Impact of Bariatric Surgery on Bone Mineral Density: Observational Study of 110 Patients Followed up in a Specialized Center for the Treatment of Obesity in France.

INTRODUCTION: Bariatric surgery is used to treat severe obesity. We aimed to investigate the incidence of clinically significant bone mineral density (BMD) loss at 6 and 12 months after bariatric surgery. METHODS: Observational study performed in a specialized center for the treatment of obesity at the University Hospital of Reims, France. Surface BMD was measured by dual x-ray absorptiometry (DEXA). A reduction of > 0.03 g/cm2 was considered clinically significant. RESULTS: A total of 110 patients were included. A clinically significant reduction in BMD was observed in 62.1% of patients at 6 months, and in 71.6% at 12 months after surgery. No case of osteoporosis was observed. There were four cases of osteopenia and one fracture post-surgery. BMD loss was related by univariate analysis to the reduction in body mass index (BMI) (p < 0.01), weight loss (p < 0.01), fat mass (p < 0.01), and lean mass (p < 0.01). Multivariable analysis found a significant association between the reduction in BMD and the excess weight loss percentage (odds ratio 1.11, 95% confidence interval (1.05-1.18), p < 0.001). CONCLUSION: There was a clinically significant reduction in BMD at 6 months after surgery in over 60% of patients undergoing bariatric surgery. BMD loss is persistent over time and predominantly situated at the femoral level, and strongly associated with weight loss. Systematic vitamin and calcium supplementation, as well as follow-up by DEXA scan seems appropriate. Systematic DEXA scan pre- and post-surgery, and annually thereafter until weight has stabilized seems appropriate.

Cost Effectiveness of Intra-Articular Hyaluronic Acid and Disease-Modifying Drugs in Knee Osteoarthritis.

BACKGROUND: The place of disease-modifying osteoarthritis drugs (DMOADs) and intra-articular hyaluronic acid (IAHA) in the therapeutic arsenal for knee osteoarthritis (OA) remains uncertain. Indeed, these treatments have demonstrated symptomatic efficacy but no efficacy for disease modification. OBJECTIVE: This report reviews the cost effectiveness of IAHA and DMOADs used in the treatment of knee OA. METHODS: A systematic literature search of the MEDLINE, Scopus, EMBASE and Cochrane databases was performed independently by two rheumatologists who used the same predefined eligibility criteria to identify relevant articles. Papers without abstracts and in languages other than English or French were excluded. Extracted costs were annualised and converted to 2015 euros (€) using the Consumer Price Index of the relevant countries and the 2013 Purchasing Power Parities between these countries and the European Union average. RESULTS: A total of 95 abstracts were selected, and 13 articles were considered for the review: nine articles on IAHA and four on DMOADs. Only one article directly compared different IAHA compounds. Articles showed substantial heterogeneity in methodological approaches. The incremental cost-effectiveness ratios (ICERs) ranged from €4000 to €57,550 and from €240 to €53,225 per quality-adjusted life-year (QALY) gained for DMOADs and IAHA, respectively. CONCLUSIONS: This review highlights substantial heterogeneity between studies, ranging from a cost saving (or dominating) position to very high ICERs, far above the acceptability threshold of €50,000/QALY. Additional research is needed to determine reliable and robust ICER estimates for knee OA therapies.

Neurogenic muscle hypertrophy.

We report the case of a 48-year-old man who presented with left calf hypertrophy 6 years after an episode of left S1 sciatica related to a herniated disk. Magnetic resonance imaging disclosed muscle hypertrophy. Electromyography showed left S1 radiculopathy with abnormal spontaneous muscle activity. Neurogenic muscle hypertrophy is a rare phenomenon that is chiefly seen when denervation occurs slowly and gradually. The typical patient is a middle-aged man who has a history of S1 radiculopathy. The soleus muscle is the main site of involvement. The pathophysiology is unclear but may involve type I fiber hypertrophy in response to the complex repetitive discharges recorded by electromyography. The natural history of neurogenic muscle hypertrophy is incompletely understood.