Inflammatory markers in chronic obstructive pulmonary disease patients with different α1 antitrypsin genotypes

Danielius Serapinas, Brigita Šitkauskienė, Raimundas Sakalauskas

Research output: Contribution to journalArticle

6 Citations (Scopus)


Introduction: Chronic obstructive pulmonary disease (COPD) has been recently defined as a systemic pulmonary inflammatory disease, and congenital α1 antitrypsin deficiency is one of the well-established genetic risk factors for chronic obstructive pulmonary disease. The aim of our study was to evaluate the possible associations of α1 antitrypsin with inflammatory markers – CRP, sCD14, TNF-α, sTNFR-1, and sTNFR-2 – in patients with COPD with different α1 antitrypsin genotypes. Material and methods: Serum biomarkers from patients (n = 355) with COPD, defined according to the GOLD criteria, were analyzed using commercial ELISA kits; α1 antitrypsin concentrations were determined by nephelometry, and α1 antitrypsin phenotyping was carried out by means of isoelectric focusing. Results: No significant differences in CRP, TNF-α, sTNFR-1, sTNFR-2, and sCD14 levels were found comparing COPD patients with different genotypes. In patients without α1 antitrypsin deficiency (PI*MM), a significant negative correlation between lung function (FEV1) and serum α1 antitrypsin (r = –0.522, p = 0.03) and CRP concentration (r = –0.590, p = 0.011) was detected. The level of α1 antitrypsin positively correlated with: a) CRP concentration (r = 0.671, p = 0.005), b) sCD14 (r = 0.510, p = 0.008) and c) sTNFR-1 (r = 0.567, p = 0.007). Conclusions: In patients without α1 antitrypsin deficiency, the positive association of α1 antitrypsin concentration with CRP, sCD14, and sTNFR-1 and the negative association with FEV1 show the importance of α1 antitrypsin as a marker of systemic inflammation.
Original languageEnglish
Pages (from-to)1053-1058
JournalArchives of medical science : AMS
Issue number6
Publication statusPublished - 2012



  • Pulmonary disease, chronic obstructive
  • Alpha-1 Antitrypsin deficiency
  • Inflammation
  • Biological markers
  • Blood

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