THU0484 Rebound-associated multiple vertebral fractures after discontinuation of denosumab: nine cases report

Background Denosumab (DNB) is an IgG monoclonal antibody with high affinity for RANKL that transiently decreases bone resorption. It increases bone mineral density (BMD) and decreases turnover markers, reducing fracture risk in patients with osteoporosis (OP). Several cases of rapid loss of BMD, severe bone turnover rebound (BTR) and associated fractures have been reported after DNB discontinuation. A clinical alert has been generated from these findings. Objectives To evaluate the clinical and demographic features in a case series of patients with multiple vertebral fractures after discontinuation of denosumab. Methods An observational descriptive study analysing data from nine patients with multiple vertebral fractures after DNB discontinuation that were admitted to our Rheumatology service between 2015 and 2017. Results Nine women with postmenopausal OP that received treatment with DNB were included (table 1). Mean age at treatment onset was 66.9±8.0 SD years. Four of them had previous fragility fractures, and one of them had risk factors for secondary OP (treatment with aromatase inhibitors, case 8). Eight patients (88.9%) had already received treatment other than DNB. Mean DNB received doses was 6±1.6 SD. Mean T-score before treatment was −2.6±0.6 SD for femoral neck (FN) and −3.0±1.3 SD for lumbar spine. Mean T-score ±SD after 6 months or more of DNB discontinuation was −3.5±0.8 and −3.3±1.8, respectively. Bone turnover markers (BTM) remained elevated (CTX mean 0.143±0.663 SD ng/ml and P1NP 152.1±122.4 SD ng/ml). There were a total of 47 fractures, and all occurred spontaneously. Most affected vertebrae were D9, D12, L3 y L5. Two patients underwent vertebroplasty, suffering both of them vertebral fractures after surgery. Table 1 Clinical features of the patients Conclusions This report of nine cases suffering multiple vertebral fractures early after the interruption of the DNB highlights the emerging concern on the subject in the scientific community and the need to clarify its pathogenic mechanism (”rebound effect”) and support in solid evidence the new recommendations on its management. Disclosure of Interest None declared