Alpha-1 antitrypsin deficiency: From the lung to the heart?
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 4325875
Author(s) Curjuric, Ivan; Imboden, Medea; Bettschart, Robert; Caviezel, Seraina; Dratva, Julia; Pons, Marco; Rothe, Thomas; Schmidt-Trucksäss, Arno; Stolz, Daiana; Thun, Gian Andri; von Eckardstein, Arnold; Kronenberg, Florian; Ferrarotti, Ilaria; Probst-Hensch, Nicole M.
Author(s) at UniBasel Curjuric, Ivan
Imboden, Medea
Dratva, Julia
Thun, Gian Andri
Probst Hensch, Nicole
Schmidt-Trucksäss, Arno
Year 2018
Title Alpha-1 antitrypsin deficiency: From the lung to the heart?
Journal Atherosclerosis
Volume 270
Pages / Article-Number 166-172
Abstract BACKGROUND AND AIMS: Alpha-1 antitrypsin (A1AT) is the most abundant serine protease inhibitor in human blood and exerts important anti-inflammatory and immune-modulatory effects. In combination with smoking or other long-term noxious exposures such as occupational dust and fumes, genetic A1AT deficiency can cause chronic obstructive pulmonary disease, a condition with elevated cardiovascular risk. The effects of A1AT deficiency on cardiovascular risk have hardly been studied today. METHODS: Using data from 2614 adults from the population-based SAPALDIA cohort, we tested associations of serum A1AT and SERPINA1 mutations with carotid intima-media thickness (CIMT, measured by B-mode ultrasonography) or self-reported arterial hypertension or cardiovascular disease in multiple regression models using a Mendelian Randomization like analysis design. Mutations Pi-S and Pi-Z were coded as ordinal genotype score (MM, MS, MZ/SS, SZ and ZZ), according to their progressive biological impact. RESULTS: Serum A1AT concentration presented a u-shaped association with CIMT. At the lower end of the A1AT distribution, an analogous, linear association between SERPINA1 score and higher CIMT was observed, resulting in an estimated 1.2% (95%-confidence interval -0.1-2.5) increase in CIMT per unit (p = 0.060). Genotype score was significantly associated with arterial hypertension with an odds ratio (OR) of 1.2 (1.0-1.5) per unit (p = 0.028). The association with cardiovascular disease was not significant (OR 1.3 (0.9-1.9)). CONCLUSIONS: Our results support a possible causal relationship between genetic A1AT deficiency and increased cardiovascular risk, which needs to be better taken into account for the management of affected patients and first-degree relatives.
ISSN/ISBN 1567-5688 ; 1878-5050
edoc-URL https://edoc.unibas.ch/60961/
Full Text on edoc No
Digital Object Identifier DOI 10.1016/j.atherosclerosis.2018.01.042
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/29432934
ISI-Number MEDLINE:29432934
Document type (ISI) Journal Article
 
   

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