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Updated: Mar 19, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody mAb by Neutralizing TNF Using an In Vitro Bioanalytical Method
Published on: September 16, 2017
Effects of TNF-α Inhibitors on Subclinical Atherosclerosis and Endothelial Function in Patients with Psoriatic
Yasmine Makhlouf1, Hiba Boussaa1, Hiba Bettaieb2
1Department of Rheumatology, Mongi Slim University Hospital, Tunis, Tunisia. University of Tunis El Manar, Faculty of Medicine of Tunis, 1007, Tunisia.
Background:
Patients with psoriatic arthritis (PsA) are at increased risk of cardiovascular disease (CVD), largely driven by systemic inflammation and accelerated atherosclerosis. Tumor necrosis factor-alpha (TNF-alpha) inhibitors have transformed PsA treatment and may exert vascular protective effects. This systematic review aimed to evaluate the impact of TNF-alpha inhibitors on atherosclerosis and endothelial dysfunction in PsA patients.
Methods:
This systematic review followed the preferred reporting items for systematic reviews guidelines. A systematic search of PubMed, Scopus, Cochrane Library and Embase databases was conducted, identifying original articles up to September 3rd, 2024. Outcomes included carotid intima-media thickness (CIMT), endothelial function, carotid plaques, and biomarkers of inflammation, lipid metabolism, and coagulation. This systematic review was registered in prospero (CRD42023451234).
Results:
Five studies met the inclusion criteria and were published between 2011 and 2020. TNF-alpha inhibitors were associated with a reduction in CIMT in one study (0.7±0.18 vs 0.8±0.26; p=0.002 for the CCA and 0.94±0.31 vs 1.24±0.52; p<0.001 for the bulb), particularly with longer treatment duration (B:-0.317, p<0.001), while two studies reported progression of CIMT over time. Carotid plaque prevalence was significantly lower in TNF-alpha-treated patients compared to those on csDMARDs (15.8% vs 40.4%; p<0.0001). No consistent improvement in endothelial function, assessed by flow-mediated dilation or reactive hyperemia index was observed. TNF-alpha inhibitors consistently reduced inflammatory markers (CRP, ESR) and some lipid parameters (LDL-C, triglycerides). One study showed significant improvement in fibrinolytic and hemostatic markers (p<0.001), especially among patients achieving minimal disease activity (p<0.005).
Conclusion:
TNF-alpha inhibitors may offer vascular benefits in PsA by attenuating subclinical atherosclerosis and systemic inflammation. However, their effects on endothelial function remain unclear. Further large-scale, controlled, and long-term studies are warranted to confirm their cardioprotective role and define their impact on clinical cardiovascular outcomes in PsA patients.
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