Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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Gewählte Publikation:

Dimai, HP; Domej, W; Leb, G; Lau, KH.
Bone loss in patients with untreated chronic obstructive pulmonary disease is mediated by an increase in bone resorption associated with hypercapnia.
J Bone Miner Res. 2001; 16(11):2132-2141 Doi: 10.1359/jbmr.2001.16.11.2132 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz: Dimai Hans Peter
Co-Autor*innen der Med Uni Graz: Domej Wolfgang
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Abstract:: This study sought to determine whether the bone loss in untreated chronic obstructive pulmonary disease (COPD) is associated with hypercapnia and/or respiratory acidosis. Bone mineral density (BMD) measured at the distal forearm of the nondominant arm (with peripheral quantitative computed tomography [pQCT]) and serum markers of bone turnover were determined in 71 male patients with untreated COPD and 40 healthy male subjects who matched the patients in age, weight, and body mass index (BMI). The COPD patients, compared with controls, had reduced pulmonary functions, lower arterial pH, and elevated arterial partial pressure of CO2 (PCO2) The BMD (in T score) was significantly lower in COPD patients than that in control subjects (-1.628 +/- 0.168 vs. -0.058 +/- 0.157; p < 0.001). The BMD of COPD patients correlated positively with arterial pH (r = 0.582; p < 0.001), negatively with PCO2 (r = -0.442; p < 0.001), and negatively with serum cross-linked telopeptide of type I collagen (ICTP), a bone resorption marker (r = -0.444; p < 0.001) but not with serum osteocalcin, a bone formation marker. Serum ICTP, but not osteocalcin, correlated with PCO2 (r = 0.593; p < 0.001) and arterial pH (r = -0.415; p < 0.001). To assess the role of hypercapnia, COPD patients were divided into the hypercapnic (PCO2 > 45 mm Hg; n = 35) and eucapnic (PCO2 = 35-45 mm Hg) group (n = 36). Patients with hypercapnia had lower BMD, lower arterial pH, and higher serum ICTP than did patients with eucapnia. Arterial pH and serum ICTP of eucapnic patients were not different from those of controls. To evaluate the role of uncompensated respiratory acidosis, COPD patients with hypercapnia were subdivided into those with compensatory respiratory acidosis (pH > or = 7.35; n = 20) and those with uncompensated respiratory acidosis (pH < 7.35; n = 15). The BMD and serum ICTP were not different among the two subgroups. In conclusion, this study presents the first associative evidence that the bone loss in COPD is at least in part attributed to an increased bone resorption that is associated primarily with hypercapnia rather than uncompensated respiratory acidosis.
Find related publications in this database (using NLM MeSH Indexing): Acidosis, Respiratory - etiology; Aged - etiology; Bone Density - etiology; Bone Remodeling - etiology; Bone Resorption - etiology; Calcium - blood; Case-Control Studies - blood; Collagen - blood; Collagen Type I - blood; Humans - blood; Hypercapnia - etiology; Male - etiology; Middle Aged - etiology; Parathyroid Hormone - blood; Peptides - blood; Pulmonary Disease, Chronic Obstructive - complications
Find related publications in this database (Keywords): chronic obstructive pulmonary disease; respiratory acidosis; hypercapnia; bone resorption; bone loss (humans)