» Articles » PMID: 34808541

Heightened Splenic and Bone Marrow Uptake of F-FDG PET/CT is Associated with Systemic Inflammation and Subclinical Atherosclerosis by CCTA in Psoriasis: An Observational Study

Abstract

Background And Aims: Psoriasis is an immune-mediated inflammatory disease with increased risk of myocardial infarction. Preclinical studies in psoriasis models show an association between chronic inflammation and immune cell proliferation in the spleen and bone marrow (BM). We sought to test the hypothesis that splenic and BM F-fluorodeoxyglucose (F-FDG) uptake is heightened in psoriasis and that higher uptake associates with systemic inflammation and subclinical atherosclerotic disease measures in this cohort.

Methods: Multimodality imaging and biomarker assays were performed in 240 participants (210 with psoriasis and 30 healthy). Splenic and BM uptake was obtained using F-FDG positron emission tomography/computed tomography (PET/CT). Coronary artery plaque characteristics including non-calcified burden (NCB) and lipid rich necrotic core (LRNC) were quantified using a dedicated software for CT angiography. All analyses were performed with StataIC 16 (Stata Corp., College Station, TX, USA).

Results: Splenic and BM F-FDG uptake was increased in psoriasis (vs. healthy volunteers) and significantly associated with proatherogenic lipids, immune cells and systemic inflammation. Higher splenic F-FDG uptake associated with higher total coronary burden (β = 0.37; p<0.001), NCB (β = 0.39; p<0.001), and LRNC (β = 0.32; p<0.001) in fully adjusted models. Similar associations were seen for BM F-FDG uptake in adjusted models (β = 0.38; β = 0.41; β = 0.24; respectively, all p<0.001).

Conclusions: Heightened splenic and BM uptake of F-FDG is associated with proatherogenic lipids, immune cells, inflammatory markers and coronary artery disease. These findings provide insights into atherogenic mechanisms in psoriasis and suggest that immune cell proliferation in the spleen and BM is associated with subclinical atherosclerosis.

Citing Articles

HDL-associated vitamin D binding protein levels are inversely associated with necrotic plaque burden in psoriasis.

Playford M, Li H, Dey A, Florida E, Teague H, Gordon S Atheroscler Plus. 2025; 59():32-38.

PMID: 39811778 PMC: 11732513. DOI: 10.1016/j.athplu.2024.12.002.


The spleen in ischaemic heart disease.

Heusch G, Kleinbongard P Nat Rev Cardiol. 2025; .

PMID: 39743566 DOI: 10.1038/s41569-024-01114-x.


Recent Advances in Targeted Management of Inflammation In Atherosclerosis: A Narrative Review.

Zubiran R, Neufeld E, Dasseux A, Remaley A, Sorokin A Cardiol Ther. 2024; 13(3):465-491.

PMID: 39031302 PMC: 11333429. DOI: 10.1007/s40119-024-00376-3.


Cortico-limbic interactions and carotid atherosclerotic burden during chronic stress exposure.

Gharios C, van Leent M, Chang H, Abohashem S, OConnor D, Osborne M Eur Heart J. 2024; 45(19):1753-1764.

PMID: 38753456 PMC: 11107120. DOI: 10.1093/eurheartj/ehae149.


Molecular Imaging of Fibroblast Activation in Rabbit Atherosclerotic Plaques: a Preclinical PET/CT Study.

Ji T, Zan C, Li L, Cao J, Su Y, Wang H Mol Imaging Biol. 2024; 26(4):680-692.

PMID: 38664355 DOI: 10.1007/s11307-024-01919-9.


References
1.
Kaiser H, Kvist-Hansen A, Krakauer M, Gortz P, Henningsen K, Wang X . Association between Vascular Inflammation and Inflammation in Adipose Tissue, Spleen, and Bone Marrow in Patients with Psoriasis. Life (Basel). 2021; 11(4). PMC: 8065955. DOI: 10.3390/life11040305. View

2.
Trompouki E, Mullen L, Fernandez-Reyes D, Yodoi J, Kim S, Schuettpelz L . Editorial: Inflammatory Signaling in Bone Marrow Failure and Hematopoietic Malignancy. Front Immunol. 2017; 8:660. PMC: 5454062. DOI: 10.3389/fimmu.2017.00660. View

3.
Goyal A, Dey A, Chaturvedi A, Elnabawi Y, Aberra T, Chung J . Chronic Stress-Related Neural Activity Associates With Subclinical Cardiovascular Disease in Psoriasis: A Prospective Cohort Study. JACC Cardiovasc Imaging. 2018; 13(2 Pt 1):465-477. PMC: 6506409. DOI: 10.1016/j.jcmg.2018.08.038. View

4.
King K, Goodell M . Inflammatory modulation of HSCs: viewing the HSC as a foundation for the immune response. Nat Rev Immunol. 2011; 11(10):685-92. PMC: 4154310. DOI: 10.1038/nri3062. View

5.
Mitroulis I, Kalafati L, Bornhauser M, Hajishengallis G, Chavakis T . Regulation of the Bone Marrow Niche by Inflammation. Front Immunol. 2020; 11:1540. PMC: 7396603. DOI: 10.3389/fimmu.2020.01540. View