GlycA Is a Novel Biomarker of Inflammation and Subclinical Cardiovascular Disease in Psoriasis

Joshi, Aditya; Lerman, Joseph B; Aberra, Tsion; Afshar, Mehdi; Teague, Heather; Rodante, Justin; Krishnamoorthy, Parasuram; Ng, Qimin; Aridi, Tarek; Salahuddin, Taufiq; Natarajan, Balaji; Lockshin, Benjamin; Ahlman, Mark A.; Chen, Marcus Y; Rader, Daniel J.; Reilly, Muredach P.; Remaley, Alan T.; Bluemke, David A.; Playford, Martin P.; Gelfand, Joel M.; Mehta, Nehal N.

doi:10.1161/circresaha.116.309637

Cited by 103 publications

(120 citation statements)

References 38 publications

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“…Atherothrombotic CVD is described as a chronic inflammatory condition, which involves processes mediated by cytokines and acute phase reactants . Indeed, higher CVD risk in chronic inflammatory conditions has been shown to be associated with higher GlycA levels . In addition, GlycA is shown to be associated with other measures of subclinical CVD.…”

Section: Discussionmentioning

confidence: 99%

Association Between Smoking and Serum GlycA and High‐Sensitivity C‐Reactive Protein Levels: The Multi‐Ethnic Study of Atherosclerosis (MESA) and Brazilian Longitudinal Study of Adult Health (ELSA‐Brasil)

Kianoush¹,

Bittencourt

Lotufo

et al. 2017

JAHA

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BackgroundInflammation is suggested to be a central feature of atherosclerosis, particularly among smokers. We studied whether inflammatory biomarkers GlycA and high‐sensitivity C‐reactive protein are associated with cigarette smoking.Methods and ResultsA total of 11 509 participants, 6774 from the MESA (Multi‐Ethnic Study of Atherosclerosis) and 4735 from ELSA‐Brasil (The Brazilian Longitudinal Study of Adult Health) were included. We evaluated the cross‐sectional association between multiple measures of smoking behavior and the inflammatory biomarkers, GlycA and high‐sensitivity C‐reactive protein, using regression models adjusted for demographic, anthropometric, and clinical characteristics. Participants were 57.7±11.1 years old and 46.4% were men. Never, former, and current smokers comprised 51.7%, 34.0%, and 14.3% of the population, respectively. Multivariable‐adjusted mean absolute difference in GlycA levels (μmol/L) with 95% confidence interval (CI) were higher for former (4.1, 95% CI, 1.7–6.6 μmol/L) and current smokers (19.9, 95% CI, 16.6–23.2 μmol/L), compared with never smokers. Each 5‐unit increase in pack‐years of smoking was associated with higher GlycA levels among former (0.7, 95% CI, 0.3–1.1 μmol/L) and current smokers (1.6, 95% CI, 0.8–2.4 μmol/L). Among former smokers, each 5‐year increase in time since quitting smoking was associated with lower GlycA levels (−1.6, 95% CI, −2.4 to −0.8 μmol/L) and each 10‐unit increase in number of cigarettes/day was associated with higher GlycA among current smokers (2.8, 95% CI, 0.5–5.2 μmol/L). There were similar significant associations between all measures of smoking behavior, and both log‐transformed GlycA and high‐sensitivity C‐reactive protein.ConclusionsAcute and chronic exposure to tobacco smoking is associated with inflammation, as quantified by both GlycA and high‐sensitivity C‐reactive protein. These biomarkers may have utility for the study and regulation of novel and traditional tobacco products.

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Section: Discussionmentioning

confidence: 99%

Association Between Smoking and Serum GlycA and High‐Sensitivity C‐Reactive Protein Levels: The Multi‐Ethnic Study of Atherosclerosis (MESA) and Brazilian Longitudinal Study of Adult Health (ELSA‐Brasil)

Kianoush¹,

Bittencourt

Lotufo

et al. 2017

JAHA

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“…Coronary plaque burden adjusted for luminal attenuation was evaluated across each of the main coronary arteries using the dedicated software QAngio CT (Medis, The Netherlands) by previously described methods by a single, blinded reader. 18, 21 Manual adjustment of inner lumen and outer vessel wall delineations were performed if needed. TB and NCB plaque volume indices, assessed as mm 2 , were calculated by dividing total vessel plaque volume by total vessel length and were attenuated for luminal intensity measures for accuracy.…”

Section: Methodsmentioning

confidence: 99%

Coronary Plaque Characterization in Psoriasis Reveals High-Risk Features That Improve After Treatment in a Prospective Observational Study

et al. 2017

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Background Psoriasis, a chronic inflammatory disease associated with an accelerated risk of MI, provides an ideal human model to study inflammatory atherogenesis in vivo. We hypothesized that the increased cardiovascular risk observed in psoriasis would be partially attributable to an elevated subclinical coronary artery disease (CAD) burden composed of non-calcified plaques with high-risk features. However, inadequate efforts have been made to directly measure CAD in this vulnerable population. As such, we sought to compare total (TB) and non-calcified (NCB) coronary plaque burden, and high-risk plaque (HRP) prevalence, between psoriasis patients (n=105), hyperlipidemic patients eligible for statin therapy under NCEP-ATP III guidelines (n=100) who were ~10 years older, and non-psoriasis healthy volunteers (HV) (n=25). Methods Patients underwent coronary computed-tomography angiography (CCTA) for TB and NCB quantification, and HRP identification, defined as low-attenuation (<30 HU), positive remodeling (>1.10), and spotty calcification. A consecutive sample of the first 50 psoriasis patients were scanned again at 1 year following therapy. Results Despite being younger and at lower traditional risk than hyperlipidemic patients, psoriasis patients had increased NCB (mean±S.D.:1.18±0.33 vs 1.11±0.32, p=0.02), and similar HRP prevalence (p=0.58). Furthermore, compared to HV, psoriasis patients had increased TB (1.22±0.31 vs 1.04±0.22, p=0.001), NCB (1.18±0.33 vs 1.03±0.21, p=0.004), and HRP prevalence beyond traditional risk (OR=6.0, 95% CI: 1.1–31.7; p=0.03). Finally, amongst psoriasis patients followed for 1-year, improvement in psoriasis severity associated with improvement in TB (β=0.45, 0.23–0.67; p<0.001) and NCB (β=0.53, 0.32–0.74; p<0.001) beyond traditional risk factors. Conclusions Psoriasis patients had greater NCB and increased HRP prevalence than HV. Additionally, psoriasis patients had elevated NCB and equivalent HRP prevalence as older, hyperlipidemic patients. Finally, modulation of target organ inflammation (eg. skin) associated with an improvement in NCB at 1 year, suggesting that control of remote sites of inflammation may translate into reduced CAD risk.

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“…As levels of CRP decrease, cardiovascular risk lowers . However, there is evidence that questions the clinical usefulness of CRP for evaluating cardiovascular risk among individuals with inflammatory conditions such as psoriasis, indicating a need for alternative CVD risk biomarkers in patients with underlying inflammatory conditions …”

Section: Goals For Treating Systemic Inflammation In Psoriasismentioning

confidence: 99%

Management of psoriasis as a systemic disease: what is the evidence?

2019

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Summary Background Psoriasis is a chronic, systemic immune‐mediated disease characterized by development of erythematous, indurated, scaly, pruritic and often painful skin plaques. Psoriasis pathogenesis is driven by proinflammatory cytokines and psoriasis is associated with increased risk for comorbidities, including, but not limited to, psoriatic arthritis, cardiovascular disease, diabetes mellitus, obesity, inflammatory bowel disease and nonalcoholic fatty liver disease compared with the general population. Objectives To explore the pathophysiological relationship between psoriasis and its common comorbidities and discuss the need for new treatment paradigms that include strategies to reduce systemic inflammation in patients with moderate‐to‐severe psoriasis. Methods This narrative review summarizes the published evidence related to the ability of biological therapies to ameliorate the consequences of systemic inflammation in patients with psoriasis. Results Current evidence suggests that preventing damage associated with inflammation, and preventing development of future inflammatory damage and comorbidities, may be a potentially achievable treatment goal for many patients with moderate‐to‐severe plaque psoriasis when biological therapies are utilized early in the disease. Encouraging data from recent studies suggest that the loftier goal of reversing existing inflammatory damage and improving signs and symptoms of inflammatory comorbidities could also possibly be attainable. Conclusions Results from ongoing prospective studies regarding the effects of biologics on markers of systemic inflammation in patients with psoriasis will strengthen the clinical evidence base that can be used to inform treatment decisions for patients with moderate‐to‐severe psoriasis. What's already known about this topic? Psoriasis is a systemic inflammatory disease and treatments are needed to optimize patient outcomes. What does this study add? This review discusses new psoriasis treatment paradigms that may potentially reduce effects of systemic inflammation. Evidence demonstrating that biological treatment may prevent or reverse inflammatory damage associated with psoriasis comorbidities is reviewed.

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GlycA Is a Novel Biomarker of Inflammation and Subclinical Cardiovascular Disease in Psoriasis

Cited by 103 publications

References 38 publications

Association Between Smoking and Serum GlycA and High‐Sensitivity C‐Reactive Protein Levels: The Multi‐Ethnic Study of Atherosclerosis (MESA) and Brazilian Longitudinal Study of Adult Health (ELSA‐Brasil)

Association Between Smoking and Serum GlycA and High‐Sensitivity C‐Reactive Protein Levels: The Multi‐Ethnic Study of Atherosclerosis (MESA) and Brazilian Longitudinal Study of Adult Health (ELSA‐Brasil)

Coronary Plaque Characterization in Psoriasis Reveals High-Risk Features That Improve After Treatment in a Prospective Observational Study

Management of psoriasis as a systemic disease: what is the evidence?

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