Telomere length and elevated iron: The influence of phenotype and HFE genotype. Issue 6 (13th May 2013)

• Record Type: Journal Article
• Authors: Mainous, Arch G.; Wright, Robert U.; Hulihan, Mary M.; Twal, Waleed O.; McLaren, Christine E.; Diaz, Vanessa A.; McLaren, Gordon D.; Argraves, W. Scott; Grant, Althea M.
• Is Part Of: American journal of hematology. Volume 88:Issue 6(2013:Jun.)
• Page Start: 492
• Page End: 496
• Publication Date: 2013-05-13
• Subjects: Hematology -- Periodicals; 616.15
• DOI: 10.1002/ajh.23438
• Languages: English
• ISSNs: 0361-8609

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Elevated body iron stores are associated with morbidity and mortality due to oxidative stress. Hereditary hemochromatosis, a common condition caused by <italic>HFE</italic> gene mutations, can lead to excess iron storage and disease but clinical penetrance of <italic>HFE</italic> gene mutations is low and many people with elevated iron stores lack <italic>HFE</italic> mutations. We analyzed data from the Hemochromatosis and Iron Overload Screening Study to assess the relationship among <italic>HFE</italic> genotype (individuals with either homozygous or compound heterozygous status for C282Y and/or H63D <italic>HFE</italic> mutations were defined as genotype positive, or G+), elevated iron phenotype (individuals exceeding gender‐specific transferrin saturation and serum ferritin threshold levels were considered phenotype positive, or P+), and leukocyte telomere length, a marker of biological aging and cumulative oxidative stress. In unadjusted analyses in comparison to individuals who were G−P−, G+P− were not significantly different (OR 0.74; 95% CI 0.26–2.04), while the G+P+ (OR 2.03; 95% CI 1.15–3.56), and G−P+ (OR 2.24; 95% CI 1.5–3.29) had increased risk of short telomeres (<=25th percentile) rather than long telomeres (>=75th percentile). In analyses adjusting for age, gender, and race/ethnicity, the effect of individuals with elevated iron phenotypes having short telomeres persisted with G+P+ individuals (OR 1.94; 95% CI 1.02–3.72), and G−P+ individuals (OR 2.17; 95% CI 1.39–3.39) being significantly different from the G−P− group. In conclusion, elevated iron phenotype, but not <italic>HFE</italic> genotype, was associated with shortened telomeres. Further studies will be needed to determine whether telomere length provides a marker for morbidities specifically associated with iron overload. Am. J. Hematol. 88:492–496, 2013. © 2013 Wiley Periodicals, Inc.</p> </abstract>