Anti-fracture Therapy Effectively Prevents Bone Loss in Women Post-Critical Illness

Anti-fracture therapy was found to be an effective intervention to prevent bone mineral density (BMD) loss in women recovering from a critical illness, according to a study published in Critical Care.¹

Neil Orford, MD, intensive care unit medical director at Barwon Health in Geelong, Australia and colleagues led a prospective observational cohort study to examine the association between post-intensive care unit (ICU) administration of anti-fracture therapy or glucocorticoids and longitudinal changes in BMD over a 2-year period. BMD was measured using dual-energy X-ray absorptiometry (DXA) at the proximal femur and lumbar spine. 

A total of 92 patients who met study inclusion criteria including duration of mechanical ventilation >24 hours were enrolled in the study during their tertiary, mixed medical, surgical, or cardiac surgical ICU stay.

Patient data were collected at ICU baseline, post-ICU discharge, 1-year post-ICU discharge, and 2-year post-ICU discharge. Of the 92 patients, 66 had 2 BMD assessments and 48 patients had all 3 BMD assessments.

Over the 2-year period following ICU hospitalization, 10 patients (6 women, 4 men) were prescribed anti-fracture therapies including alendronate (5 patients), denosumab (2 patients), strontium ranelate (2 patients), and risedronate (1 patient).

In 53 measurements from 43 women of annual change in BMD over the 2-year period there was a significant decrease in BMD observed in year 1 vs year 2 for spine BMD (-1.1±2.0 vs 3.0±1.7%, P =.02) but not in femur BMD (−0.3±1.9% vs 0.6±1.7%, P =.6).

There was also a significant difference in women who did and did not receive anti-fracture therapy for the femur (3.1±2.4% vs −2.8±1.7%, P =.04) and the spine (5.1±2.5% vs −3.2±1.8%, P =.01).

However, use and disuse of glucocorticoids in women was not associated with a difference in an annual change in BMD of the femur (−0.2±2.7% vs 0.5±1.6%, P =.8) or the spine (0.5±2.9% vs 1.4±1.6%, P =.8), respectively.

In women who did not receive anti-fracture therapy or glucocorticords there was a decrease in femur BMD from year 1 to 2 (−2.8±1.3% vs −1.9±0.7, P =.6,) and spine BMD from year 1 to 2 (−4.8±1.4% vs −1.3±1.8%, P =.08).

In the 48 male patients with 61 measurements of annual change in BMD over the 2-year period, there was a greater decrease in femur BMD at year 2 compared with year 1 (−0.9±2.1% vs −2.5±2.1%, P =.030), respectively.

There was no difference in the annual change in spine BMD in men from year 1 to year 2 (0.9±4.0% vs 2.1±4.0%, P =.45), respectively.

In men, there was no association between anti-fracture therapy use and disuse and annual change of BMD in the femur (−0.4±2.5% vs −3.0±2.0%, P =.1) or the spine (2.4±4.8% vs 0.7±3.6%, P =.6), respectively. Since only one male participant received glucocorticoids, the researchers did not perform analysis in this field.

In men not receiving anti-fracture therapy or glucocorticords, the annual decrease in femur BMD was significantly greater in year 2 than year 1 (−1.9±0.7% vs −3.2±0.7%, P =.03). There was no difference in annual change in spine BMD between year 1 and year 2 (0.0±1.2% vs 0.9±1.5%, P =.6).

“This implies that anti-resorptive therapy may be an effective intervention to prevent bone loss in women with critical illness as has been shown in other at-risk patients,” the researchers concluded.

Limitations and Disclosures