Relationship of annual change in bone mineral density with extent of emphysematous lesions and pulmonary function in patients with COPD

Abstract

Background

Osteoporosis is a well-known comorbidity in COPD. It is associated with poor health status and prognosis. Although the exact pathomechanisms are unclear, osteoporosis is suggested to be either a comorbidity due to shared risk factors with COPD or a systematic effect of COPD with a cause–effect relationship. This study aimed to evaluate whether progression of osteoporosis is synchronized with that of COPD.

Materials and methods

Data from 103 patients with COPD included in the Hokkaido COPD cohort study were analyzed. Computed tomography (CT) attenuation values of thoracic vertebrae 4, 7, and 10 were measured using custom software, and the average value (average bone density; ABD_4,7,10) was calculated. The percentage of low attenuation volume (LAV%) for each patient was also calculated for evaluation of emphysematous lesions. Annual change in thoracic vertebral CT attenuation, which is strongly correlated with dual-energy X-ray absorptiometry-measured bone mineral density, was compared with that in FEV_1.0 or emphysematous lesions.

Results

In the first CT data set, ABD_4,7,10 was significantly correlated with age (ρ=−0.331; p=0.0006), body mass index (BMI; ρ=0.246; p=0.0136), St George’s Respiratory Questionnaire (SGRQ) activity score (ρ=−0.248; p=0.0115), eosinophil count (ρ=0.229; p=0.0198), and LAV% (ρ=−0.372; p=0.0001). However, ABD_4,7,10 was not associated with FEV_1.0. After adjustment for age, BMI, SGRQ activity score, and eosinophil count, no significant relationship was found between ABD_4,7,10 and LAV%. Annual change in ABD_4,7,10 was not associated with annual change in LAV% or FEV_1.0.

Conclusion

Progression of osteoporosis and that of COPD are not directly related or synchronized with each other.

Keywords:

• osteoporosis
• quantitative CT analysis
• FEV_1.0
• low attenuation volume
• automatic analysis
• systemic effect

Acknowledgments

This study was supported by a scientific research grant from the Ministry of Education Science, Culture and Sports of Japan (17390239 and 2139053); a grant to the Respiratory Failure Research Group from the Ministry of Health, Labor and Welfare, Japan; Nippon Boehringer Ingelheim; Pfizer, Inc.; Daiichi Sankyo Co. Ltd; and Chugai Pharmaceutical Co., Ltd. The sponsor of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report. We would like to thank Editage (www.editage.jp) for English language editing.

Disclosure

The authors report no conflicts of interest in this work.