Background: Patients with rheumatoid arthritis (RA) have an increased risk of cardiovascular (CV) diseases. TNFa blockade in RA patients has been associated with weight gain, increase in fat mass and variations in serum adipokines. Adiponectin (Adp), a protein produced by adipocytes, plays a beneficial role in insulin sensitivity and CV disease prevention, especially its high molecular weight (HMW) isoform.

Objectives: To analyse the changes in serum adipokines and especially Adp (total and HMW) and body composition during TCZ therapy in RA.

Methods: Multicenter open-label study. All patients enrolled had active RA (2010 ACR/EULAR criteria and DAS28≥ 3.2) with previous inadequate response to a csDMARDs and/or bDMARDs. They all were TCZ naïve and received TCZ IV. Patients were evaluated at baseline,1,3,6 and 12 months. Clinical assessment included body mass index (BMI), waist circumference, DAS28 and HAQ scores. Laboratory parameters of inflammation (ESR, CRP, IL-6), lipid parameters (total chol., LDL and HDL chol., triglycerides), metabolic parameters (glycemia, insulin), serum Adp (total and HMW), leptin, resistin, and ghrelin were measured at each time point. Body composition (lean mass, fat mass,% of fat, fat in the android and gynoid regions) was evaluated at baseline, 6, and 12 months (DEXA, Lunar GE). Our primary criteria was the changes in Adp (total and HMW) at 6 months.

Results: 107 patients (78 F; mean age ± SD: 56.6 yr ± 13.5; disease duration: 9.9 yr ± 8.1; previous bDMARD: 64.5%; corticosteroids: 69%; concomitant csDMARD: 72.8%) were included. 97 were still on treatment at month 6 and 77 completed the study. Most of the patients (95%) received TCZ 8 mg/kg by infusion. Patients were responding to TCZ with a significant DAS28 decrease between baseline and months 6 and 12 (p<0.0001). HAQ, ESR, and CRP levels significantly decreased along the study (p<0.0001). BMI and abdominal circumference significantly increased at month 6 and 12, as well as lean mass (p=0.0097 at month 6 and 0.021 at month 12). Fat mas,% of fat and android fat did not change over the study. Total chol and LDL chol increased while glycaemia and insulin remained stable. Both total and HMW Adp increased from baseline to month 6 and month 12 (total Adp: baseline vs month 6: p=0.055; HMW Adp: baseline vs month 6: p=0.02, baseline vs month 12: p=0.057). Serum leptin, resistin and ghrelin did not change during the follow-up.

Conclusion: These variations in Adp during TCZ treatment may have a positive impact on the CV risk of RA patients and may contribute to the protective role of TCZ against the CV burden in RA.

Acknowledgement: ADIPRAT study group This work was supported by a grant from ROCHE CHUGAI

Disclosure of Interests: ERIC TOUSSIROT Grant/research support from: Roche Chugai, Hubert MAROTTE: None declared, Denis Mulleman Speakers bureau: Pfizer, Novartis, Grifols, Gregoire CORMIER: None declared, Fabienne COURY-LUCAS: None declared, Philippe Gaudin Speakers bureau: Roche, Chugai, BMS, Abbvie, Servier, Pfizer, MSD, UCB, ESAOTE, Genévrier, Janssen, Novartis, Lilly, Biogen, Amge, Emmanuelle Dernis: None declared, Christine BONNET: None declared, Richard DAMADE: None declared, Jean Luc GRAUER: None declared, Tassadit AIT-ABDESSELAM: None declared, Caroline GUILLIBERT KARRAS : None declared, Frederic Lioté Grant/research support from: institutional grants from Grunenthal, Ipsen Pharma/Menarini, Novartis, SOBI for the European Crystal Network Workshops, Consultant for: Grunenthal, Novartis, Pascal Hilliquin Consultant for: Roche SAS, Antoinette SACCHI: None declared, Jean Marie BERTHELOT: None declared, Marc PUYRAVEAU: None declared, Gilles DUMOULIN: None declared

DOI: 10.1136/annrheumdis-2019-eular.4675