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Published on: September 16, 2017
Decrease of asymmetric dimethyl arginine after anti-TNF therapy in patients with rheumatoid arthritis
Francesca Romana Spinelli1, Manuela Di Franco, Alessio Metere
1Department of Internal Medicine and Medical Specialities, Rheumatology Unit, Sapienza University of Rome, 00161, Rome, Italy.
Tumor necrosis factor (TNF) inhibitors may reduce levels of asymmetric dimethyl arginine (ADMA), a marker linked to cardiovascular risk in rheumatoid arthritis (RA). Further research is needed to confirm ADMA
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Pharmacology
Background:
- Chronic inflammatory diseases like rheumatoid arthritis (RA) are linked to higher rates of atherosclerosis and cardiovascular events.
- Asymmetric dimethyl arginine (ADMA) impairs endothelial function, an early stage of atherosclerosis, by inhibiting nitric oxide synthase.
- Tumor necrosis factor (TNF) can inhibit ADMA's enzymatic degradation, suggesting anti-TNF therapies might normalize ADMA levels.
Purpose of the Study:
- To investigate the impact of TNF inhibitors on serum ADMA levels in patients with RA.
- To explore the potential of anti-TNF therapy in managing cardiovascular risk factors associated with RA.
Main Methods:
- The study assessed serum ADMA levels in patients undergoing treatment with TNF inhibitors for RA.
- Observational study design to evaluate the effect of anti-TNF agents on ADMA concentrations.
Main Results:
- Preliminary findings suggest that anti-TNF drugs may influence serum ADMA levels in RA patients.
- A potential correlation between TNF inhibition and ADMA level modulation was observed.
Conclusions:
- Anti-TNF agents might play a role in regulating ADMA levels in rheumatoid arthritis.
- Longer-term studies are required to validate the role of ADMA in cardiovascular risk assessment for RA patients treated with anti-TNF therapy.
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