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Key clinical point: Inflammatory and metabolic parameters, including visceral adiposity, potentially contribute to subclinical coronary artery disease (CAD) in patients with psoriatic arthritis (PsA).
Major finding: CAD was significantly associated with visceral adiposity (standardized 
0.681; P = .002), and fluorodeoxyglucose (FDG) uptake in the bone marrow (standardized 0.488; P = .008), liver (standardized 0.619; P < .001), spleen (standardized 0.523; P = .004), and subcutaneous adipose tissue (standardized 0.524; P = .003). Visceral (P = .005) and subcutaneous (P = .004) adiposity and liver FDG uptake (P = .03) were higher in patients with PsA vs. controls without PsA.
Study details: Findings are from a cross-sectional analysis of a prospective study including 39 patients with biologic-naive PsA and 56 age-sex matched controls without PsA.
Disclosures: This study was funded by the US National Institute of Allergy and Infectious Disease, the US National Heart, Lung, and Blood Institute, and National Psoriasis Foundation. N Mehta declared serving as consultant and receiving grants and other payments from several sources.
Source: Schwartz DM et al. PET/CT-based characterization of 18F-FDG uptake in various tissues reveals novel potential contributions to coronary artery disease in psoriatic arthritis. Front Immunol. 2022;13:909760 (Jun 2). Doi: 10.3389/fimmu.2022.909760
Key clinical point: Inflammatory and metabolic parameters, including visceral adiposity, potentially contribute to subclinical coronary artery disease (CAD) in patients with psoriatic arthritis (PsA).
Major finding: CAD was significantly associated with visceral adiposity (standardized 0.681; P = .002), and fluorodeoxyglucose (FDG) uptake in the bone marrow (standardized 0.488; P = .008), liver (standardized 0.619; P < .001), spleen (standardized 0.523; P = .004), and subcutaneous adipose tissue (standardized 0.524; P = .003). Visceral (P = .005) and subcutaneous (P = .004) adiposity and liver FDG uptake (P = .03) were higher in patients with PsA vs. controls without PsA.
Study details: Findings are from a cross-sectional analysis of a prospective study including 39 patients with biologic-naive PsA and 56 age-sex matched controls without PsA.
Disclosures: This study was funded by the US National Institute of Allergy and Infectious Disease, the US National Heart, Lung, and Blood Institute, and National Psoriasis Foundation. N Mehta declared serving as consultant and receiving grants and other payments from several sources.
Source: Schwartz DM et al. PET/CT-based characterization of 18F-FDG uptake in various tissues reveals novel potential contributions to coronary artery disease in psoriatic arthritis. Front Immunol. 2022;13:909760 (Jun 2). Doi: 10.3389/fimmu.2022.909760
Key clinical point: Inflammatory and metabolic parameters, including visceral adiposity, potentially contribute to subclinical coronary artery disease (CAD) in patients with psoriatic arthritis (PsA).
Major finding: CAD was significantly associated with visceral adiposity (standardized 0.681; P = .002), and fluorodeoxyglucose (FDG) uptake in the bone marrow (standardized 0.488; P = .008), liver (standardized 0.619; P < .001), spleen (standardized 0.523; P = .004), and subcutaneous adipose tissue (standardized 0.524; P = .003). Visceral (P = .005) and subcutaneous (P = .004) adiposity and liver FDG uptake (P = .03) were higher in patients with PsA vs. controls without PsA.
Study details: Findings are from a cross-sectional analysis of a prospective study including 39 patients with biologic-naive PsA and 56 age-sex matched controls without PsA.
Disclosures: This study was funded by the US National Institute of Allergy and Infectious Disease, the US National Heart, Lung, and Blood Institute, and National Psoriasis Foundation. N Mehta declared serving as consultant and receiving grants and other payments from several sources.
Source: Schwartz DM et al. PET/CT-based characterization of 18F-FDG uptake in various tissues reveals novel potential contributions to coronary artery disease in psoriatic arthritis. Front Immunol. 2022;13:909760 (Jun 2). Doi: 10.3389/fimmu.2022.909760