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

Abstract

IntroductionChronic 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 methodsSerum 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.ResultsNo 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).ConclusionsIn 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.

α1-Antitrypsin level in patients with spontaneous pneumothorax

“…The AAT deficiency phenotypes in patients with spontaneous pneumothorax could indicate a lack of antiprotease activity. However, we found that the AAT level was significantly higher in the patients with spontaneous pneumothorax without AAT deficiency than in the controls and was even similar to the level in COPD patients reported in other studies [16]. One study of 32 patients with spontaneous pneumothorax presented similar results [11].…”

“…The prevalence of AAT deficiency in Lithuania has not been reported, but it could be estimated to be sim-a1-Antitrypsin level in patients with spontaneous pneumothorax ilar to that in other European developed countries, i.e., 1 : 3000-5000 [6,16]. This might signify that more than 900 ZZ subjects remain undiagnosed.…”

Chronic Obstructive Pulmonary Disease and its Non-Smoking Risk Factors in India

“…In last fi ve years, due to the advent of genome-wide association studies (135)(136)(137), the genetics of COPD has moved beyond α-1 antitrypsin gene (138)(139)(140)(141)(142). Several genetic variants are reported to be associated with COPD in Indian population namely PIM3 allele of alpha-1-antitrypsin gene ( 143 ), GSTT1, GSTM1 and GSTM3 ( 144 , 145 ), PiZ and Pi S ( 146 ), cytokine gene polymorphisms (IL1B, IL1RN, TNF-α, and IL4) ( 144 ), CYP2E1 and NAT2 ( 147 ), GSTP1 and mEPHX ( 148 ), COX2 and p53 ( 149 ), CYP1A1, CYP1A2, and CYBA ( 150 ), TIMP-1 and α1AT ( 151 ).…”

The spectrum of microdeletian syndromes at the hospital of Lithuanian university of health sciences

“…Also there are more known microdeletion syndromes such as Smith-Magenis (17p11.2), Cri du Chat (5p15.2) and 3) which are rare (HALDER et al, 2013;KURTOVIC-KOZARIC et al, 2016). Pathogenesis of microdeletian syndromes is different than monogenous diseases (SERAPINAS et al, 2012;SERAPINAS et al, 2013;DAUGELAITE et al, 2015).…”