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This study aims to investigate pre-clinical esophageal involvement in systemic sclerosis (SSc) by high-resolution impedance manometry (HRiM), its associations with disease features including lung involvement, and its predictivity of esophageal symptoms overtime. Charts of 45 asymptomatic (no heartburn/regurgitation/dysphagia) SSc patients (96% females; mean age 46 years) with at least one follow-up (FU) visit and complete clinical, serological, functional, and radiological assessment, including high-resolution computed tomography (HRCT) of the chest and lung function tests, that had undergone esophageal HRiM were retrospectively evaluated. Esophagogastric junction-contractile integral (EGJ-CI) and esophageal body motility, as evaluated by mean distal contractile integral (DCI), were assessed. SSc patients had a normal esophageal motility in 7/45 cases, a defective EGJ-CI in 28, an ineffective esophageal motility (IEM) in 17, and aperistalsis in 12. Defective EGJ-CI was associated with IEM/aperistalsis in 20 cases, while 9 patients had isolated IEM. Defective EGJ-CI and/or IEM/aperistalsis were associated with a diffusing lung capacity for CO < 80% of predicted value (all p < 0.05), while defective EGJ-CI was also associated with interstitial lung disease on HRCT (p = 0.03). Prevalence of any HRiM abnormality was higher in anti-centromere antibody negative patients (all p < 0.05). IEM/aperistalsis independently increased the risk of esophageal symptoms by 2.3-fold (95% CI 1.1–5.7) and was associated with their higher cumulative incidence with respect to patients with other HRiM patterns at FU (χ2= 4.63; p = 0.03). SSc patients asymptomatic for esophageal involvement can have HRiM abnormalities in up to 84% of cases. A baseline-impaired motility is a risk factor for symptomatic esophageal disease.

Background A reduced basal lower esophageal sphincter (LES) pressure (LES Objectives We aimed to investigate potential associations of a reduced basal LES pressure at first observation with the development of new gastrointestinal symptoms and with self-administered questionnaires devoted to assess the impact of gastrointestinal involvement on quality of life during follow-up (FU) in SSc patients. Methods SSc patients meeting the 2013 ACR/EULAR criteria for disease classification with measurement of basal LES pressure at the first observation and at least one FU visit with complete clinical evaluation were enrolled. The gastroesophageal reflux disease questionnaire (GerdQ) (2, 3) was administered to explore the impact of esophageal symptoms on patient9s disease perception and to estimate the risk for GERD. Associations between reduced basal LES pressure and new onset gastrointestinal symptoms at FU were analyzed by Fisher9s exact test, while the GerdQ score in SSc patients with or without a reduced basal LES pressure was analyzed by Mann-Whitney U test. Results Fifty-nine SSc patients, aged 47±13 years, were investigated (75% females; median disease duration 7 years, range 0.5–43). Eighty % of patients had a limited SSc subset (lcSSc); 20% had a diffuse subset (dcSSc). All patients were ANA positive (36% had anti-centromere antibodies, 39% anti-Scl70+; 5% anti-RNApolymerase III; 1.7% anti-PmScl; 1.7% anti-U1RNP). All patients were under proton pomp inhibitors ± prokinetics during FU. Forty-two % of patients had already esophageal symptoms at baseline; 32% developed new esophageal symptoms and 40% new gastric and/or intestinal symptoms during observation (median FU 4 years; range 0.5–15.5). Baseline basal LES pressure was reduced in 63% of patients. Out of these, 49% had also esophageal symptoms. Median GerdQ score at the end of FU was significantly higher in patients with baseline reduced LES pressure (7, range 3–14 versus 6, range 2–11; p Conclusions Our data suggest that evaluation at baseline of esophageal involvement in SSc patients by esophageal manometry can predict the development of more severe symptoms over time, as evaluated by the association with a higher score at GerdQ also in initially asymptomatic patients. Larger studies need to be carried out to confirm this association. References Sjogren RW. Arthritis Rheum 1994; 37: 1265–82 Jonasson C et al. Aliment Pharmacol Ther 2013; 37: 564–72 Chunlertrith K et al. Clin Exp Rheumatol 2014; 32 (6 Suppl 86): S98–102 Disclosure of Interest None declared