21 research outputs found

    What was your fracture risk evaluated by FRAX® the day before your osteoporotic fracture?

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    Osteoporotic fracture (OF) is one of the major causes of morbidity and mortality in industrialized countries. Switzerland is among the countries with the greatest risk. Our aim was (1) to calculate the FRAX® in a selected Swiss population the day before the occurrence of an OF and (2) to compare the results with the proposed Swiss FRAX® thresholds. The Swiss Association Against Osteoporosis proposed guidelines for the treatment of osteoporosis based on age-dependent thresholds. To identify a population at a very high risk of osteoporotic fracture, we included all consecutive patients in the active OF pathway cohort from the Lausanne University Hospital, Switzerland. FRAX® was calculated with the available data the day before the actual OF. People with a FRAX® body mass index (BMI) or a FRAX® (bone mineral density) BMD lower than the Swiss thresholds were not considered at high risk. Two-hundred thirty-seven patients were included with a mean age of 77.2years, and 80% were female. Major types of fracture included hip (58%) and proximal humerus (25%) fractures. Mean FRAX® BMI values were 28.0, 10.0, 13.0, 26.0, and 37.0% for age groups 50-59, 60-69, 70-79, and 80-89years old, respectively. Fifty percent of the population was not considered at high risk by the FRAX® BMI. FRAX® BMD was available for 95 patients, and 45% had a T score < −2.5 standard deviation. Only 30% of patients with a normal or osteopenic BMD were classified at high risk by FRAX® BMD. The current proposed Swiss thresholds were not able to classify at high risk in 50 to 70% of the studied population the day before a major O

    “Inflammaging” and bone in the OsteoLaus cohort

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    In this large population-based cohort, we did not find a relation between the coined concept of “inflammaging” (hs-CRP, IL-6, IL-1β and TNF-α within the normal range) and bone parameters, measured in terms of prevalent and incident fractures, bone mass density and trabecular bone score

    Severe Rebound-Associated Vertebral Fractures After Denosumab Discontinuation: 9 Clinical Cases Report

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    Abstract Context: Denosumab inhibits bone resorption, increases bone mineral density, and reduces fracture risk. Denosumab was approved for the treatment of osteoporosis and the prevention of bone loss in some oncological situations. Denosumab discontinuation is associated with a severe bone turnover rebound (BTR) and a rapid loss of bone mineral density. The clinical consequences of the BTR observed after denosumab discontinuation are not known. Cases Description: We report 9 women who presented 50 rebound-associated vertebral fractures (RAVFs) after denosumab discontinuation. A broad biological and radiological assessment excluded other causes than osteoporosis. These 9 cases are unusual and disturbing for several reasons. First, all vertebral fractures (VFs) were spontaneous, and most patients had a high number of VFs (mean = 5.5) in a short period of time. Second, the fracture risk was low for most of these women. Third, their VFs occurred rapidly after last denosumab injection (9-16 months). Fourth, vertebroplasty was associated with a high number of new VFs. All the observed VFs seem to be related to denosumab discontinuation and unlikely to the underlying osteoporosis or osteopenia. We hypothesize that the severe BTR is involved in microdamage accumulation in trabecular bone and thus promotes VFs. Conclusion: Studies are urgently needed to determine 1) the pathophysiological processes involved, 2) the clinical profile of patients at risk for RAVFs, and 3) the management and/or treatment regimens after denosumab discontinuation. Health authorities, physicians, and patients must be aware of this RAVF risk. Denosumab injections must be scrupulously done every 6 months but not indefinitely

    Functional neurological signs in hypermobile Ehlers–Danlos syndrome and hypermobile spectrum disorders with suspected neuropathic pain

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    Abstract Background The hypermobile Ehlers–Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD) are connective tissue disorders characterized by generalized joint hypermobility, associated with chronic pain and several symptoms, such as fatigue, dysautonomia, as well as psychiatric co‐morbidities. Clinical observations of unusual manifestations during systematic sensory testing raised the question of a possible co‐existence with a functional neurological disorder (FND). Hence, this study aimed to assess the presence of positive functional neurological signs (FNS) in a cohort of patients with hEDS/HSD. Methods The clinical data of hEDS/HSD patients (N = 24) were retrospectively analyzed and compared to a prospectively recruited age‐/sex‐matched healthy control group (N = 22). Four motor‐ and three sensory‐positive FNS were assessed. Results Twenty‐two patients (92%) presented at least one motor or sensory FNS. Five patients (21%) presented only a single FNS, 14 presented between 2 and 4 FNS (58%), and 3 patients presented 5 or more FNS (12%). None of the healthy controls presented motor FNS, and only two presented a sensory FNS. Conclusions The presence of FNS in hEDS/HSD deserves better clinical detection and formal diagnosis of FND to offer more adequate care in co‐morbid situations. In fact, FND can severely interfere with rehabilitation efforts in hEDS/HSD, and FND‐targeted physical therapy should perhaps be combined with EDS/HSD‐specific approaches

    Comment gérer l'effet rebond à l'arrêt du dénosumab et éviter les fractures vertébrales multiples?

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    L'arrêt du dénosumab est associé à un effet rebond sévère associant élévation des marqueurs du remodelage osseux pour deux ans et perte du gain de densité osseuse. A l'arrêt du dénosumab, en l'absence de prescription d'un puissant bisphosphonate, la fréquence des fractures vertébrales multiples est élevée. Le nombre médian de fractures vertébrales est de 5 dans les 7 à 20 mois (médiane 11) suivant la dernière injection de dénosumab. Un bisphosphonate puissant prescrit à l'arrêt du traitement de dénosumab pourrait réduire ce risque. Cette stratégie nécessite un suivi serré des marqueurs du remodelage osseux et un ajustement du traitement si le remodelage osseux n'est pas suffisamment contrôlé
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