Background:The Janus Kinase (JAKi) inhibitors Baricitinib (BAR) and Tofacitinib (TOF) are indicated for moderate to severe active rheumatoid arthritis (RA). Data about safety, effectiveness in refractory patients and adherence in real clinical practice in our population are scarce.Objectives:An evaluation of safety, adherence and reasons to consider suspension of JAKi in routine clinical practice.Methods:Retrospective observational study of patients with RA treated with BAR and TOF according to usual clinical practice between September 2017 - December 2019. Data were collected from the electronic medical record and from the Dominion® Outpatient Drug Dispensing program.Demographic, clinical, laboratory and treatment-related variables were collected, including reasons for discontinuing JAKi (inefficiency and toxicity). Adherence was calculated using the Compliance Questionnaire on Rheumatology (CQR-5), and the average possession ratio (RMP), which is defined as the number of days with treatment dispensed between the total days of the period analyzed, considering the adherent patient when RMP had a ≥ 0.8.Laboratory abnormalities were defined according to normal limit values (NLV) and specifications of data sheet. A descriptive analysis was performed using proportions, medians and interquartile ranges (IQR) using the SPSS v.15 program.Results:Thirty patients were included in treatment with BAR and nine with TOF. The median age was 62.9 (RIQ 49.9-74.4), 34 (87.2%) were women, 28 (71.2%) anti-CCP and 32 (82.1%) were rheumatoid factor positive, with erosive disease in 34 (87,2%) patients. In the previous treatment, 9 (23.1%) were naive to biological, 6 (15.4%) had received 1 biological, 18 (46.1%) 2 biologicals, and 6 (15.4%) ≥ 3 biologicals. The median treatment time was 8.4 months (RIQ 6.5-20.3) in BAR and 13.2 (RIQ 3.9-20.7) in TOF.The reasons for consider suspension shown in Table 1.Table 1.Treatment DiscontinuationBARICITINIBInitial DAS28[median (IQR)]Final DAS28[median (IQR)]Continue treatmentn (%): 17/30 (55.6)4.20 (2.95-5.72)2.60 (1.70-2.77)Reasons for suspension-Refractory n (%): 7/13 (55.8%)4.38 (4.16-5.43)4,16 (3.56-5.23)-Side effects n (%): 4/13 (30.7)4.16 (3.45-4.84)3.15 (2.69-4.41) ◦Thrombocytosis (1) ◦Herpes Zoster (1) ◦Anemia (1) ◦Tubaritis (1)-Patient decisión n (%): 2/13 (15.4)TOFACITINIBContinue treatmentn (%): 6/9 (66.6)4.82 (3.28-6.20)2.61 (2.45-3.70)Reasons for suspension-Refractory n (%): 2/3 (66.6)5.27 (5.23-5.31)5.48 (5.04-5.92)-Side effects n (%): 1/3 (33.33)Based on the CQR5 questionnaire, all patients treated with BAR and TOF were adherent “HIGH” class, and a median of RMP = 1.01 (IQR = 0.93-1.06) was obtained for BAR and RMP = 1, 00 (IQR = 0.91-1.01) for TOF, all adherents (≥ 0.8).Table 2.Safety results of the treatment shows the safety results.Side EffectBaricitinib(n, %)Tofacitinib(n, %)Hb <11 g/dl7 (23,3)0Hb < 8 g/dl0 (0)/Hb Recovery >11 g/dl2/7 (28,6)/Neutrophils < 1500/mm30 (0)/Lymphocytes < 1000/mm33 (10,0)2 (22,2)Platelets > 600 × 103/mm31 (3,3)0AST o ALT > 1 NLV4 (13.3)0 (0)Hypercholesterolemia (> 1 NLV)13 (43.3)5 (55.5)Infections13 (43.3)0 (0)Herpes zoster6 (20,0)0 (0)Conclusion:In our population, mostly refractory to biological, more than half of the patients maintain treatment with JAKi, with optimal adherence. The main reason for the suspension of both drugs was inefficiency. The most frequent adverse effects were hypercholesterolemia in both groups and infections in BAR, with a high frequency of herpes zoster. No cardiovascular or thromboembolic events were observed.Disclosure of Interests:Cristina Valero: None declared, Alberto Calvo Garcia: None declared, Noelia García Castañeda: None declared, Ana Ortiz: None declared, Irene Llorente Speakers bureau: Gebro, Janssen, Sanofi, Lilly., Blanca Varas: None declared, Santos Castañeda: None declared, Rosario Garcia de Vicuna Grant/research support from: BMS, Lilly, MSD, Novartis, Roche, Consultant of: Abbvie, Biogen, BMS, Celltrion, Gebro, Lilly, Mylan, Pfizer, Sandoz, Sanofi, Paid instructor for: Lilly, Speakers bureau: BMS, Lilly, Pfizer, Sandoz, Sanofi, Esther Ramirez: None declared
Background:Vaspin is a novel anti-inflammatory adipokine associated with cardiovascular (CV) disease and inflammation in chronic inflammatory conditions different from axial spondyloarthritis (axSpA).1 Given the high incidence of CV disease (mainly due to accelerated atherosclerosis) exhibited by axSpA patients,2 we wondered if vaspin could also be a key molecule in this process. However, data on the role of vaspin regarding atherosclerotic disease in the context of axSpA is scarce.3Objectives:To evaluate the implication of vaspin, at the genetic and serological level, in subclinical atherosclerosis and CV risk in axSpA.Methods:510 patients who fulfilled the ASAS criteria for axSpA4 were included in this study. Carotid ultrasound (US) was performed to evaluate the presence of subclinical atherosclerosis. Three vaspin gene variants (rs2236242 T/A, rs7159023 G/A and rs35262691 T/C) were genotyped by TaqMan probes. Serum vaspin levels were assessed by Enzyme-Linked ImmunoSorbent Assay. Analysis was performed using a statistical software.Results:Serum vaspin levels were significantly higher in female patients than in males and also in obese patients when compared to those with normal weight (p<0.05). At the genetic level, we disclosed that the minor allele of rs2236242 (A) was associated with lower serum vaspin levels in axSpA, while the rs7159023 minor allele (A) was linked to higher serum levels (p<0.05). When the three polymorphisms assessed were combined conforming haplotypes, we disclosed that the TGC haplotype related to high serum levels of vaspin (p=0.01). However, no statistically significant association was observed between vaspin and markers of subclinical atherosclerosis, both at the genetic and serological level.Conclusion:Our results revealed that vaspin is linked to CV risk factors that may influence on the atherosclerotic process in axSpA. Additionally, we disclosed that serum vaspin concentration is genetically modulated in a large cohort of patients with axSpA.References:[1]Adv Exp Med Biol. 2019;1111:159-88.[2]Front Med (Lausanne). 2018;5:62.[3]Braz J Med Biol Res. 2016;49(7):e5231.[4]Ann Rheum Dis. 2009;68(2):ii1-44.Acknowledgements:Personal funds: RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF); SR-M: RD16/0012/0009 (ISCIII-ERDF); VP-C: PREVAL18/01 (IDIVAL); LL-G: INNVAL20/06 (IDIVAL).Disclosure of Interests:Javier Rueda-Gotor: None declared, Raquel López-Mejías: None declared, Sara Remuzgo-Martínez: None declared, Verónica Pulito Cueto: None declared, Alfonso Corrales: None declared, Leticia Lera-Gómez: None declared, Virginia Portilla: None declared, Iñigo González-Mazón: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Rosa Expósito: None declared, Cristina Mata: None declared, Javier Llorca: None declared, Vanessa Hernández-Hernández: None declared, Carlos Rodríguez-Lozano: None declared, Nuria Barbarroja Puerto: None declared, Rafaela Ortega Castro: None declared, Noelia García Castañeda: None declared, Cristina Fernández-Carballido: None declared, Maria Paz Martínez-Vidal: None declared, David Castro-Corredor: None declared, Joaquín Anino-Fernández: None declared, Diana Peiteado: None declared, Chamaida Plasencia: None declared, E Galindez: None declared, María L. García Vivar: None declared, Oreste Gualillo: None declared, Juan Carlos Quevedo-Abeledo: None declared, Santos Castañeda: None declared, Iván Ferraz-Amaro: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Fernanda Genre: None declared
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