Chi Chiu Mok1, Kar Li Chan2, Ling Yin Ho3 and Chi Hung To4, 1Tuen Mun Hospital, Hong Kong, China, 2Tuen Mun Hospital, Tsing Yi, Hong Kong, China, 3Tuen Mun Hospital, Hong Kong SAR, China, 4Hospital Authority, Hong Kong, Hong Kong
Background/Purpose: To study the prevalence and risk factors of fragility fractures in a longitudinal cohort of patients with SLE.
Methods: All patients who fulfilled ≥4 1997 ACR criteria for SLE and have been registered in our cohort database were included. Symptomatic fragility fractures were identified from the SLE organ damage index (SDI) data and verified by record review. A longitudinal cohort of 383 SLE patients who had a baseline DEXA scan performed in 2011 was followed for new fragility fractures over time. These patients were stratified into 2 groups according to previous fracture or osteoporosis, defined as a DEXA T score < -2.5 or Z score < -2.0 at the hip, femoral neck or lumbar spine. The cumulative incidence of new fractures was studied by Kaplan-Meier's analysis and risk factors by Cox regression, adjusted for confounders.
Results: Of 1140 SLE patients (age34.7±14.4 years; 91.5% women), 102 fractures (hip [n=15]; vertebral [n=54]; limbs (non-hip) [n=14]; digital/rib [n=19]) developed in 91(8.0%) patients over 13.1 years. The prevalence of major osteoporotic and hip fractures was 0.56 and 0.10 per 100 patient-years, respectively. A longitudinal cohort (N=383) of SLE was further analyzed (age at DEXA scan 40.5±13 years; 94% women). Osteoporosis was present in 105 patients (13 with fractures) at baseline and 8 patients had osteopenia with fractures. Patients with osteoporosis/previous fractures (N=113), compared to those without (N=270), were more likely to have childhood onset disease (< 18 years), longer SLE duration and a higher prevalence of thrombocytopenia, hemolytic anemia or neuropsychiatric manifestations that required immunosuppressive therapies. Use of glucocorticoids (79% vs 62%; p=0.002) and MMF/AZA (55% vs 42%; p=0.02), BMI≤18kg/m2 (14% vs 7%; p=0.04), premature menopause (< 45 years) (14% vs 4%; p=0.001) were also more frequent in the osteoporosis/fracture group. However, no difference in the SLEDAI scores was observed between the 2 groups at baseline (3.7±3.8 vs 4.1±3.3; p=0.26). Over 153±41 months, new symptomatic fragility fractures developed in 34(8.9%) patients (vertebral [n=19], hip [n=2], limbs (non-hip) [n=6], digital/rib [n=7]; incidence 0.69 per 100 patient-years). The cumulative risk of new fragility fractures at 3,5,10 and 15 years was 1.8%, 3.7%, 14.7%, 22.2%; and 1.5%, 1.9%, 3.9%, 6.7%, respectively, in the osteoporosis/previous fracture and non-osteoporosis groups (p< 0.001). Cox regression showed that increasing age (HR1.08[1.03-1.12]; p=0.001), osteoporosis/previous fracture (HR3.47[1.59-7.59]; p=0.002) and a family history of fracture (HR4.31[1.41-13.2]; p=0.01) were independently associated with the development of new fractures after adjustment for SLE duration, childhood onset disease, low BMI, chronic smoking, premature menopause, use of glucocorticoids and immunosuppressive agents and clinical manifestations. In those patients using prednisolone at baseline, there was no significant relationship between the daily dosage and new fractures.
Conclusion: In a longitudinal cohort of SLE followed for 12 years, new fragility fracture developed in 8.9% of patients. Increasing age, osteoporosis, a personal or family history of fractures were major risk factors.
Disclosures: C. Mok, None; K. Chan, None; L. Ho, None; C. To, None.
