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Whole-genome characterisation in clinical microbiology enables to detect trends in infection dynamics and disease transmission. Here, we report a case of bacteraemia due to Campylobacter fetus subsp. fetus in a rural worker under cancer treatment that was diagnosed with cellulitis; the patient was treated with antibiotics and recovered. The routine typing methods were not able to identify the microorganism causing the infection, so it was further analysed by molecular methods and whole-genome sequencing. The multi-locus sequence typing (MLST) revealed the presence of the bovine-associated ST-4 genotype. Whole-genome comparisons with other C. fetus strains revealed an inconsistent phylogenetic position based on the core genome, discordant with previous ST-4 strains. To the best of our knowledge, this is the first C. fetus subsp. fetus carrying the ST-4 isolated from humans and represents a probable case of zoonotic transmission from cattle.

Summary Osteoporosis is a frequent complication related to spinal cord injury (SCI), and data on osteoporosis treatment after SCI is scarce. Treatment with denosumab increases lumbar and femoral BMD and decreases bone turnover markers in individuals with recent SCI. This drug may be a promising therapeutic option in SCI-related osteoporosis. Introduction Osteoporosis development is a frequent complication related to SCI, especially at the sublesional level. Nevertheless, data on osteoporosis treatment after SCI is scarce, particularly short term after injury, when the highest bone loss is produced. The aim of this study was to analyze the efficacy of denosumab in the treatment of SCI-related osteoporosis. Methods Fourteen individuals aged 39 ± 15 years with osteoporosis secondary to recent SCI (mean injury duration 15 ± 4 months) were treated with denosumab for 12 months. Bone turnover markers (BTMs) (PINP, bone ALP, sCTx), 25-hydroxyvitamin D (25OHD) levels and bone mineral density (BMD) at the lumbar spine (LS), total hip (TH), and femoral neck (FN) were assessed at baseline and at 12 months. All participants received calcium and vitamin D supplementation. Results At 12 months, SCI denosumab-treated participants showed a significant increase in BMD at TH (+2.4 ± 3.6 %, p  = 0.042), FN (+3 ± 3.6 %, p  = 0.006), and LS (+7.8 ± 3.7 %, p  < 0.001) compared to baseline values. Denosumab treatment was associated with significant decreases in BTMs (bone ALP −42 %, p  < 0.001; PINP −58 %, p  < 0.001, sCTx −57 %, p  = 0.002) at 12 months. BMD evolution was not related to BTM changes or 25OHD serum levels. No skeletal fractures or serious adverse events were observed during follow-up. Conclusions Treatment with denosumab increases lumbar and femoral BMD and decreases bone turnover markers in individuals with recent SCI. This drug may be a promising therapeutic option in SCI-related osteoporosis.

Summary Spinal cord injury (SCI) has been associated with a marked bone loss after injury and a consequent increased risk of osteoporosis. The evaluation of bone mineral density shortly after SCI is a simple and effective method for predicting the development of osteoporosis during the first year after SCI. Introduction Spinal cord injury (SCI) has been associated with a marked bone loss after injury and a consequent increased risk of osteoporosis and fractures. The aim of this study was to analyze the factors associated with osteoporosis development short-term after SCI. Methods We included patients with complete recent SCI (<6 months) evaluating bone turnover markers (P1NP, bone ALP, and sCTx), 25-OH-vitaminD (25OHD) levels, and lumbar and femoral BMD (Lunar, Prodigy) at baseline, 6 and 12 months after SCI. The risk factors for osteoporosis analyzed included the following: age, gender, BMI, toxic habits, bone turnover markers, 25OHD levels, lumbar and femoral BMD, level, severity and type of SCI, and days-since-injury. Osteoporosis was defined according to WHO criteria. Results Thirty-five patients aged 35 ± 16 years were included, and 52 % developed osteoporosis during the 12-month follow-up. These latter patients had lower BMD values at femur and lumbar spine and higher bone turnover markers at baseline. On multivariate analysis, the principal factors related to osteoporosis development were as follows: total femur BMD <1 g/cm 2 (RR, 3.61; 95 % CI 1.30–10.06, p  = 0.002) and lumbar BMD <1.2 g/cm 2 at baseline (0.97 probability of osteoporosis with both parameters under these values). Increased risk for osteoporosis was also associated with increased baseline values of bone ALP (>14 ng/mL) (RR 2.40; 95 % CI 1.10–5.23, p  = 0.041) and P1NP (>140 ng/mL) (RR 3.08; 95 % CI 1.10–8.57, p  = 0.017). Conclusions The evaluation of BMD at the lumbar spine and femur short-term after SCI is a simple, effective method for predicting the development of osteoporosis during the first year after SCI. Our results also indicate the need to evaluate and treat these patients shortly after injury.

SummaryThere is marked bone loss after spinal cord injury (SCI); however, its pathogenesis and clinical management remain unclear. The increased circulating levels of receptor activator of nuclear factor kB ligand (RANKL) associated with bone loss shortly after SCI and the prevention of bone loss with denosumab treatment suggest a contributory role of RANKL in SCI-induced osteoporosis.IntroductionBone turnover and bone loss are markedly increased shortly after SCI. However, the pathogenesis and clinical management of this process remain unclear, especially the role of the osteoprotegerin (OPG)/RANKL system in this disorder. The aim of this study was to analyze serum levels of OPG and RANKL in bone loss associated with recent SCI and the effect of denosumab treatment on these mediators.MethodsTwenty-three males with recent complete SCI were prospectively included. Serum OPG and RANKL levels, bone turnover markers (PINP, bone ALP, CTX), and bone mineral density (BMD) were assessed at baseline, at 6 months of follow-up, prior to initiating denosumab, and 6 months after treatment. The results were compared with a healthy control group.ResultsAt baseline, SCI patients showed higher RANKL levels vs. controls which were correlated with days-since-SCI and total hip BMD loss at 6 months. OPG levels were similar to controls at baseline. After denosumab treatment, OPG showed no changes, whereas RANKL levels became undetectable in 67% of patients. Patients with undetectable RANKL during treatment showed better response in femoral BMD and bone markers vs. patients with detectable RANKL at 6 months of denosumab. Increased parathormone (PTH) levels during treatment were negatively correlated with RANKL changes.ConclusionsRANKL levels are increased after SCI and related to BMD loss at the proximal femur, becoming undetectable after denosumab treatment. The effect of denosumab on preventing sublesional bone loss, especially in patients with undetectable levels during treatment, suggests a contributory role of RANKL in this process.

BackgroundThe 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.ObjectivesTo 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 <1.230 (degraded microarchitecture). TBS values were compared with a healthy control group of similar age and gender.Results:5/24 patients (21%) had a degraded microarchitecture, 4 (17%) a partially degraded microarchitecture and 15 (63%) normal TBS. All patients with TBS <1230 were over 40 years old. 21/24 patients had a previous history of multiple fractures. Regarding BMD, 54% of the patients had osteoporosis, 42% osteopenia and one had normal values. Most patients had a mutation in the COL1A1 gene (63%). A correlation was observed between TBS and age (r=−0.5, p=0.006) and LS BMD (r=0.5, p=0.014), showing a trend to significance with BMI (r=−0.4, p=0.058). No significant differences were observed on comparing TBS in patients and controls (1.321 vs. 1.391, p=N .S.).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, Odén A, Harvey NC, et al. J Bone Miner Res2016;31:940–8.Disclosure of Interest:None declared

SummaryMarked trabecular and cortical bone loss was observed at the proximal femur short-term after spinal cord injury (SCI). 3D-DXA provided measurement of vBMD evolution at both femoral compartments and cortical thinning, thereby suggesting that this technique could be useful for bone analysis in these patients.IntroductionSCI is associated with a marked increase in bone loss and risk of osteoporosis development short-term after injury. 3D-DXA is a new imaging analysis technique providing 3D analysis of the cortical and trabecular bone from DXA scans. The aim of this study was to assess the evolution of trabecular macrostructure and cortical bone using 3D-DXA in patients with recent SCI followed over 12 months.MethodsSixteen males with recent SCI (< 3 months since injury) and without antiosteoporotic treatment were included. Clinical assessment, bone mineral density (BMD) measurements by DXA, and 3D-DXA evaluation at proximal femur (analyzing the integral, trabecular and cortical volumetric BMD [vBMD] and cortical thickness) were performed at baseline and at 6 and 12 months of follow-up.ResultsvBMD significantly decreased at integral, trabecular, and cortical compartments at 6 months (− 8.8, − 11.6, and − 2.4%), with a further decrease at 12 months, resulting in an overall decrease of − 16.6, − 21.9, and − 5.0%, respectively. Cortical thickness also decreased at 6 and 12 months (− 8.0 and − 11.4%), with the maximal decrease being observed during the first 6 months. The mean BMD losses by DXA at femoral neck and total femur were − 17.7 and − 21.1%, at 12 months, respectively.ConclusionsMarked trabecular and cortical bone loss was observed at the proximal femur short-term after SCI. 3D-DXA measured vBMD evolution at both femoral compartments and cortical thinning, providing better knowledge of their differential contributory role to bone strength and probably of the effect of therapy in these patients.

BackgroundSpinal cord injury (SCI) has been associated with a marked increase in bone loss and bone remodeling, especially short-term after injury. However, the pathogenesis and clinical management of this process remain unclear, as well as the role of the key regulators of bone remodeling, the OPG/RANKL system.ObjectivesTo analyze the role of the regulators of bone remodeling, OPG and RANKL, in the bone loss associated with recent SCI as well as the effect of antiosteoporotic therapy with denosumab in these bone regulators in a prospective study.MethodsTwenty-three male patients (aged 18 - 67 years [mean 36 ± 16 years]) with recent (<6 months) complete SCI were prospectively included (43.5% paraplegic, 56.5% tetraplegic). Patients were followed every 6 months. All patients received calcium and vitamin D supplementation. Antiosteoporotic therapy with denosumab was recommended when patients developed densitometric osteoporosis during follow-up. Serum levels of OPG and RANKL (Biomedica, Vienna, Austria), bone turnover markers (PINP, bone ALP, sCTX) and bone mineral density (BMD) at the lumbar spine and total hip were assessed at baseline (99±30 days after SCI), prior to initiating antiosteoporotic treatment (14±4 months post-SCI) and during antiosteoporotic therapy with denosumab (6 months after initiating treatment). The results were compared with a healthy control group.ResultsAt baseline, SCI patients showed a significant increase in RANKL serum levels compared to controls (3.4±1.7 vs. 2.3±1.6 pg/mL, p=0.022) which correlated with days-since-SCI (r=0.589, p=0.005) and became undetectable after denosumab treatment in 67% of the patients (p=0.001). OPG serum levels were similar to controls at baseline (87.7±38.7 vs. 71.7±25.4, p=0.1) and did not change with denosumab treatment. No differences were observed in RANKL and OPG levels on comparing tetraplegic vs. paraplegic patients. Neither were RANKL or OPG levels related to the increase in bone loss and bone turnover markers after SCI. Patients with undetectable RANKL serum levels after denosumab treatment did not present further sublesional bone loss but increased total hip BMD (+2.5±1.3%, p=0.005), and bone markers markedly decreased (PINP: -53%, p=0.007; sCTX: -68%, p=0.005).ConclusionsThis study shows that short-term after SCI there is an increase in RANKL serum levels which become undetectable after denosumab treatment. The preventive effect of denosumab on sublesional bone loss further suggests a contributory role of RANKL in this clinical process.AcknowledgementWork funded by a Grant from the SEIOMM (Spanish Society for Bone and Mineral Research).Disclosure of InterestNone declared

Background Spinal cord injury (SCI) has been associated with marked bone loss and an increased risk of fractures under the SCI level. Objectives To analyze the effect of recent complete SCI on bone turnover and BMD evolution and factors related to bone loss. Methods Prospective study including patients with complete motor SCI (ASIA A or B) (<6 months). Bone turnover markers (bone formation: P1NP, bone ALP; resorption: sCTx) and BMD (lumbar spine and femur (DXA)) were assessed in all patients at baseline and at 6 and 12 months. Risk factors for osteoporosis, SCI level (paraplegia/tetraplegia), lesion type (spastic/flaccid), SCI severity (ASIA score) and fractures were evaluated, comparing results with a control group. Results 42 patients (40M:2F) (mean age 35±14years) were included 100±33days after SCI (ASIA A 39:B 3). 55% had paraplegia and 78% spasticity. 24 were followed-up at 6 months and 22 at 12 months. Compared to controls, bone turnover markers were markedly increased just after SCI (P1NP:194±124 vs. 50±19ng/ml,p<0.001; bone ALP:15±7 vs. 12±4ng/ml,p=0.04; sCTx1.48±0.52 vs. 0.49±0.23ng/ml,p<0.001), with maintained, although with less increased, values at 6 and 12 months. BMD decreased progressively at proximal femur (-13±5% at 6months, p<0.001; -20±8% at 12months, p<0.001), with no significant changes at lumbar BMD. At 12 months 59% of the SCI patients presented densitometric osteoporosis. Patients with higher sCTX values after SCI (3rd tertile) had the highest femur BMD loss at 12 months (-23%). No relationship was observed between BMD and bone marker changes, or SCI level or lesion type. Conclusions Patients with complete SCI have increased bone turnover after injury with marked bone loss under the injury level of ∼-20% of BMD at the proximal femur at one year, being more marked in individuals with the highest sCTX levels. Awareness of this complication and its therapeutic approach are mandatory. Acknowledgements Work funded by a grant from Fundaciό La Maratό de TV3. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.5116

Summary The effect of ascites on bone densitometry has been assessed in 25 patients with advanced cirrhosis, and it was concluded that ascites over 4 l causes inaccuracy of BMD measurements, particularly at the lumbar spine. This fact must be considered when assessing bone mass in patients with decompensated cirrhosis. Introduction Bone mineral density (BMD) measured by dual-energy x-ray absorptiometry (DXA) is the best procedure for assessment of osteoporosis and fracture risk, but BMD values at the central skeleton may be influenced by changes in soft tissues. Therefore, we have studied the effect of ascites on BMD. Methods BMD was measured by DXA at the lumbar spine, femoral neck and total hip, just before and shortly after therapeutic paracentesis in 25 patients with advanced liver cirrhosis. Changes in BMD, lean and fat mass, abdominal diameter and weight, as well as the amount of removed ascites were measured. Results The amount of drained ascites was 6.6 ± 0.5 l (range: 3.0 to 12.7 l). After paracentesis, BMD increased at the lumbar spine (from 0.944 ± 0.035 to 0.997 ± 0.038 g/cm 2 , p  < 0.001) and at the total hip (from 0.913 ± 0.036 to 0.926 ± 0.036 g/cm 2 , p  < 0.01). Patients with a volume of drained ascites higher than 4 l showed a significant increase in lumbar BMD (7.0%), compared with patients with a lower amount (1.5%) ( p  < 0.03). The decrease in total soft tissue mass correlated with the amount of removed ascites ( r  = 0.951, p  < 0.001). Diagnosis of osteoporosis or osteopenia changed after paracentesis in 12% of patients. Conclusion Ascites over 4 l causes inaccuracy of BMD measurements, particularly at the lumbar spine. This fact must be considered when assessing bone mass in patients with advanced cirrhosis.