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Changes in bone mineral density in women before critical illness: a matched control nested cohort study.

Archives of Osteoporosis 2018 November 6
The contribution of premorbid bone health to accelerated bone loss following critical illness is unknown. This study compared bone density in women before critical illness to women who did not become critically ill. Overall bone density was similar, although femoral neck bone mass increased immediately prior to critical illness.

PURPOSE: The relative contribution of acute and chronic factors to accelerated loss of bone mineral density (BMD) following critical illness is unknown. This study compared the BMD trajectory of women before critical illness to the BMD trajectory of women who did not become critically ill.

METHODS: This prospective, nested, age- and medication-matched, case-control study compared trajectory of BMD in women in the Geelong Osteoporosis study (GOS) requiring admission to an Australian Intensive Care Unit (ICU) between June 1998 and March 2016, to women not admitted to ICU. The main outcome was age and medication use adjusted change in BMD.

RESULTS: A total of 52 women, with a mean age of 77 ± 9 years were admitted to ICU, predominantly post-surgery (75%), during the study period. A greater age-adjusted annual rate of decline was observed for pre-ICU women compared to no-ICU women for AP spine BMD (-0.010 ± 0.002 g/cm2 vs -0.005 ± 0.002 g/cm2 , p = 0.01) over the 15-year study period. In participants with multiple BMDs 2 years before critical illness, a significantly greater increase in femoral neck BMD compared to age- and medication-matched controls was observed (difference in BMD, ICU vs no-ICU = 0.037 ± 0.013 g/cm2 , p = 0.006).

CONCLUSION: In a cohort of women with predominantly surgical ICU admission, bone health prior to critical illness was comparable to age- and medication-matched controls, with a relative increase in femoral neck bone mass immediately prior to critical illness. These findings suggest critical illness-related bone loss cannot be entirely explained as a continuation of pre-morbid bone trajectory.

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