SAT0545 ULTRASONOGRAPHIC ENTHESEAL AND JOINT INVOLVEMENT IN PATIENTS WITH ACUTE ANTERIOR UVEITIS: A MONOCENTRIC CROSS-SECTIONAL STUDY.
Authors: G. Citriniti, P. Macchioni, N. Girolimetto, L. Cimino, C. Salvarani
Journal: Annals of the Rheumatic Diseases (2020)

Background: Few studies have been investigating ultrasonographic (US) changes at peripheral entheses and joints in patients with anterior acute uveitis (AAU) 1 and none has been comparing non granulomatous uveitis (AANGU) with granulomatous uveitis (AAGU). Objectives: To investigate prevalence of US entheses and joints abnormalities in a consecutive series of AAU patients and to compare US findings in AANGU HLA-B27 positive and HLA-B27 negative, with AAGU patients. Methods: 121 consecutive patients diagnosed with AAU [91 AANGU (40 B27-, 61 B27+) and 20 AAGU, M/F 32/29, mean age 45.4± 12.8 y, mean disease duration 44± 84 m] from the Immunology Eye Unit (AUSL-IRCCS Reggio Emilia, Italy) entered the study. Patients with Fuchs uveitis were enrolled as controls (AAGU group). A complete rheumatological examination, including 68/66 peripheral joint count, entheses and bone spine mobility evaluation, was conducted. Using an Esaote MyLabClass, 18-6MHz linear multifrequency transducer both in B-mode and PD-mode, 6 entheses were evaluated bilaterally for the presence of any elementary lesion, structural damage and active enthesitis, according to OMERACT definitions 2 . The following sites were studied: lateral epicondyle of humerus, distal quadriceps insertion into the patella, proximal and distal patellar tendon insertions, calcaneal insertion of Achilles tendon and plantar fascia. Knee and ankle joints, were evaluated for synovial hypertrophy, effusion and PD signal. Extensor and flexor tendons of the foot and ankle were also examined for tendon sheath effusion, synovial hypertrophy and PD signal. Results: Abnormal US findings, consisting in the presence of at least one entheseal abnormality, were detected in 110/121 patients (90.2%), the mean number of abnormal entheses per patient was 6.71±5.46. At the enthesis level, structural damage was significantly higher in AANGU, as compared with AAGU (30.9% vs 21.7%, p&lt;0.001) and in AANGU B27+ as compared with B27- (27% vs 36%, p &lt; 0.001). The presence of PD signal at enthesis was significantly increased in AANGU vs AAGU (7.1% vs 0.4%, p &lt; 0.001) but also among AANGU B27+ vs AANGU B27- pts (5.9% vs 9%, p = 0.040). Analysis based on patient-level data showed a significantly higher percentage of patient in AANGU group having at least one enthesis exhibiting PD signal, when compared with AAGU (31% vs 5%, p = 0.023) (Table 1). The prevalence of US joint and tendon sheath alterations was negligible in the entire AAU population (&lt;1%) without any difference between groups. Table 1. US findings at the patient level Total n = 121 AAGU n = 20 AANGU n = 101 AANGU B27– n = 40 AANGU B27+ n = 61 AANGU vs AANGU AAGU vs AANGU B27 - AAGU vs AANGU B27 + AANGU B27- vs AANGU B27+ Entesophyte, n. (%) 109 (90,1%) 16 (80%) 93 (92,1%) 39 (97,5%) 54 (88,5%) 0,111 0,038 0,451 0,142 Entheseal erosion, n. (%) 12 (9,9%) 0 12 (11,9%) 5 (12,5%) 7 (11,5%) 0,213 0,159 0,184 1 Hypoechogenicity, n. (%) 5 (5,1%) 0 5 (5%) 3 (7,5%) 2 (3,3%) 0,589 0,544 1 0,382 Thickened enthesis, n. (%) 118 (97,5%) 19 (95%) 96 (98%) 37 (97,4%) 59 (97,3%) 0,440 1 0,440 1 Doppler signal at enthesis, n. (%) 32 (26,4%) 1 (5%) 31 (30,7%) 13 (32,5%) 18 (29,5%) 0,024 0,023 0,032 0,750 Active enthesitis, n. (%) 10 (8,3%) 0 10 (9,9%) 5 (12,5%) 5 (8,2%) 0,211 0,159 0,326 0,512 Structural damage, n. (%) 109 (90,1%) 16 (80%) 93 (92,1%) 39 (97,5%) 54 (88,5%) 0,111 0,038 0,451 0,142 Results are presented as number and percentage of patients having at least 1 entheseal abnormality, with significance Conclusion: US entheseal structural damage is frequent in AAU patients, whereas US active enthesitis has a low prevalence. At the patient level, the presence of PD signal at enthesis seems to be associated with AANGU, without apparent influence of HLA-B27 positivity. References: [1]Muñoz-Fernández S, et al. Arthritis Rheum. 2009;60(7):1985-1990. [2]Balint P V, et al. Ann Rheum Dis. 2018;77(12):1730-1735. Disclosure of Interests: None declared