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Treatment with Tocilizumab can significantly regulate the level of
adipokines, resulting in lower cardiovascular risk in rheumatoid arthritis
patients.
According to a recent study of Clinical and Experimental Rheumatology, Tocilizumab (TCZ), an interleukin-6 receptor antagonist, found to have good cardiovascular safety as it significantly regulates the adiponectin and chemerin serum levels, without affecting treatment response among rheumatoid arthritis (RA) patients. Adipokines have an essential part in rheumatoid arthritis pathophysiology and present a connection between the disease and overweight. It also shows an association with increased cardiovascular (CV) risk along with altered disease-modifying anti-rheumatic drugs response.
This study aimed to discover the effects of intravenous (IV) tocilizumab (TCZ) on serum levels of visfatin, adiponectin, chemerin, leptin and resistin. A total of 44 patients received 8 mg/kg IV TCZ once every 4 weeks for six months. Out of these 44 patients; 20 received only TCZ and the rest of the patients received TCZ with MTX (methotrexate). Health Assessment Questionnaire (HAQ), body mass index and DAS28-ESR was measured at baseline and each month before every infusion. Adipokines serum levels were taken at baseline and six months after the treatment.
Both groups showed remarkable improved HAQ, ESR and DAS28-ESR at the follow-up end. During the evaluation of lipid profile it was observed that only total cholesterol levels exhibited a rise. All the patients presented with increased adiponectin and decreased chemerin levels, without any significant biochemical and clinical parameters. Resistin and leptin levels showed no changes. These findings explain that TCZ can regulate chemerin and adiponectin serum levels in RA patients, freely from the disease treatment response and this explains the CV safety of TCZ.
Clinical and Experimental Rheumatology
Tocilizumab modulates serum levels of adiponectin and chemerin in patients with rheumatoid arthritis: potential cardiovascular protective role of IL-6 inhibition.
Fioravanti A et al.
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