ArticleInternational journal of chronic obstructive pulmonary disease2013
Deficiency of α-1-antitrypsin influences systemic iron homeostasis.
Article in International journal of chronic obstructive pulmonary disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Immunological and homeostatic pathways of alpha -1 antitrypsin: a new therapeutic potential.Frontiers in immunology · 2024Review
- Lung microhaemorrhage drives oxidative/inflammatory damage in αERJ open research · 2023Article
- Neonatal cholestasis, hyperferritinemia, hypoglycemia and deafness: a diagnostic challenge.BMJ case reports · 2019Article
- Normalizing serum hepcidin but not α-1-antitrypsin level during effective treatment of chronic hepatitis C.Clinical and experimental hepatology · 2017Article
- The "Iron"-y of Iron Overload and Iron Deficiency in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2017Article
- Impaired hepcidin expression in alpha-1-antitrypsin deficiency associated with iron overload and progressive liver disease.Human molecular genetics · 2015Article
- The role of iron in pulmonary pathology.Multidisciplinary respiratory medicine · 2015Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is evidence that proteases and antiproteases participate in the iron homeostasis of cells and living systems. We tested the postulate that α-1 antitrypsin (A1AT) polymorphism and the consequent deficiency of this antiprotease in humans are associated with a systemic disruption in iron homeostasis. Archived plasma samples from Alpha-1 Foundation (30 MM, 30 MZ, and 30 ZZ individuals) were analyzed for A1AT, ferritin, transferrin, and C-reactive protein (CRP). Plasma samples were also assayed for metals using inductively coupled plasma atomic emission spectroscopy (ICPAES). Plasma levels of A1AT in MZ and ZZ individuals were approximately 60% and 20% of those for MM individuals respectively. Plasma ferritin concentrations in those with the ZZ genotype were greater relative to those individuals with either MM or MZ genotype. Plasma transferrin for MM, MZ, and ZZ genotypes showed no significant differences. Linear regression analysis revealed a significant (negative) relationship between plasma concentrations of A1AT and ferritin while that between A1AT and transferrin levels was not significant. Plasma CRP concentrations were not significantly different between MM, MZ, and ZZ individuals. ICPAES measurement of metals confirmed elevated plasma concentrations of nonheme iron among ZZ individuals. Nonheme iron concentrations correlated (negatively) with levels of A1AT. A1AT deficiency is associated with evidence of a disruption in iron homeostasis with plasma ferritin and nonheme iron concentrations being elevated among those with the ZZ genotype.
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