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Low-trauma fractures increase 1-year mortality risk in adults with neurodevelopmental delays
Compared with typical adults, those with neurodevelopmental disabilities may be more susceptible to early mortality following a low-trauma fracture, according to findings published in Bone.
“For clinicians treating adults with neurodevelopmental disabilities, there may need to [place] greater emphasis on treating and/or monitoring health complications immediately and/or more aggressively following a low-trauma fracture than the type of care they would typically provide their adult patient without neurodevelopmental disabilities,” Daniel G. Whitney, PhD, assistant professor in the department of physical medicine and rehabilitation at the University of Michigan, told Endocrine Today. “The findings from this study may underrepresent the extent of this problem, as our sample of adults with neurodevelopmental disabilities may represent a healthier and less skeletally fragile sector of these populations.”
Whitney and colleagues analyzed data from 3,749 adults with neurodevelopmental disabilities (mean age, 57 years; 45.2% men) and 585,910 nondisabled adults (mean age, 64 years; 34.4% men) who sustained a low-trauma fracture between 2012 and 2016. Data were from Optum Clinformatics Data Mart, a nationwide claims database from a single private payer in the U.S. Individuals with neurodevelopmental disabilities were identified by at least one claim for intellectual disabilities, cerebral palsy or autism spectrum disorders. Researchers used Cox proportional hazard ratios to estimate mortality rates for adults with and without neurodevelopmental disabilities using HRs at 1, 3, 6 and 12 months after fracture.
During 12 months of follow-up, 182 adults with neurodevelopmental disabilities (4.9%; mean age, 70 years; 46.2% men) and 25,456 nondisabled adults (4.3%; mean age, 79 years; 38.3% men) died.
For nondisabled adults, the crude mortality rate was 13.6 at 1 month, 9.02 at 3 months, 6.61 at 6 months and 4.96 at 12 months. For adults with neurodevelopmental disabilities, crude mortality rates were 12.46 (RR = 0.92; 95% CI, 0.67-1.26) at 1 month, 8.48 (RR = 0.94; 95% CI, 0.75-1.18) at 3 months, 7.16 (RR = 1.08; 95% CI, 0.91-1.29) at 6 months and 5.4 (RR = 1.09; 95% CI, 0.94-1.26) at 12 months. In analyses stratified by neurodevelopmental disability, only adults with intellectual disabilities had a greater crude mortality rate at 6 months (RR = 1.46; 95% CI, 1.17-1.83) and 12 months (RR = 1.49; 95% CI, 1.23-1.79).
Post-fracture mortality
After adjustments for age, sex, race, U.S. region and comorbidities, adults with neurodevelopmental disabilities had greater postfracture mortality rates at 3 months (HR = 1.27; 95% CI, 1.02-1.59), 6 months (HR = 1.45; 95% CI, 1.22-1.73) and 12 months (HR = 1.46; 95% CI, 1.27-1.69) vs. nondisabled adults. When stratified by the type of neurodevelopmental disability, adults with intellectual disabilities (HR = 1.8; 95% CI, 1.49-2.17) and adults with autism spectrum disorders (HR = 1.63; 95% CI, 1.12-2.38), but not adults with cerebral palsy, had greater 12-month postfracture mortality risk vs. nondisabled adults.
In analyses stratified by fracture location, lower-extremity fractures were associated with greater crude mortality rate (RR = 1.69; 95% CI, 1.22-2.35) and adjusted mortality risk (HR = 2.41; 95% CI, 1.73-3.35) for adults with neurodevelopmental disabilities vs. nondisabled adults. Researchers found that upper-extremity fractures were associated with greater adjusted mortality risk (HR = 1.76; 95% CI, 1.23-2.5) for adults with and without neurodevelopmental disabilities.
Underlying causes
“Many research directions should be taken,” Whitney said. “From a clinical and epidemiologic perspective, more research is needed to determine factors following a low-trauma fracture that increase risk for mortality, such as chronic diseases, medications, infections or a dramatic decline in physical activity or function. More research is needed to determine causality between fracture and adverse health complications and premature mortality, as well as the temporal sequence of skeletal fragility, health complications and premature mortality.”
Additionally, from a basic research perspective, understanding the biological mechanisms of a fracture event increasing risk for mortality is urgently needed, Whitney said, as well as an understanding of the biological mechanisms increasing fracture susceptibility, such as inflammation, lipid metabolites or muscle-bone interactions. – by Regina Schaffer
For more information:
Daniel G. Whitney, PhD, can be reached at the University of Michigan, Department of Physical Medicine and Rehabilitation, 325 E. Eisenhower Parkway, Ann Arbor, MI 48108; email: dgwhit@umich.edu.
Disclosures: The authors report no relevant financial disclosures.
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