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Inhaled corticosteroids reduce exacerbation frequency in COPD but it is not known whether the presence of emphysema, with decreased alveolar volume, results in impaired bioactivity. The systemic effects of fluticasone 2000 μg daily were compared in patients with COPD who did and did not have emphysema (COPDE and COPD, respectively, both n = 10). The two groups had comparable airflow obstruction. The presence of emphysema was defined by carbon monoxide transfer factor <60% in conjunction with appropriate spirometric, clinical, and radiological findings. Systemic bioactivity was assessed using overnight 10 hour urinary cortisol excretion corrected for creatinine (OUCC) as a marker of adrenal suppression and serum osteocalcin as an indicator of bone metabolism. OUCC and osteocalcin were measured at baseline and after 2 weeks of fluticasone.
OUCC values did not differ significantly between the COPD and COPDE groups before or after starting treatment with fluticasone, but in both groups fluticasone resulted in significant suppression of OUCC. Similarly, the serum osteocalcin concentration did not differ significantly between the two groups before or after starting treatment with fluticasone, but osteocalcin was significantly suppressed following fluticasone.
The results suggest that the degree of cortisol and osteocalcin suppression is similar in COPD patients with or without emphysema. The authors hypothesise that the site of absorption of fluticasone may therefore be more proximal than the alveoli. Patients with COPD on high dose fluticasone are susceptible to systemic adverse effects whether or not they have a significant component of emphysema.
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