This study aimed to examine serum tenascin C (TNC) in different subsets of axial spondyloarthritis (axSpA) patients. Sixty-one patients fulfilling the Assessment of SpondyloArthritis international Society classification criteria for axSpA and 20 healthy subjects (HS) were included in study. Based on imaging, patients were classified as non-radiographic (n=16) and radiographic (n=45) axSpA. TNC serum levels were determined by ELISA. Disease-related factors including the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and C-reactive protein (CRP) levels were determined. TNC levels were elevated in axSpA patients [535.3 (457.7–677.2) ng/ml] compared to HS [432.1 (329.1–565.9) ng/ml, p=0.007]. Dividing axSpA into radiographic and non-radiographic subsets, the difference in TNC was observed between the radiographic subset and HS [535.3 (434.5–677.2) vs. 432.1 (329.1–565.9) ng/ml, p=0.022]. TNC levels did not correlate with disease activity measures (serum CRP or BASDAI). Nevertheless, the weak correlation of TNC levels with different disease stages (r=0.25, p=0.025) was found, with the highest levels in patients with syndesmophytes. TNC levels are elevated across various subsets of axSpA, and although not related to systemic disease activity, TNC levels might reflect chronic structural spinal changes in axSpA patients. However, its specific role in bone metabolism should be elucidated in further studies.

Background: Acute anterior uveitis (AAU) is a relatively common extra-musculoskeletal manifestation of axial spondyloarthritis (axSpA); however, data on the prevalence of active sacroiliitis in patients with AAU are limited. Methods: 102 patients with AAU and 39 healthy subjects (HS) underwent clinical assessment and sacroiliac joint MRI. Patients with absence of active sacroiliitis were reassessed after two years. International Spondyloarthritis Society (ASAS) classification criteria for axSpA (regardless of patient’s age) and expert opinion for definitive diagnosis of axSpA were applied. Results: Although chronic back pain was equally present in both groups, bone marrow edema (BME) in SIJ and BME highly suggestive of axSpA was found in 52 (51%) and in 33 (32%) patients with AAU compared with 11 (28%) and none in HS, respectively. Out of all AAU patients, 41 (40%) patients fulfilled the ASAS classification criteria for axSpA, and 29 (28%) patients were considered highly suggestive of axSpA based on clinical features. Two out of the 55 sacroiliitis-negative patients developed active sacroiliitis at the two-year follow-up. Conclusions: One-third of patients with AAU had active inflammation on SIJ MRI and clinical diagnosis of axSpA. Therefore, patients with AAU, especially those with chronic back pain, should be referred to a rheumatologist, and the examination should be repeated if a new feature of SpA appears.

Aim: Heat shock protein 90 (Hsp90) is a molecular chaperone regulating immune response. We aimed to assess systemic Hsp90 as a biomarker for spondyloarthritis (SpA). Materials & methods: Total of 80 axial SpA (axSpA) and 22 psoriatic arthritis patients and a corresponding number of age- and sex-matched healthy controls (HC) were included. Plasma Hsp90 levels were measured by ELISA. Results: Hsp90 was significantly increased in axSpA patients compared with HC (median interquartile range: 15.7 [10.5–19.8] vs 8.3 [6.6–11.8] ng/ml, p < 0.001). Moreover, Hsp90 was superior to C-reactive protein in differentiating axSpA (and both radiographic axSpA [r-axSpA] and nonradiographic-axSpA) from HC. Hsp90 levels correlated with bone marrow edema of sacroiliac joints in r-axSpA patients (r = 0.594, p = 0.019). Conclusion: Hsp90 could become a biomarker for active inflammation in r-axSpA, and can better distinguish axSpA patients from healthy subjects than C-reactive protein.

Career situation of first and presenting authorStudent for a master or a PhD.IntroductionHsp90 is a highly conserved molecular chaperone that regulates activation of innate immunity, antigen presentation, and the induction of proinflammatory cytokines and chemokines. These properties predispose Hsp90 to its potential role in the pathogenesis of autoimmune inflammatory rheumatic diseases.ObjectivesThe aim of this study was to assess plasma Hsp90 in patients with axial spondyloarthritis (axSpA), psoriatic arthritis (PsA), rheumatoid arthritis (RA) and healthy controls (HC) and to determine its potential association with disease activity and clinical features.MethodsA total of 136 patients, that were divided into groups according to the type of a rheumatic disease (SpA, RA, PsA), and age-/sex- matched healthy individuals were included. Plasma Hsp90 levels were measured by ELISA (eBioscience, Vienna, Austria). Data are presented as median (IQR).ResultsPlasma Hsp90 levels were significantly increased in axSpA and in RA patients compared to HC. The increased plasma levels of Hsp90 in PsA compared to HC did not reach statistical significance. Hsp90 concentrations were higher in RA patients with an altered serum lipid profile: low-density lipoprotein (LDL: r=0.352, p=0.048), high-density lipoprotein (HDL: r=−0.349, p=0.046) and atherogenic index (calculated as log (triglycerides/HDL)) (AI: r=0.454, p=0.009). Furthermore, Hsp90 levels in r-axSpA patients positively correlated with the MRI presence of active inflammatory lesions in sacroiliac joints (SPARCC MRI score for SI joints: r=0.594, p=0.020). Increased Hsp90 levels in PsA patients were associated with the count of joint deformities (r=0.526, p=0.025). No further statistically significant associations were found between Hsp90 plasma levels and RA-, axSpA- or PsA-specific clinical features.ConclusionsWe demonstrated elevated plasma concentrations of Hsp90 in RA and in axSpA patients compared to healthy controls. Hsp90 could be associated with early alterations of serum lipids and development of atherosclerosis in RA. Furthermore, in r-axSpA, Hsp90 may represent an independent marker of SI joint inflammation, whereas in PsA, plasma Hsp90 correlates with joint deformities. These data suggest that Hsp90 could become a potential biomarker of structural changes in SpA.ReferenceNone.AcknowledgementsSupported by AZV-16–33542A and MHCR 023728.Disclosure of InterestNone declared.