Pos1269 investigating the trajectory of functional disability in systemic sclerosis: group based trajectory modelling of the health assessment questionnaire disability index

Background Up to 70% of people with systemic sclerosis (SSc) report impaired physical function [1,2] , which can negatively impact quality of life [3] . The Health Assessment Questionnaire Disability Index (HAQ DI) is a self-administered measure of function, where higher scores (range 0-3) indicate worse function. Objectives To identify trajectories, clinical correlates and associations of functional disability in SSc. Methods Australian Scleroderma Cohort Study participants meeting ACR/EULAR criteria for SSc recruited within 5 years of SSc onset were included. Participants needed to have ≥2 HAQ DI scores available within 10 years of SSc onset. Group based trajectory modelling (GBTM) was used to identify the number and shape of HAQ DI score trajectories over 10 years. Between group comparisons were made using the chi-squared test for discrete variables and the two-sample t-test or Wilcoxon rank sum test for continuous variables. Generalised estimating equations were used to model longitudinal data involving repeated measures. Survival analyses were performed using Kaplan Meier and Cox proportional hazard modelling. Results 426 participants were included with incident SSc and ≥2 HAQ DI scores, with median time between HAQ DI scores of 1.1 (IQR 1.0-1.4) years. Median age at SSc onset was 53 years (IQR 44-61 years), 83% were female and 33% had dcSSc. We found two HAQ DI trajectory groups: low/stable disability (n=221, 52%), and high/increasing disability (n=205, 48%; Figure 1). Participants with high/increasing disability were older (p=0.01) and more likely to have dcSSc (p<0.01), PAH (p<0.01) and multiple cardiovascular risk factors (p<0.01; Table 1). High/increasing disability was associated with markers of poor hand function such as digital ulcers and synovitis (p<0.01), upper and lower GI involvement (both p<0.01) and proximal muscle weakness and atrophy (both p<0.001). Use of immunosuppression (p<0.001), including prednisolone (p<0.001), was more frequent in those with high/increasing disability. Those with high/increasing disability had worse survival after adjusting for age, sex, dcSSc, PAH and ischaemic heart disease (HR 1.9, 95% CI 1.0-3.8, p=0.05), as did those with increasing baseline HAQ DI scores (HR 1.8, 95%CI 1.2-2.7, p=0.01). Conclusion Two trajectories of functional disability in SSc were identified. Those with poorer function had a distinct clinical phenotype and survival compared to those with less functional disability. Further work is required to identify if amelioration of disease-specific features associated with higher HAQ DI scores results in a commensurate improvement in physical function. References [1]Zaghlol RS, Dawa GA, Makarm WK. Functional Disability Among Systemic Sclerosis Patients: Relation to Disease Characteristics and Quality of Life Parameters. Curr Rheumatol Rev 2021. [2]Guillevin L, Hunsche E, Denton CP, et al. Functional impairment of systemic scleroderma patients with digital ulcerations: results from the DUO Registry. Clin Exp Rheumatol 2013; 31 (2 Suppl 76): 71-80. [3]Hossain S, Choudhury MR, Haque MM, Yeasmin S, Hossain F, Zaman MM. Functional disability and health-related quality of life among systemic sclerosis patients in Bangladesh. BMC Rheumatol 2022; 6 (1): 60. Figure 1 : Trajectory groups Table 1 : Clinical features and treatments in trajectory groups Variable High/Increasing HAQ DI (N = 205) Low/Stable HAQ DI (N= 221) p-value Age at SSc onset (y) 56 (44-63) 52 (41-59) <0.01 DcSSc 97 (47%) 43 (20%) <0.01 ANA Centromere 64 (32%) 104 (47%) <0.01 Scl 70 42 (21%) 32 (15%) 0.09 IHD 32 (16%) 15 (7%) <0.01 HTN 126 (62%) 85 (39%) <0.01 PAH 22 (11%) 8 (4%) <0.01 ILD 78 (63%) 54 (69%) 0.358 Digital ulcers 117 (57%) 90 (41%) <0.01 Synovitis 118 (58%) 89 (40%) <0.01 Proximal weakness 75 (37%) 31 (14%) <0.01 Muscle atrophy 64 (31%) 24 (11%) <0.01 Upper GI symptoms 196 (96%) 193 (87%) <0.01 Lower GI symptoms 188 (92%) 175 (79%) <0.01 Immunosuppression 165 (81%) 121 (55%) <0.01 Prednisolone 126 (62%) 81 (37%) <0.01 Acknowledgements JLF holds a NHMRC Postgraduate Scholarship (GNT2013842) and an Australian Government Research Training Program Scholarship. LR holds an Arthritis Australia – ARA Victoria Fellowship. MN holds an NHMRC Investigator Grant (GNT1176538). KB holds an NHMRC Investigator Grant (GNT1197169). Disclosure of Interests Jessica Fairley Speakers bureau: Boerhinger Ingelheim, Dylan Hansen: None declared, Murray Baron: None declared, Susanna Proudman Speakers bureau: Boehringer Ingelheim, Consultant of: Boehringer Ingelheim, Jo-Anne Sahhar Speakers bureau: Boehringer Ingelheim, Gene-Siew Ngian: None declared, Jenny Walker Speakers bureau: Boehringer Ingelheim, Lauren Host: None declared, Kathleen Morrisroe: None declared, Wendy Stevens Consultant of: Boehringer Ingelheim, Laura Ross: None declared, Mandana Nikpour Speakers bureau: Janssen, Boehringer Ingelheim, GSK, Consultant of: Janssen, Boehringer Ingelheim, Astra Zeneca, GSK.