 41 years) were young with low cardiovascular risk. Psoriasis area severity index scores (median 5.4; interquartile range 2.8-8.3) were consistent with mild-to-moderate skin disease severity. Increasing psoriasis area severity index score was associated with an increase in aortic target-to-background ratio (β=0.41, P=0.001), an association that changed little after adjustment for age, sex, and Framingham risk score. We observed evidence of increased neutrophil frequency (mean psoriasis, 3.7±1.2 versus 2.9±1.2; P=0.02) and activation by lower neutrophil surface CD16 and CD62L in blood. Serum levels of S100A8/A9 (745.1±53.3 versus 195.4±157.8 ng/mL; P<0.01) and neutrophil elastase-1 (43.0±2.4 versus 30.8±6.7 ng/mL; P<0.001) were elevated in psoriasis. Finally, S100A8/A9 protein was related to both psoriasis skin disease severity (β=0.53; P=0.02) and vascular inflammation (β=0.48; P=0.02). CONCLUSIONS: Psoriasis severity is associated with vascular inflammation beyond cardiovascular risk factors. Psoriasis increased neutrophil activation and neutrophil markers, and S100A8/A9 was related to both skin disease severity and vascular inflammation.
OBJECTIVE: To understand whether directly measured psoriasis severity is associated with vascular inflammation assessed by (18)F-fluorodeoxyglucose positron emission tomography computed tomography. APPROACH: In-depth cardiovascular and metabolic phenotyping was performed in adult psoriasispatients (n=60) and controls (n=20). Psoriasis severity was measured using psoriasis area severity index. Vascular inflammation was measured using average aortic target-to-background ratio using (18)F-fluorodeoxyglucose positron emission tomography computed tomography. RESULTS: Both the psoriasispatients (28 men and 32 women, mean age 47 years) and controls (13 men and 7 women, mean age 41 years) were young with low cardiovascular risk. Psoriasis area severity index scores (median 5.4; interquartile range 2.8-8.3) were consistent with mild-to-moderate skin disease severity. Increasing psoriasis area severity index score was associated with an increase in aortic target-to-background ratio (β=0.41, P=0.001), an association that changed little after adjustment for age, sex, and Framingham risk score. We observed evidence of increased neutrophil frequency (mean psoriasis, 3.7±1.2 versus 2.9±1.2; P=0.02) and activation by lower neutrophil surface CD16 and CD62L in blood. Serum levels of S100A8/A9 (745.1±53.3 versus 195.4±157.8 ng/mL; P<0.01) and neutrophil elastase-1 (43.0±2.4 versus 30.8±6.7 ng/mL; P<0.001) were elevated in psoriasis. Finally, S100A8/A9 protein was related to both psoriasis skin disease severity (β=0.53; P=0.02) and vascular inflammation (β=0.48; P=0.02). CONCLUSIONS:Psoriasis severity is associated with vascular inflammation beyond cardiovascular risk factors. Psoriasis increased neutrophil activation and neutrophil markers, and S100A8/A9 was related to both skin disease severity and vascular inflammation.
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