THU0346 Determinants of sonographic glandular damage in a large cohort of patients with primary sjÖgren’s syndrome and its impact on salivary gland dysfunction
Authors: C. Baldini, N. Luciano, F. Ferro, E. Calabresi, E. Elefante, V. Donati, S. Bombardieri, M. Mosca
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Salivary gland ultrasonography (SGUS) has increasingly appeared as a valid tool to characterise major salivary glands involvement in primary Sjögren's syndrome (pSS). An international score based on the number and location of the hypoechoic areas in the gland has been proposed for diagnostic purposes. Recently, a specific interest in using SGUS to estimate major salivary gland damage has also arisen in order to individualise patients treatment. <h3>Objectives</h3> a) to investigate frequency and severity of salivary gland damage in a large monocentric cohort of pSS patients; b) to explore determinants that could be associated with salivary gland damage accrual. <h3>Methods</h3> Sonographic data from a monocentric cohort of 311 pSS patients were collected from 2012 to 2017. SGUS had been performed according to a standard protocol that evaluated the echostructure of each gland graded on a 5-point scale (0–4). Salivary gland damage was defined by the presence of hyperechoic bands in more than 50% of the glandular parenchyma and on the basis of the size of the four glands. <h3>Results</h3> We included in the study 311 patients. The median age of the patients was 58 years (IQR, 49–68) and the median disease duration was 3 years (IQR, 0–9). Out of the cohort, 163 (52.4%) patients underwent SGUS examination within 3 years from the diagnosis, 91 (29.3%) within 4 to 10 years and 57 (18.3%) 10 years or more after the diagnosis. At SGUS evaluation 134/311 (43.1%) pSS patients did not present any findings of damage, whereas 177/311 (56.9%) presented at least one element of damage. SGUS damage inversely correlated with USFR (r=-0.382, p-value=0.001). At the univariate analysis SGUS damage was associated to disease duration, number and location of the hypo-anechoic areas, focus score, ESSDAI score, hypergammaglobulinemia, and positivity for anti-Ro/SSA, anti-La/SSB, Rheumatoid Factor (RF) and cryoglobulins. In the linear regression, duration of the follow-up, number and location of the hypo-anechoic areas and presence of cryoglobulins remained independently associated with SGUS damage. In 138/311 (44.4%) patients, SGUS was repeated prospectively at least twice during a median follow-up of 24 months (IQR, 12–36). Notably, 23/138 (16.7%) patients presented a damage progression. Presence of hyperechoich bands in the submandibular glands at the baseline evaluation was an independent risk factor for damage progression, whereas pSS low disease activity (ESSDAI &lt;5) was protective against damage accrual. <h3>Conclusions</h3> Ultrasonographic damage resulted quite frequent in pSS patients and significantly associated with salivary gland dysfunction. Notably, pSS patients with normal echostructure of their glands were those less prone to develop SGUS damage during the disease course, whereas those presenting localised, diffuse or scattered hypo-anechoic areas were at higher risk of damage accrual. <h3>Disclosure of Interest</h3> None declared