Steve Iliffe

Multicentre cluster randomised trial comparing a community group exercise programme and home-based exercise with usual care for people aged 65 years and over in primary care

BACKGROUNDnRegular physical activity (PA) reduces the risk of falls and hip fractures, and mortality from all causes. However, PA levels are low in the older population and previous intervention studies have demonstrated only modest, short-term improvements.nnnOBJECTIVEnTo evaluate the impact of two exercise promotion programmes on PA in people aged ≥u200965 years.nnnDESIGNnThe ProAct65+ study was a pragmatic, three-arm parallel design, cluster randomised controlled trial of class-based exercise [Falls Management Exercise (FaME) programme], home-based exercise [Otago Exercise Programme (OEP)] and usual care among older people (aged ≥u200965 years) in primary care.nnnSETTINGnForty-three UK-based general practices in London and Nottingham/Derby.nnnPARTICIPANTSnA total of 1256 people ≥u200965 years were recruited through their general practices to take part in the trial.nnnINTERVENTIONSnThe FaME programme and OEP. FaME included weekly classes plus home exercises for 24 weeks and encouraged walking. OEP included home exercises supported by peer mentors (PMs) for 24 weeks, and encouraged walking.nnnMAIN OUTCOME MEASURESnThe primary outcome was the proportion that reported reaching the recommended PA target of 150 minutes of moderate to vigorous physical activity (MVPA) per week, 12 months after cessation of the intervention. Secondary outcomes included functional assessments of balance and falls risk, the incidence of falls, fear of falling, quality of life, social networks and self-efficacy. An economic evaluation including participant and NHS costs was embedded in the clinical trial.nnnRESULTSnIn total, 20,507 patients from 43 general practices were invited to participate. Expressions of interest were received from 2752 (13%) and 1256 (6%) consented to join the trial; 387 were allocated to the FaME arm, 411 to the OEP arm and 458 to usual care. Primary outcome data were available at 12 months after the end of the intervention period for 830 (66%) of the study participants. The proportions reporting at least 150 minutes of MVPA per week rose between baseline and 12 months after the intervention from 40% to 49% in the FaME arm, from 41% to 43% in the OEP arm and from 37.5% to 38.0% in the usual-care arm. A significantly higher proportion in the FaME arm than in the usual-care arm reported at least 150 minutes of MVPA per week at 12 months after the intervention [adjusted odds ratio (AOR) 1.78, 95% confidence interval (CI) 1.11 to 2.87; pu2009=u20090.02]. There was no significant difference in MVPA between OEP and usual care (AOR 1.17, 95% CI 0.72 to 1.92; pu2009=u20090.52). Participants in the FaME arm added around 15 minutes of MVPA per day to their baseline physical activity level. In the 12 months after the close of the intervention phase, there was a statistically significant reduction in falls rate in the FaME arm compared with the usual-care arm (incidence rate ratio 0.74, 95% CI 0.55 to 0.99; pu2009=u20090.042). Scores on the Physical Activity Scale for the Elderly showed a small but statistically significant benefit for FaME compared with usual care, as did perceptions of benefits from exercise. Balance confidence was significantly improved at 12 months post intervention in both arms compared with the usual-care arm. There were no statistically significant differences between intervention arms and the usual-care arm in other secondary outcomes, including quality-adjusted life-years. FaME is more expensive than OEP delivered with PMs (£269 vs. £88 per participant in London; £218 vs. £117 in Nottingham). The cost per extra person exercising at, or above, target was £1919.64 in London and £1560.21 in Nottingham (mean £1739.93).nnnCONCLUSIONnThe FaME intervention increased self-reported PA levels among community-dwelling older adults 12 months after the intervention, and significantly reduced falls. Both the FaME and OEP interventions appeared to be safe, with no significant differences in adverse reactions between study arms.nnnTRIAL REGISTRATIONnThis trial is registered as ISRCTN43453770.nnnFUNDINGnThis project was funded by the NIHR Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 18, No. 49. See the NIHR Journals Library website for further project information.

Can exercise interventions designed to reduce falls improve bone quality [Abstract]

In this symposium, we will review the association of inflammatory arthritis with altered bone health. It has long been recognised that joint conditions such as rheumatoid arthritis and ankylosing spondylitis are associated with reduced bone density and increased fracture risk. Such conditions may be associated with high levels of inflammation, with stimulation of the inflammatory cascade and production of pro-inflammatory cytokines (Il-1, IL-10, IL-6, TNF-α), all of which are well-recognised to cause both localised and generalised osteoporosis. In addition, arthritis patients may be physically inactive because of recurrent arthritis flares, or may be receiving long term corticosteroid therapy. In this session we will review bone health in two other arthritic conditions, namely gout and HIV arthritis. We will also review novel ways of assessing bone microarchitecture in arthritis through high resolution peripheral quantitative computed tomography scans of the radius and tibia. Participants are invited to share their own observations in clinical practice, and propose a research agenda in this important area.This is an abstract of a paper presented at the Congress on Osteoporosis, Osteoarthritis and Musculoskeletal Diseases (WCO-IOF-ESCEO World), Malaga, Spain, April 14-17th. The final publication is available at Springer via http://dx.doi.org/10.1007/s00198-016-3519-5.

Can exercise protect against vertebral deformity? The proact65+bone study [Abstract]

S OF OSTEOPOROSIS CONFERENCE 2016 Invited Plenary Lecture Abstracts IS1 FROM FAMILY HISTORY TO EPIGENETICS OF OSTEOPOROSIS Trevor Cole West Midlands Regional Genetics Service and Birmingham Health Partners, Birmingham Women’s Hospital NHS Foundation Trust, Birmingham, UK With the development of greater genetic knowledge and the advent of more powerful genomic technologies there has been a greater impetus to develop more personalised service delivery and treatments for both rare diseases and common disorders. The “flagship” of such developments was in the field of oncology but similar models are now widespread and this includes disorders associated with bone fragility. Osteoporosis in the general population most frequently presents as an isolated finding, but to date, when presenting to a combined bone and genetic clinic is more likely to be seen as “compounding morbidity” in a patient or family with one of the many different rare causes of bone fragility such as osteogenesis imperfecta. Over 140 such rare bone fragility conditions are listed on the London dysmorphology database. These may present antenataly right through into old age, each with differing severity but often exacerbated by osteoporosis in those surviving into adulthood. One important lesson learnt from such clinical experience is that taking a good clinical history, including a family history, not a reliance on genomic testing, is frequently the most valuable first step in recognising the aetiology and identifying whether other family members should be seen in clinic. In past decades genetic studies in osteoporosis focused on large genomic wide association studies or rare Mendelian families in the belief that a small number of genes would be identified as the cause for more widespread osteoporosis in the general population. It was hoped such findings could be translated into simple algorithms to predict future osteoporotic risk as well as identifying novel therapeutic targets. More recently it has become apparent that this is an over-simplification and not only are there many more genetic influences present than originally suspected, but that many of these may relate to epigenetic phenomena, a mechanism by which gene expression may be modified. This now opens up a whole new therapeutic opportunity as our epigenome is modifiable by many pharmacological and nonpharmacological interventions. It also likely provides new insights into the mechanisms behind well recognised influences on osteoporosis such as physical activity. While basic research continues to focus on the genomic and epigenomic basis of osteoporosis and bone fragility disorders we will illustrate there is still plenty of scope to introduce simple practical measures, such as taking a family history, into the clinic which will improve the clinical management as well as identifying potential patient cohorts to participate in studies investigating the aetiology and future therapeutic trials. IS2 DIABETES AND BONE Serge Ferrari Geneva University Hospital and Faculty of Medicine, Geneva, Switzerland Type 1 diabetes that develops during childhood or adolescence impairs bone formation and thereby peak bone mass acquisition. Taken together with their increased risk of falls due to other diabetes complications, these bone alterations in adults with type 1 diabetes result in a 6 to 12 fold increased risk of hip fractures and also in a higher risk of vertebral and non-vertebral fractures. This increased fracture probability is also reflected in the FRAX tool when it is used without BMD in T1DM subjects. Subjects with type 2 diabetes (T2DM) also have a 50 % to two fold increased risk of fracture, depending on the skeletal site, despite the fact their aBMD is on average higher than in the non-diabetic population. Their increased Osteoporos Int (2016) 27 (Suppl 2):S609–S685 DOI 10.1007/s00198-016-3743-zThis is an abstract of a paper presented at the Osteoporosis Conference 2016, Birmingham, UK, 7-9 November 2016. The final publication is available at link.springer.com via http://dx.doi.org/10.1007/s00198-016-3743-z.This is an abstract of a paper presented at the Osteoporosis Conference 2016, Birmingham, UK, 7-9 November 2016. The final publication is available at link.springer.com via http://dx.doi.org/10.1007/s00198-016-3743-z.