Surgically induced weight loss contributed to a decrease in blood pressure and markers of renal inflammation. The reduced levels of CRP and urinary cytokines suggest that bariatric surgery attenuates systemic and renal inflammatory status.

BackgroundPrevalance of iron deficiency (ID) in systemic sclerosis (SSc) is unclear and can occur related to several causes.ObjectivesThis cross sectional study aims to analyse association between ID and disease characteristics in SSc patients who does not have an overt cause for ID.MethodsWe identified 227 consecutive SSc patients who had iron laboratory studies (serum iron, total iron binding capacity and ferritin) with concurrent full blood count and serum C-reactive protein (CRP) measurement between May 2015 and November 2017. Exclusion criteria were as follows: not having serum CRP levels within 1 month of iron studies, chronic kidney disease (eGFR <60 ml/min), haemoglobinopathies, major surgery within one year, overt gastrointestinal (GI) or genitourinary blood loss, active GI cancer and vascular lesions of GI (GAVE, intestinal telengiectasia). Patients who have ferritin levels below cut-off values or were already on iron replacement were considered as iron deficient. To define iron deficient status, threshold levels of serum ferritin 30 ng/mL and 100 ng/mL were used to denote those with normal and high CRP levels (>5 mg/L) respectively. WHO classification system was used to determine the presence and severity of anaemia. Relationship between demographic and disease characteristics and serum iron status was analysed using Fisher’s exact and Mann-Whithey U test.Results178 patients (76.4% female) were eligible for final analysis. Clinical characteristics are reported in table 1. Median age and disease duration (interquartile range, IQR) were 54.6 (44.8–66.1) and 4.9 (2.1–4.8) years, respectively. ID was present in 43.2% of the patients and 41.6% of these patients was not anaemic. Iron deficient patients were more frequently female and had longer disease duration. Among female patients, ID was significantly more prevalent before the age of 50 (77.6% vs 0%, p<0.001).Abstract THU0398 – Table 1Comparison of demographics and disease characteristics between iron deficient and iron replete patientsConclusionsUnexplained iron deficiency is frequent in scleroderma patients and a significant number of these patients do not have frank anaemia. Female sex and longer disease duration is associated with iron deficiency. Increased frequency in young female patients can be related to menstrual blood loss and further study to evaluate this association is required.Disclosure of InterestNone declared

No abstract

BackgroundPulmonary fibrosis (PF) is an important complication of systemic sclerosis (SSc), being a leading cause of disease related death. Some studies suggest that the timing of PF development differs between patients with different autoantibodies.ObjectivesWe set out to assess a large single-centre SSc cohort, focusing on the timing of clinically significant PF (csPF), and to compare this within subgroups with different disease-specific autoantibodies, in particular anti-centromere antibody (ACA), anti-topoisomerase I antibody (ATA) and anti-RNA polymerase antibody (ARA).MethodsPatients with confirmed SSc and information on autoantibodies were included. PF was confirmed on high-resolution CT and defined as clinically significant based on at least one of the following: FVC <70%; a drop in FVC >15%; DLCO<70% with no pulmonary hypertension (PH) present; or a drop in DLCO>15% with no PH. Only subjects who had first available lung function test result within the first 3 years from onset were included. 1-Kaplan-Meier (1 KM) estimation was used to calculate cumulative incidence of csPF. To assess the timing of highest rates of csPF development, hazard rates were calculated within intervals of 12 months over the follow-up.ResultsA total of 450 subjects, 75 (16.7%) male, mean age of onset 47.4 years, were included in the study. Of those 225 (50%) had diffuse cutaneous SSc, 105 (23.3%) carried ACA, 113 (25.1%) ATA and 72 (16%) ARA. Mean follow-up was 12 years, interquartile range 8–16 years. Over the entire follow-up period, 196 (43.6%) of the subjects developed csPF.Using 1 KM estimation, for the whole cohort, over the first 20 years of disease, approximately half of the patients developed csPF. Three quarters of the patients who developed csPF had reached this endpoint by 5 years (38.2%) with much lower incidence thereafter (at year 10, 15 and 20%–43%, 47% and 49.6%, respectively).Analysis within subgroups showed that, ACA was associated with a very low risk of csPF development (cumulative incidence of 5.9%, 8.1%, 9.8% at 5, 10 and 15 years from SSc onset). On the other hand, ATA +patients had a remarkably high risk of csPF development, which ultimately occurred in the majority of cases, with cumulative incidence of 77.6% at 5 years, 82.7% at 10 years and 87.1% at 15 years. Rates of csPF development among ARA+patients were higher than those in ACA+, but still much lower than ATA+, and even after 20 years of follow-up, the cumulative incidence of csPF among them was less than a half of that among ATA +patients (23.7%, 33% and 41% at years 5, 10 and 15, figure 1).The hazard of csPF among ACA +patients was highest in the second year from SSc onset (3%) and in the subsequent years varied between 0% and 1.8%. On the other hand, among ATA +patients hazard of csPF was 28.3% in year 1, 44.9% in year 2, peaked at 52.5% in year 3 and went down sharply thereafter. Although hazard was much lower among ARA+patients, this still peaked at year 3 (2.8%, 6.1% and 12.1% at year 1, 2 and 3 respectively) and declined after.ConclusionsOur ...