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Bone turnover markers are decreased in GC-treated subjects with DM. Decreased OC levels in GC-treated patients were associated with an increased risk of DM. These results suggest the involvement of OC in glucose homeostasis regulation in DM. Osteocalcin (OC) is involved in the regulation of glucose homeostasis. Glucocorticoid (GC) treatment is associated with impaired osteoblast function, decreased OC levels, and the development and/or worsening of pre-existing diabetes mellitus (DM). Whether decreased OC levels in GC-treated subjects contribute to DM is not well known. The aim of this study was to analyse whether OC levels in GC-treated patients are associated with the presence of DM. One hundred twenty-seven patients (aged 61.5 ± 17.9 years) on GC treatment were included. GC dose, treatment duration, presence of DM and bone formation (OC, bone ALP, PINP) and resorption markers (urinary NTX, serum CTX) were analysed. The cut-offs of each bone turnover marker (BTM) for the presence of DM were evaluated and optimised with the Youden index and included in the logistic regression analysis. Among the patients, 17.3% presented DM. No differences were observed in GC dose or duration or the presence of fractures. Diabetics showed lower levels of OC (7.57 ± 1.01 vs. 11.56 ± 1; p

To estimate the incidence of clinical fragility fractures in postmenopausal women with rheumatoid arthritis (RA) and analyze risk factors for fracture.Incidence of clinical fragility fractures in 330 postmenopausal women with RA was compared to that of a control population of 660 age-matched postmenopausal Spanish women. Clinical fractures during the previous five years were recorded. We analyzed associations with risk factors for fracture in both populations and with disease-related variables in RA patients.Median age of RA patients was 64 years; median RA duration was eight years. Sixty-nine percent were in remission or on low activity. Eighty-five percent had received glucocorticoids (GCs); 85 %, methotrexate; and 40 %, ≥1 biologic DMARD. Fifty-four patients and 47 controls had ≥1 major osteoporotic fracture (MOF). Incidence of MOFs was 3.55 per 100 patient-year in patients and 0.72 in controls (HR: 2.6). Risk factors for MOFs in RA patients were age, previous fracture, parental hip fracture, years since menopause, BMD, erosions, disease activity and disability, and cumulative dose of GCs. Previous fracture in RA patients was a strong risk for MOFs (HR: 10.37).Of every 100 postmenopausal Spanish women with RA, 3-4 have a MOF per year. This is more than double that of the general population. A previous fracture poses a high risk for a new fracture. Other classic risk factors for fracture, RA disease activity and disability, and the cumulative dose of GCs are associated with fracture development.

Objective To analyse the clinical utility of trabecular bone score (TBS) evaluation for fracture risk assessment in glucocorticoid (GC)-treated patients compared with BMD assessment. Methods One hundred and twenty-seven patients on GC treatment were included [mean age 62 (18) years, 63% women] in this cross-sectional study. The medical history, anthropometric data, lumbar and femoral BMD (DXA) [considering osteoporosis (OP): T-score ⩽−2.5], TBS (considering degraded microarchitecture: Results All patients were receiving GC treatment for autoimmune diseases during 47.7 (68.9) months at a mean daily dose of 14.5 mg; 17% had VF, 28% any type of fragility fracture (VF + non-VF), 29% OP and 52% degraded microarchitecture. Degraded microarchitecture was significantly more frequent than densitometric OP in patients with VF (76% vs 38%) and with any fragility fracture (69% vs 36%). For VF, TBS and BMD sensitivity, specificity, PPV, and NPV were 0.76, 0.53, 0.25 and 0.92, and 0.38, 0.72, 0.22 and 0.85, respectively. Specificity increased to 0.89 for VF and 0.9 for any fragility fracture on combining BMD+TBS. TBS had better ability than BMD to discriminate between patients with fracture, especially VF (area under the curve = 0.73). Conclusion TBS seems to have greater discriminative power than BMD for fracture risk assessment in GC-treated patients, confirming the utility of this method as a complementary tool in the diagnosis of GC-induced OP.

Periostin is a matricellular protein with a preferential location in cortical bone and periosteal tissue, and tartrate-resistant acid phosphatase 5b (TRAP5b) is a marker of osteoclast numbers. In Paget's disease of bone (PDB), there is increased cortical thickening and probably increased periosteal apposition, along with increased osteoclast numbers.To analyse if circulating periostin is a biomarker for PDB, and if it is associated with disease activity and involvement of long bones that represent major cortical contribution. Also, to analyse whether TRAP5b, a scarcely explored bone resorption marker, is useful in the assessment of PDB.We recruited 42 patients with PDB (13F/29M; 71 ± 11.6 yrs). 71.4% had active disease, 66.6% had polyostotic disease and 54.8% had long bone involvement. Blood and urine samples were taken between 8:00 and 10:00 A.M. after an overnight fast. Periostin and TRAP5b were measured in serum, using commercial ELISA assays (Biomedica and IDS, respectively). Serum total ALP, PINP, CTX, bone ALP and urinary NTX were measured. Reference values for periostin and TRAP5b were obtained from 45 healthy subjects.Serum periostin did not differ between patients and controls (989.4 ± 173.2 vs. 966.9 ± 195.4 pMol/L, p = 0.572). No significant differences were observed between patients with and without active disease (964.5 ± 168.8 vs.1051.6 ± 175.6 pMol/L, p = 0.143), involvement or not of long bones (1022.2 ± 145.8 vs 949.7 ± 198.2 pMol/L, p = 0.181) and monostotic or polyostotic disease (963.8 ± 198.7 vs 1002.2 ± 161.4 pMol/L, p = 0.505). There were significant correlations between serum periostin and all bone turnover markers (bone ALP, PINP, uNTX, sCTX and TRAP5b) in PDB patients with active disease, but not in the inactive PDB group. Serum TRAP5b was significantly higher in PDB patients than in controls (4.43 ± 1.76 vs. 3.21 ± 1.02 U/L, p 0.001), in those with active disease (4.98 ± 1.76 vs. 3.07 ± 0.72 U/L, p 0.001) and in patients with polyostotic disease than in those with monostotic disease (4.81 ± 1.79 vs 3.68 ± 1.5 U/L, p = 0.005). TRAP5b levels were not influenced by previous bisphosphonate treatment (4.14 ± 1.42 vs. 4.84 ± 2.02 U/L, p = 0.206).Periostin is not useful for assessing PDB, whilst TRAP5b, which has been a scarcely explored bone turnover marker until now, may be useful in the analysis of this disease, providing new information on the resorption process. In addition, periostin levels correlate with all classical BTMs in active PDB, suggesting that this marker may reflect periosteal and cortical metabolism in accelerated bone turnover states.

Giant cell arteritis (GCA) is a primary large vessel vasculitis in which glucocorticoid (GC) therapy is the mainstay of treatment. During GC tapering, relapses may occur in about half of GC...

Prevalence and risk factors of vertebral fractures in postmenopausal RA women were assessed in 323 patients and compared with 660 age-matched women. Of patients, 24.15% had at least one vertebral fracture vs.16.06% of controls. Age, glucocorticoids and falls were the main fracture risks. Vertebral fractures were associated with disease severity. Introduction There is little quality data on the updated prevalence of fractures in rheumatoid arthritis (RA) that may have changed due to advances in the therapeutic strategy in recent years. This study was aimed at analysing the prevalence and risk factors of vertebral fractures in postmenopausal women with RA and comparing it with that of the general population. Methods We included 323 postmenopausal women diagnosed with RA from 19 Spanish Rheumatology Departments, randomly selected and recruited in 2018. Lateral radiographs of the thoracic and lumbar spine were obtained to evaluate morphometric vertebral fractures and the spinal deformity index. We analysed subject characteristics, factors related to RA, and fracture risk factors. The control group consisted of 660 age-matched Spanish postmenopausal women from the population-based Camargo cohort. Results Seventy-eight (24.15%) RA patients had at least one vertebral fracture. RA patients had increased fracture risk compared with controls (106 of 660, 16.06%) (p = 0.02). Logistic regression analysis showed that age (OR 2.17; 95% CI 1.27-4.00), glucocorticoids (OR 3.83; 95% CI 1.32-14.09) and falls (OR 3.57; 95% CI 1.91-6.86) were the independent predictors of vertebral fractures in RA patients. The subgroup with vertebral fractures had higher disease activity (DAS28: 3.15 vs. 2.78, p = 0.038) and disability (HAQ: 0.96 vs. 0.63, p = 0.049), as compared with those without vertebral fractures. Conclusion The risk of vertebral fracture in RA is still high in recent years, when compared with the general population. The key determinants of fracture risk are age, glucocorticoids and falls. Patients with vertebral fractures have a more severe RA.

Objective The aim of this study was to quantify the incidence of all clinical fractures, including traumatic and fragility fractures, in patients aged 50 years and older, and to describe their distribution by fracture location, sex and age. Methods The incidence of clinical fractures at 10 hospitals in Catalonia, with a reference population of 3 155 000 inhabitants, was studied. For 1 week, from 30 May to 5 June 2016, we reviewed the discharge reports of the Traumatology section of the Emergency Department to identify all fractures diagnosed in patients ≥50 years of age. As a validation technique, data collection was carried out for 1 year at one of the centres, from 1 December 2015 to 30 November 2016. The fracture incidence, including the 95% CI, was estimated for the entire sample and grouped by fracture type, location, sex and age. Results A total of 283 fractures were identified. Seventy per cent were in women, with a mean age of 72 years. The overall fracture incidence was 11.28 per 1000 person-years (95% CI: 11.10, 11.46), with an incidence of traumatic and fragility fractures of 4.15 (95% CI: 4.04, 4.26) and 7.13 per 1000 person-years (95% CI: 6.99, 7.28), respectively. The incidence of fractures observed in the validation sample coincided with that estimated for the whole of Catalonia. The most common fragility fractures were of the hip, forearm, humerus and vertebrae. Conclusion The results of this study are the first to estimate the incidence of clinical fragility fractures in Spain, grouped by location, age and sex.

espanolIntroduccion y objetivo La displasia fibrosa (DF) puede asociarse al desarrollo de osteomalacia hipofosfatemica por la produccion de FGF-23 en el tejido oseo displasico. En este estudio se analizan los valores de FGF-23 en pacientes con DF y su relacion con la actividad de la enfermedad y con los valores de fosfato serico. Pacientes y metodos Se incluyo a 12 pacientes adultos con DF. Se revisaron las caracteristicas clinicas, los parametros analiticos y los tratamientos realizados y su relacion con los valores de FGF-23. Resultados Seis de 12 pacientes (50%) tenian un aumento del FGF-23; estos pacientes tenian una edad, una extension y una actividad de la enfermedad similares a aquellos con FGF-23 normal. No se observaron diferencias entre los valores de fosfato serico entre ambos grupos (FGF-23 alto: 3,9±0,9mg/dl vs. FGF-23 normal: 3,5±0,6mg/dl). Ningun paciente con aumento de FGF-23 tenia valores de fosfato serico bajos. Conclusion Los pacientes adultos con DF presentan con frecuencia un aumento del FGF-23 sin repercusion en los niveles sericos de fosfato, lo que indica una alteracion en el procesamiento de esta proteina en el tejido oseo displasico en esta patologia. EnglishIntroduction and objective Fibrous dysplasia (FD) can be associated with the development of hypophosphatemic osteomalacia, caused by the production of FGF-23 by dysplastic bone tissue. This study analysed FGF-23 levels in patients with FD, and their association with disease activity and serum phosphate values. Patients and methods Twelve adult patients with FD were included in the study. Clinical history, disease extension and activity and treatments received were reviewed, and the relationship of those values with FGF-23 and serum P levels was analysed. Results FGF-23 was elevated in 6/12 patients (50%). Patients with high FGF-23 levels had similar age and disease activity and extension than those who did not. No differences were observed in serum phosphate values between both groups (increased FGF-23: 3.9±0.9 mg/dl vs. decreased FGF-23: 3.5±0.6 mg/dl). In fact, none of the patients with increased FGF-23 had low serum phosphate values. Conclusion Adult FD patients frequently present elevated FGF-23 values with no serum phosphate level repercussion, suggesting an alteration in the processing of this protein in the dysplastic bone tissue for this pathology.

Background Glucocorticoid-induced osteoporosis (GIOP) is the one of the most common forms of secondary osteoporosis (OP). Fractures in GIOP frequently occur with higher than expected bone mineral density (BMD) values. The Trabecular Bone Score (TBS) is a gray-level textural index derived from DXA images that provides information about bone microarchitecture and fracture risk independently of BMD; therefore, TBS measurement could be useful for identifying patients with high fracture risk associated with glucocorticoid (GC) treatment. Objectives To analyse the clinical utility of TBS for fracture risk assessment in GC treated patients and compare it with BMD assessment, the gold-standard diagnostic test. Methods 127 patients on chronic GC treatment (≥5mg/day) were included (mean age 62±18 years, 63% women) in this cross-sectional study. The medical history and anthropometric data were collected, as well as measurements of bone metabolism parameters, bone densitometry (DXA) at lumbar spine and femur (considering OP when T-score ≤-2.5), TBS (considering degraded microarchitecture [DMA] with values Results Most of the patients were receiving GC treatment for vasculitis or polymyalgia rheumatica over a mean period of 47.7±69 months at a mean daily dose of 14.5mg. 17% had VF, 28% any type of fragility fracture (VF + no-VF), 29% OP and 71% DMA. In patients with VF, low TBS (DMA) was more common than densitometric OP (76%, p=0.03 vs. 38%, p=n.s). Similar results were observed when analysing patients with any fragility fracture (69%, p=0.02 vs. 36%, p=n.s). The diagnostic accuracy of TBS was greater than BMD on evaluating VF, with a sensitivity, specificity, PPV and NPV of 0.76, 0.53, 0.25 and 0.92 for TBS and 0.38, 0.72, 0.22, and 0.85 for BMD, respectively. Specificity increased to 0.89 for VF and 0.9 for any fragility fracture on combining both assessments (OP+DMA). Conclusion TBS has greater discriminative power than BMD measurement and could be useful as a complementary tool for fracture risk assessment in GIOP. Disclosure of Interests Helena Florez: None declared, Jose Hernandez-Rodriguez : None declared, Africa Muxi: None declared, Josep Lluis Carrasco: None declared, Sergio Prieto-Gonzalez: None declared, Silvia Ruiz-Gaspa : None declared, Maria C. Cid Grant/research support from: Kiniksa Pharmaceuticals, Consultant for: Roche, GSK, Janssen, Abbvie, Speakers bureau: Boehringer-Inhelheim, Vifor, Ana Monegal Speakers bureau: Eli Lilly, Amgen, Nuria Guanabens Consultant for: Advisory Boards from Amgen, Alexion and UCB, Speakers bureau: Fees and lectures from Eli Lilly, Pilar Peris Speakers bureau: Personal Fees and Non-financial support (attendance to congresses) from Amgen and Eli Lilly

Background Glucocorticoid-induced osteoporosis (GIOP) is a common form of secondary osteoporosis (OP). Fractures in GIOP frequently occur with higher bone mineral density (BMD) than expected and typically at treatment initiation, complicating the identification of patients at risk for fracture. Objectives Identify risk factors associated with fragility fracture development in GC-treated patients. Methods 127 patients (aged 62±18years, 63% women, 46% postmenopausal) on GC treatment (prednisone ≥5mg/day, >3months) were included. Clinical data collected included: risk factors for OP and fractures, dose and GC-treatment duration, previous fractures and disease activity, anthropometric data, bone metabolism parameters (including gonadal axis study), BMD analysis (DXA; OP: T-score ≤-2.5), TBS (degraded microarchitecture [DMA]: Results Most patients received GC treatment for vasculitis or polymyalgia rheumatica during 47.7±69 months (mean daily dose: 14.5mg). 17% had VF, 28% had fragility fracture (VF + non-VF), 29% OP and 71% DMA. Patients with VF received more GC-boluses (57.1% vs. 29.5%,p=0.03), were older (68±13 vs. 60±19 years, p=0.02), postmenopausal (100% vs. 67%, p=0.015) and/or men with testosterone 100, p=0.01) and having received GC-boluses (OR 3.40; IC95% 1-11.8, p=0.01) were the principal factors associated with VF. Hypogonadism (OR 7.1; IC95% 1.5-38.7, p=0.01) and having a FRAX >20 (OR 6.97; IC95% 1.3-51.7, p=0.02) were factors related to the presence of fragility fractures. Men with testosterone Conclusion Hypogonadism is a major risk factor for developing fractures in GC-treated men and women, whereas receiving GC-boluses is related to VF, indicating the importance of evaluating the gonadal axis in these patients. References [1] Buckley L, et al. Arthritis Care Res. 2017 Disclosure of Interests Helena Florez: None declared, Jose Hernandez-Rodriguez : None declared, Africa Muxi: None declared, Josep Lluis Carrasco: None declared, Sergio Prieto-Gonzalez: None declared, Silvia Ruiz-Gaspa : None declared, Maria C. Cid Grant/research support from: Kiniksa Pharmaceuticals, Consultant for: Roche, GSK, Janssen, Abbvie, Speakers bureau: Boehringer-Inhelheim, Vifor, Ana Monegal Speakers bureau: Eli Lilly, Amgen, Nuria Guanabens Consultant for: Advisory Boards from Amgen, Alexion and UCB, Speakers bureau: Fees and lectures from Eli Lilly, Pilar Peris Speakers bureau: Personal Fees and Non-financial support (attendance to congresses) from Amgen and Eli Lilly

Background Rheumatoid arthritis (RA) is a risk factor for the development of fragility fractures, but there is little quality data on its prevalence. Conversely, osteoporosis is one of the most frequent comorbidities of RA. Objectives To determine the prevalence of vertebral fractures in postmenopausal women with RA and to analyse their characteristics and associated risk factors. Methods We included 346 postmenopausal women diagnosed with RA according to the ACR/EULAR 2010 criteria in 19 Spanish Rheumatology Departments, randomly selected from the registry of RA patients in each center, recruited during 2018. Lateral radiographs of the dorsal and lumbar spine were obtained from all patients, to evaluate morphometric vertebral fractures. Expert rheumatologists identified vertebral fractures and classified them into mild (grade 1: reduction of height of 20-25%), moderate (grade 2: reduction of 26-40%) and severe (grade 3: reduction > 40%), according to the Genant grading scale. The spinal deformity index (SDI) was calculated by assigning numbers 1, 2 and 3 to each fractured vertebra and adding the total score of each patient. The study variables were: a) age, body mass index (BMI), b) factors related to RA: time of evolution, FR, ACPA, and c) fracture risk factors: prior fragility fracture, parental hip fracture, glucocorticoids, smoking, alcohol intake ≥3 units daily, secondary osteoporosis and time since menopause. Results The mean age was 66.8 (SD: 10.1) years and the median evolution of the disease, 8.00 [RIQ: 3.00-15.5] years. 77.2% (n: 267) and 75.7% (n: 252) had FR and ACPA +, respectively. The mean duration of the postmenopausal period was 15.0 (SD: 9.6) years. 23.4% (n: 79) of patients had at least one vertebral fracture; 10.7% (n: 36) had a single fracture and 12.7% (n: 43), multiple fractures. The most fractured vertebrae were D12, L1 and L2 (fractured in > 5% of patients). The median SDI was 3 [RIQ: 2-5]. The vertebrae with the highest mean IDE were D8, D10, D11 and L1 (all mean IDE ≥ 2).An association was found between the presence of vertebral fractures and age, height, postmenopausal period, time of disease progression, glucocorticoid treatment and parental hip. No linear association was found between SDI and age, time of evolution of the disease, BMI and time since menopause. Conclusion One out of every 4 postmenopausal women with RA has at least one vertebral fracture. Vertebrae of the dorso-lumbar hinge are the most frequently involved and the magnitude of the spinal deformity is relevant. Vertebral fractures are related to the time of evolution of RA and to the risk factors for fracture. Disclosure of Interests Carmen Gomez Vaquero: None declared, Dacia Cerda: None declared, Cristina Hidalgo: None declared, JA Martinez Lopez: None declared, Luis Marcelino Arboleya Rodriguez: None declared, Javier Aguilar del Rey: None declared, Silvia Martinez Pardo: None declared, Inmaculada Ros: None declared, Xavier Suris Speakers bureau: Lilly, Pfizer, MSD, Dolors Grados: None declared, Chesus Beltran: None declared, Evelyn Suero-Rosario: None declared, Inmaculada Gomez Gracia: None declared, Asuncion Salmoral: None declared, Irene Martin-Esteve: None declared, Helena Florez: None declared, Antonio Naranjo: None declared, Santos Castaneda Consultant for: Amgen, BMS, Pfizer, Lilly, MSD, Roche, Sanofi, UCB, Soledad Ojeda Grant/research support from: AMGEN, Speakers bureau: AMGEN, S Garcia Carazo: None declared, Alberto Garcia-Vadillo: None declared, Laura Lopez Vives: None declared, A Martinez-Ferrer: None declared, Helena Borrell: None declared, Pilar Aguado: None declared, Raul Castellanos-Moreira Speakers bureau: MSD, Lilly, Nuria Guanabens Consultant for: Advisory Boards from Amgen, Alexion and UCB, Speakers bureau: Fees and lectures from Eli Lilly

Fibrous dysplasia is a skeletal disorder that is associated with a wide spectrum of clinical manifestations, including localized asymptomatic forms and extensive severe forms with severe bone deformities and endocrinological alterations, depending on age, location, extent and associated processes. Although the treatment of choice is based on bisphosphonates, the therapeutic efficacy of these agents in the control of disease activity remains uncertain. This article reviews the current data available on the treatment of this disease as well as the preliminary data on new therapeutic approaches.

Resumen La displasia fibrosa es un trastorno esqueletico que dependiendo de la edad, la localizacion, la extension y los procesos asociados puede presentarse con un amplio espectro de manifestaciones clinicas, desde formas localizadas asintomaticas a formas extensas graves con deformidades oseas importantes o incluso alteraciones endocrinologicas. Si bien el tratamiento de eleccion lo constituyen los bisfosfonato, la eficacia en el control de la actividad de la enfermedad continua siendo incierta. En este articulo se revisan los datos sobre el tratamiento de esta entidad, asi como los resultados preliminares de nuevas dianas terapeuticas.

Background:Increasing evidence indicates that osteocalcin (OC) is involved in the regulation of glucose homeostasis. Glucocorticoid (GC) treatment is associated with impaired osteoblast function and decreased OC levels and also with the development of CG-induced diabetes mellitus (GIDM). However, whether decreased OC levels in GC-treated subjects contribute to GIDM is not well known.Objectives:To analyse whether OC levels in GC-treated patients are associated with the presence of GIDM.Methods:127 patients (aged 62±18years, 63% women) on GC treatment for autoimmune diseases (≥5mg/day, >3 months) were included. Clinical and anthropometric data were analysed, including the GC dose and treatment duration, presence of GIDM, fragility fractures, densitometric osteoporosis and bone formation (OC, bone alkaline phosphatase [BAP], PINP) and resorption markers (urinary NTX, serum CTX). The cut-offs of each bone marker for the presence of GIDM were estimated and optimized with the Youden index and included in the logistic regression analysis (adjusted for BMI, age and GC doses).Results:17.3% of patients presented GIDM. Diabetic subjects were older (70.5±12.2 vs. 59.6±18.4, p=0.001) and had a higher BMI than non-diabetics (30±5.2 vs. 26±4.2, p=0.002). No differences were observed in GC dose or duration or in the presence of vertebral fractures. Diabetics showed lower levels of OC (7.57±1.01 vs. 11.56±1; pConclusion:Decreased OC levels in GC-treated patients are associated with an increased risk of GIDM, a finding that was not observed with other bone turnover markers, further confirming the involvement of OC in the glucose homeostasis regulation in this entity.Disclosure of Interests:None declared

Background:Incidence of clinical fractures in rheumatoid arthritis (RA) is not as well-known as hip or vertebral fracture incidence.Objectives:1. To estimate the incidence of clinical fragility fractures in a population of postmenopausal women diagnosed with RA and compare it with that of the general population; 2. To analyze the risk factors for fracture.Methods:330 postmenopausal women with RA from 19 Spanish Rheumatology Departments, randomly selected from the registry of RA patients in each center. The control group consisted of 660 Spanish postmenopausal women from the Camargo Cohort. Clinical fractures during the previous 5 years were recorded. Assessed risk factors for fracture were: sociodemographic characteristics, BMD and variables related to RA.Results:Median age of RA patients was 64 yrs. vs. 63 yrs. in controls (ns). Evolution of the disease was 8 yrs. 78% and 76% had RF and ACPA+, respectively. 69% of patients were in remission or low activity. 85% had received glucocorticoids and methotrexate and 40% at least one biological DMARD. We identified 105 fractures (87 fragility and 18 traumatic) in 75 patients. Fifty-four patients and 47 controls had at least one major fracture (MF) (p< 0.001). Incidence of MF was 3.55 per 100 patient-year in patients and 0.72 in controls. Risk factors for MF in RA patients were age, previous fracture, parental hip fracture, postmenopausal period, hip BMD and cumulative dose of glucocorticoids. In controls, risk factors were age, age at menopause and lumbar BMD.Among RA-associated factors, MFs were associated with erosions, disease activity and disability. Previous fracture in RA patients was a strong risk for MF (HR: 10.37 [95% CI: 2.95-36.41]).Conclusion:Between 3 and 4 of every 100 postmenopausal women with RA have a major fracture per year, four times more than the general population. Disease activity and disability associated with RA, the cumulative dose of glucocorticoids and mainly previous fracture are associated with the development of fragility fractures.References:NoneAcknowledgments:Funded in part by ISCIII (PI18/00762) that included FEDER funds from the EU.Disclosure of Interests:Carmen Gómez Vaquero: None declared, Jose Manuel Olmos: None declared, J. Luis Hernández: None declared, Dacia Cerda: None declared, Cristina Hidalgo: None declared, JA Martínez López: None declared, Luis Marcelino Arboleya Rodríguez: None declared, Javier Aguilar del Rey: None declared, Silvia Martinez Pardo: None declared, Inmaculada Ros: None declared, Xavier Surís: None declared, Dolors Grados Canovas: None declared, Chesús Beltrán Audera: None declared, Evelyn Suero-Rosario: None declared, Inmaculada Gómez Gracia: None declared, Asunción Salmoral: None declared, Irene Martín-Esteve: None declared, Helena Florez: None declared, Antonio Naranjo Grant/research support from: amgen, Consultant of: UCB, Speakers bureau: AMGEN, Santos Castañeda: None declared, Soledad Ojeda Speakers bureau: AMGEN, LILLY, GEBRO, S García Carazo: None declared, Alberto García-Vadillo: None declared, Laura López Vives: None declared, À Martínez-Ferrer: None declared, Helena Borrell Paños: None declared, Pilar Aguado: None declared, Raul Castellanos-Moreira: None declared, Cristian Tebé: None declared, Núria Guañabens: None declared

Objective Denosumab is an antiresorptive drug with demonstrated efficacy in the treatment of osteoporosis. However, discontinuation of this agent is associated with increased bone turnover and rapid bone loss, and more recently, with the development of vertebral fractures (VF) in some patients. Therefore, the aim of the study was to analyze the clinical characteristics, bone metabolism parameters and evolution of a group of patients who developed vertebral fractures after denosumab discontinuation. In addition, we reviewed the literature on this subject. Methods During a period of 28 months (September 2015–January 2018) 7 women presenting spontaneous vertebral fractures after denosumab discontinuation were attended in the Rheumatology Department of our centre. We analyzed their clinical characteristics, bone metabolism parameters and evolution and reviewed the literature related to this subject. Results The patients had received denosumab during 24–58 months (median 38), and developed a median of 5 VF per patient at 8–20 months (median 10) since the last dose of denosumab. Only 2 patients presented previous VF, and most (5 patients) received previous bisphosphonate treatment. After VF all restarted antiosteoporotic treatment with no further fractures during follow-up (median 19 months). Conclusions In this short series, previous bisphosphonate treatment does not seem to be a protective factor for the development of VF. The possible development of VF following discontinuation of denosumab must be taken into account in the clinical practice of physicians and dentists. Nonetheless, further studies are needed to improve the identification of patients at risk and the most adequate sequential treatment options.

Background Denosumab (Dmab) is an antiresorptive treatment with demonstrated efficacy in osteoporosis. However, discontinuation of Dmab has been associated with rapid bone loss, and recently, the development of vertebral fractures (VF) in some patients. It is essential to identify the risk factors for these adverse events and follow its evolution. Objectives To analyse the clinical characteristics, parameters of bone metabolism and evolution of patients developing VF after Dmab discontinuation. Methods Six women with spontaneous VF after Dmab discontinuation were included (median age 66 years56–75). The clinical history, cause of osteoporosis, treatments received, fractures, Dmab treatment duration and discontinuation period were reviewed. Additionally, the clinical and densitometric evolution, and bone mineral parameters were also analysed after Dmab discontinuation. Results All the patients had postmenopausal osteoporosis, and one was receiving glucocorticoid treatment; 3/6 patients had previous fractures (2 VF and 1 calcaneus); 4/6 had previously received antiosteoporotic treatment (hormone replacement therapy, risedronate, alendronate, zoledronate [once or consecutively)] during 1–23 years. All had received Dmab for 24–53 months (median 37). The reasons for treatment discontinuation were: dental indication (1 patient), BMD improvement (T-score −1.2) (1 patient), poor adherence,1 prescription problems and/or delay in administration.3 The median bone mineral density T-scores prior to VF were −2.6 (-1.2/–4) at the lumbar spine and −3.0 (-0.6/–3.7) at the femoral neck. The mean time between the last Dmab dose and VF was 9.5 months,8–20 with a median of 5 VFs/patient.2–8 No patient showed 25-OH vitamin D Conclusions Discontinuation of Dmab is associated with an increase in bone turnover markers and bone loss which can be associated with the development of spontaneous VF. Previous bisphosphonate therapy does not seem to decrease this risk. Further studies are needed to assess the optimal antiresorptive treatment and its duration after Dmab discontinuation. Disclosure of Interest None declared

Background The trabecular Bone Score (TBS) is a novel gray-level textural analysis measurement that can be applied to DXA images to estimate trabecular microarchitecture and has been shown to be related to direct measures of bone microarchitecture and fracture risk. Osteogenesis impefecta (OI) is a congenital bone disease characterised by a low bone mineral density (BMD) and poor bone quality and strength. The usefulness of TBS in OI has been scarcely evaluated. Objectives To analyse the clinical usefulness of TBS determination in patients with OI and its relation with anthropometric and clinical features (especially concerning skeletal fractures and BMD results). Methods: Twenty-four patients (18 F:6 M) with OI with a mean age of 38±15 years19–63 attending a Metabolic Bone Disease Unit were included. The clinical reports of the patients were reviewed, with especial attention to the clinical features (weight, height and body mass index [BMI]), previous fractures, disease severity, associated mutations and treatments received. Lumbar spine (LS), total hip (TH), and femoral neck (FN) BMD were measured using DXA equipment (Lunar) in all patients. TBS was analysed in LS, and the results were classified in three categories1: TBS >1.310 (normal), TBS 1.230–1.310 (partially degraded microarchitecture), TBS Results: 5/24 patients (21%) had a degraded microarchitecture, 4 (17%) a partially degraded microarchitecture and 15 (63%) normal TBS. All patients with TBS Conclusions: TBS measurement does not seem to be useful for evaluating bone strength in patients with OI. Despite most patients presenting a history of multiple fractures, only 21% showed degraded microarchitecture with TBS. Reference: [1] McCloskey EV, Oden A, Harvey NC, et al. J Bone Miner Res2016;31:940–8. Disclosure of Interest: None declared

Introduction and objective Fibrous dysplasia (FD) can be associated with the development of hypophosphatemic osteomalacia, caused by the production of FGF-23 by dysplastic bone tissue. This study analysed FGF-23 levels in patients with FD, and their association with disease activity and serum phosphate values. Patients and methods Twelve adult patients with FD were included in the study. Clinical history, disease extension and activity and treatments received were reviewed, and the relationship of those values with FGF-23 and serum P levels was analysed. Results FGF-23 was elevated in 6/12 patients (50%). Patients with high FGF-23 levels had similar age and disease activity and extension than those who did not. No differences were observed in serum phosphate values between both groups (increased FGF-23: 3.9 ± 0.9 mg/dl vs. decreased FGF-23: 3.5 ± 0.6 mg/dl). In fact, none of the patients with increased FGF-23 had low serum phosphate values. Conclusion Adult FD patients frequently present elevated FGF-23 values with no serum phosphate level repercussion, suggesting an alteration in the processing of this protein in the dysplastic bone tissue for this pathology.

Background Fibrous dysplasia of bone (FD) is an uncommon skeletal disorder, caused by missense mutations of the GNAS1 gene and is characterized by the development of fibro-osseous lesions that replace normal bone. FD can present with a broad spectrum of clinical manifestations, including the development of hypophosphatemic osteomalacia which is due to the production of the phosphaturic hormone fibroblast growth factor 23 (FGF-23) by the dysplastic bone tissue. Nevertheless, the prevalence of this clinical complication is not well known. Objectives To analyse the serum levels of FGF-23 in patients with FD and determine their relationship with the extension and activity of the disease, as well as with serum phosphate levels. Methods Twelve patients (7F:5M) with FD with a mean age of 50.67±16.4 years (24–79) were included. The clinical reports of the patients were reviewed, with special attention to the extension and activity of the disease, number and location of the affected bones, clinical complications and treatments received. Serum FGF-23 values were recorded in all subjects (determined by Immunotopics, CA, USA [measuring FGF23 C- terminal], normal value Results Serum levels of FGF-23 were increased (>130 RU/ml) in 6/12 patients (50%). In patients with and without high FGF-23 levels the number of affected bones (2.2±2 vs . 1.9±1, respectively) and the skeletal locations of FD were similar as was the age in both groups of patients (48.2±14 vs . 53.2±19 years). In addition, FD disease activity and extension were similar in the two groups as were the bone turnover marker values (FAO, PINP and CTx). Strikingly, differences between serum phosphate values were not observed between the two groups (FGF23 >130: 3.9±0.9 mg/dl vs . FGF23 Conclusions Patients with FD frequently present elevated FGF-23 values with no effects on serum phosphate levels, thereby suggesting the presence of an alteration in processing this protein in the dysplastic bone tissue in this disease. The role of denosumab treatment in FD and its repercussion on FGF-23 levels need further study. Disclosure of Interest None declared

Acute generalised exanthematous pustulosis (AGEP) is a rare toxicoderma characterised by an acute onset rash, with many sterile pustules on the surface, high fever and increased acute phase reactants. We report the case of a patient who presented to the dermatology department with an AGEP and polyarthritis, in which a novel CARD14 mutation was identified. The pathophysiological mechanism of AGEP remains unclear, although mutations in the IL36RN gene have been identified in a small subset of AGEP patients. Similarly, mutations in the CARD14 gene have been linked to pustular types of psoriasis and familiar cases of pityriasis rubra pilaris; however, there are no reports associating mutations in the CARD14 gene with AGEP.