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FRI0272 Early damage assessment and prediction of damage accrual in primary sjÖgren's syndrome using salivary gland ultrasonography during 2 years of follow-up

Background Early detection and prediction of glandular damage in primary Sjögren's syndrome (pSS) is of pivotal importance in patients' stratification and treatment. Recently, ultrasonography (SGUS) has appeared as a promising tool for the assessment of salivary gland involvement in pSS. However, few studies have specifically explored its role in the early identification of salivary gland damage and in monitoring disease progression over the follow-up. Objectives a) to explore the contribution of SGUS in the early assessment of pSS-induced glandular damage and in monitoring damage accrual during the follow-up b) to identify predictive factors associated with the development and progression of sonographic changes in salivary glands. Methods An inception cohort of 54 pSS (AECG 2002) patients was included in this study at the diagnosis and prospectively followed after 6, 12 and 24 months. Demographic, clinical data and the ESSDAI of the patients were collected at each study visit as well as SGUS score that was calculated every time by the same radiologist. Sonographic assessment of glandular damage was performed by evaluating the size of the parotid and submandibular glands (normal/reduced) and the presence/absence of hyperechoic bands in more than 50% of the glands (i.e fibrosis). Descriptive statistics and logistic regression were used for the data analysis. Results We included 54 patients (51F:3 M) with a median duration of symptoms before diagnosis of 11 months (range 36–5 mo) and a median (IQR) ESSDAI at baseline of 5 (1–8). We found that at baseline 13 patients out of 54 (24.1%) already presented one element of damage in their SGUS evaluation, 14/54 (25.9%) more than one element of damage, whereas only 27/54 (50%) of patients did not present any sonographic sign suggestive for damage. In particular, hyperechoic bands were detected in the parotid glands of 12/54 (22%) patients and in the submandibular glands of 21/54 (38.9%); reduced parotid and submandibular gland size were described in 5/54 (9.3%) and in 10/54 (18.5%) of the cases, respectively. Predictive factors associated with sonographic salivary gland damage at the diagnosis were the ESSDAI at baseline (OR =1.13 [95% CI 1.0 to 1.27], p=0.04) and the positivity for Rheumatoid factor (RF) (OR =4.47 [95% CI 1.29 to 15], p=0.02). During the follow-up, 15/54 (27.8%) patients presented a progression of their salivary gland damage. We specifically observed a significant increase in the frequency of reduced parotid (9.3% vs 25.9%, p=0.004) and submandibular gland size (18.5% vs 33.3%, p=0.008) at the end of follow-up. Predictive factors for damage accrual during follow-up were: minor salivary gland focus score (OR =3.5 [95% CI 1.1 to 10.6], p=0.03) and the ESSDAI at baseline (OR =1.64, [95% CI 1.0 to 2.6]p=0.03). Conclusions Sonographic assessment of glandular damage apparently revealed a relative high frequency of already established signs of glandular damage in pSS patients at baseline, especially in patients with positive RF and higher ESSDAI. When routinely used, SGUS may accurately allowed to monitor damage accrual over the follow-up, ultimately contributing to a better clinical management of patients. Disclosure of Interest None declared