Increased serum levels of carbohydrate-deficient transferrin in patients with chronic obstructive pulmonary disease

Citation
U. Nihlen et al., Increased serum levels of carbohydrate-deficient transferrin in patients with chronic obstructive pulmonary disease, SC J CL INV, 61(5), 2001, pp. 341-347
Citations number
33
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION
ISSN journal
00365513 → ACNP
Volume
61
Issue
5
Year of publication
2001
Pages
341 - 347
Database
ISI
SICI code
0036-5513(2001)61:5<341:ISLOCT>2.0.ZU;2-C
Abstract
Objective: The reason that only a minority of smokers develop chronic obstr uctive pulmonary disease (COPD) is still largely unknown. Glycosylation def ects are involved in the pathological mechanisms in cystic fibrosis (CF), w here chronic progressive obstructive lung disease dominates the clinical pi cture. Whether defects of protein glycosylation occur in COPD has not previ ously been examined. Increase in carbohydrate-deficient transferrin (CDT) i n serum seems to function as an indicator of general defects of N-glycosyla tion. Recently, one study observed high serum CDT concentrations in CF pati ents. We examined whether subjects with COPD also have increased serum CDT levels. Method and results: A total of 131 randomly selected individuals, 4 5-64 years of age, underwent a medical examination, spirometry and blood te sts. Serum CDT was determined using high performance liquid chromatography. In subjects diagnosed as having COPD (n=15), multiple logistic regression analyses demonstrated a significant relationship between the diagnosis of C OPD and CDT, even after all efforts were made to take the influence of age and smoking into account (odds ratio 3.16, 95% CI 1.11-8.95). Also, in subj ects with COPD there was an inverse partial correlation between forced expi ratory volume in 1s (FEV1) and serum CDT (r = -0.81, p=0.001). Conclusion: These results suggest that protein glycosylation defects occur in COPD and, in addition, might be involved in the pathogenetic mechanisms of the disea se. It seems that further investigation of the protein glycosylation in COP D is warranted.