IMPAIRED GLUCOSE-TOLERANCE IN PATIENTS WITH CHRONIC HYPOXIC PULMONARY-DISEASE

Citation
A. Hjalmarsen et al., IMPAIRED GLUCOSE-TOLERANCE IN PATIENTS WITH CHRONIC HYPOXIC PULMONARY-DISEASE, Diabetes & metabolism, 22(1), 1996, pp. 37-42
Citations number
22
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
12623636
Volume
22
Issue
1
Year of publication
1996
Pages
37 - 42
Database
ISI
SICI code
0338-1684(1996)22:1<37:IGIPWC>2.0.ZU;2-1
Abstract
This study investigated glucose metabolism and glucose-mediated hormon e responses in patients with chronic respiratory hypoxaemia. Glucose a s well as insulin, glucagon, adrenaline, cortisol and growth hormone ( GH) were measured before and at 30, 60 and 120 min during an oral gluc ose-tolerance test. The following chronic obstructive pulmonary diseas e (COPD) patients were studied: 10 normoxaemic (mean paO(2) 10.9+/-0.4 kPa), 10 hypoxaemic (mean paO(2) 7.6+/-0.2 kPa before, and 10.6+/-0.4 after 24-h oxygentherapy, and 6 hypoxaemic patients on long-term oxyg en therapy (LTOT) (mean paO(2) 10.9+/-0.7 kPa before, and 7.1+/-0.3 af ter 4 h with less than 0.5 litre oxygen per minute). The hypoxaemic pa tients were tested both with and without (or reduced) oxygen therapy. Twenty healthy sex- and age-matched subjects served as controls. Plasm a glucose at 120 min was significantly higher in LTOT patients than in controls (p < 0.01), normoxaemic patients (p < 0.01) or hypoxaemic pa tients (p < 0.01). The areas under the curve for plasma glucose and in sulin were significantly higher in both the LTOT and hypoxaemic groups compared to controls (p < 0.01 and 0.05, respectively). Glucose value s for normoxaemic COPD patients were similar to those for controls. Gl ucagon, adrenaline, cortisol and GH levels did not differ significantl y between the groups. A 4-h low-dose or oxygen-free interval in the LT OT group or 24 h of oxygen supplementation in the hypoxaemic group did not affect glucose and hormone levels significantly. It is concluded that severely hypoxaemic COPD patients have altered glucose metabolism which cannot he readily explained by changes in glucoregulatory hormo nes or short-term alterations in oxygenation.