The aim of this study was to investigate the role of IL‐12 in patients with RA. IL‐12 (p70) and its associated cytokines were measured in sera and synovial fluid (SF) using an enzyme‐linked immunosorbent method. Seven American College of Rheumatology (ACR) core set measures as well as IL‐12 levels were sequentially monitored at the commencement and 4 months after treatment with a low‐dose steroid and disease‐modifying anti‐rheumatic drugs (DMARDs). In sera, 64 (42.2%) of 152 RA patients had detectable concentrations of IL‐12 (p70), whereas one (1.4%) of 69 osteoarthritis (OA) patients and five (10%) of 50 healthy controls had detectable IL‐12 (P < 0.001). The median level of circulating IL‐12 was also higher in RA patients (P < 0.001). In SF, the number of patients with detectable IL‐12 and the median IL‐12 levels were significantly higher in RA patients (n = 53) than in OA patients (n = 22). In paired samples (n = 53) of sera and SF from RA patients, IL‐12 levels were higher in the SF than in sera (P < 0.001). Patients with detectable IL‐12 (n = 51) in sera had higher tender joint scores (P = 0.003), swollen joint scores (P < 0.001) and C‐reactive protein (CRP; P = 0.036), than those without (n = 55). Four months after treatment with DMARDs, the improved group showed a larger IL‐12 decrease than the non‐improved group (P = 0.017). The levels of IL‐12 correlated positively with those of IL‐2, interferon‐gamma, IL‐6, and tumour necrosis factor‐alpha, but were correlated inversely with those of IL‐10. Our results demonstrate that IL‐12 levels reflect RA disease activity and that IL‐12 is involved in the production of proinflammatory cytokines. An IL‐12 blockade could be useful for the treatment of RA.

BackgroundNovel modalities, such as salivary ultrasonography (SGUS) and shear wave elastography (SWE), have previously been introduced to evaluate Sjögren’s syndrome (SS). However, in secondary SS (sSS), the diagnostic performance of SGUS and its relationship with clinicopathological characteristics have not yet been clearly defined.ObjectivesIn this study, we aimed to investigate sSS in RA patients using SGUS and SWE and sought to determine its pathological correlations.MethodsThirty-one RA patients who presented with sicca symptoms were included to be evaluated on SS, and were compared with 18 primary SS (pSS) patients. All subjects were assessed through SGUS and SWE, as well as conventional diagnostic approaches for SS, including minor salivary gland biopsy (MSGB). In SGUS evaluation, two separate scoring systems, suggested by Hocevar and OMERACT, were used.ResultsAmong 31 RA patients with sicca symptoms, 19 (61.2%) were diagnosed as sSS. RA patients with sSS showed significantly lower positivity for anti-Ro/La antibody than did pSS patients. Similar to pSS, SGUS showed good diagnostic performance in differentiating sSS from RA patients with simple sicca symptoms. The sSS and pSS patients exhibited significantly higher lymphoid infiltration areas in MSGB than RA patients without SS. Focus score and lymphoid infiltration areas correlated well with sonographic severity. The severity of fibrosis in MSGB showed better positive correlation with SWE than with SGUS.ConclusionsSS is frequent in RA patients and presents with less positivity for anti-Ro/La antibodies than does pSS. Similar to pSS, SGUS and SWE show good diagnostic performance for sSS, reflecting histopathologic severity well in MSGB.References[1] Jousse-Joulin S, Milic V, Jonsson MV et al. Is salivary gland ultrasonography a useful tool in Sjögren’s syndrome? A systematic review. Rheumatology (Oxford) 2016;55:789-800.[2] Mossel E, van Ginkel MS, Haacke EA et al. Histopathology, salivary flow and ultrasonography of the parotid gland: three complementary measurements in primary Sjögren’s syndrome. Rheumatology (Oxford) 2022;61:2472-82.[3] Arslan S, Durmaz MS, Erdogan H, Esmen SE, Turgut B, Iyisoy MS. Two-Dimensional Shear Wave Elastography in the Assessment of Salivary Gland Involvement in Primary Sjögren’s Syndrome. J Ultrasound Med 2020;39:949-56.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

BackgroundJanus kinase inhibitor (JAKi) and tumor necrosis factor inhibitor (TNFi) both effectively reduce inflammation, and both increases serum lipid levels. However, in the recent phase 3b-4 trial, major adverse cardiovascular events were higher with tofacitinib than TNFi. Cholesterol is still primary to the development of atherosclerosis, which collaborates with inflammation. Even in the young population, mildly abnormal lipid levels were associated with an increased future risk of atherosclerotic cardiovascular disease events.ObjectivesTo assess the effects of biological and targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs) on lipid profiles in patients with moderate-to-severe rheumatoid arthritis (RA).MethodsThis retrospective single-center observational study included patients with RA who initiated and maintained tumor necrosis factor-α inhibitor (TNFi), abatacept, tocilizumab, and Janus kinase inhibitor (JAKi) for at least 6 months. Changes in lipid profile were assessed at months 3 and 6, and associations with clinical efficacy, concomitant medications, and co-morbidities were evaluated.ResultsThis study included 114 patients treated with TNFi, 81 patients with abatacept, 103 patients with tocilizumab, and 89 patients with JAKi. Median percent change from baseline to 6 months in total cholesterol, low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and non-HDL-C levels were higher in tocilizumab and JAKi versus TNFi and abatacept recipients (16% and 15% vs 6% and 3%, 19% and 24% vs 8% and 3%, 5% and 9% vs 3% and 0%, 19% and 19% vs 7% and 8%, respectively). The significant change in non-HDL-C was associated with JAKi (versus TNFi, OR, 2.671; 95% CI, 1.44–4.956), tocilizumab (versus TNFi, OR, 1.996; 95% CI, 1.087–3.665), concomitant glucocorticoids (OR, 2.802, 95% CI 1.344–5.843), and statin (OR, 0.419; 95% CI 0.230–0.765), and presence of rheumatoid factor (OR, 3.252, 95% CI, 1.029–10.276). However, the change in disease activity in 28 joints was not associated with a significant non-HDL-C change.ConclusionRegardless of disease activity changes, tocilizumab and JAKi-associated increases in serum non-HDL-C levels were observed. Combination with glucocorticoids may induce elevations in non-HDL-C, whereas statins may decrease in non-HDL-C.References[1] Nurmohamed MT, Heslinga M, Kitas GD. Cardiovascular comorbidity in rheumatic diseases.Nat Rev Rheumatol2015;11:693-704.[2] Robertson J, Peters MJ, McInnes IB, et al.Changes in lipid levels with inflammation and therapy in RA: a maturing paradigm.Nat Rev Rheumatol2013;9:513-23.[3] Brunner FJ, Waldeyer C, Ojeda F, et al.Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium.Lancet2019;394:2173-83.AcknowledgementsThis work was supported by National Research Foundation of Korea grants funded by the Ministry of Science, ICT and Future Planning (Grant 2015R1A3A2032927 to W.U. Kim).Disclosure of InterestsNone Declared.