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Serum Iron, Transferrin Saturation, Ferritin, and Dietary Data in Age-Related Macular Degeneration
Abstract
Iron (Fe) is a tightly metabolically controlled mineral and growth factor for all living cells. Iron not bound in erythrocyte hemoglobin is transported by the plasma iron transport protein transferrin (Tf) and bound within cells by ferritin. Apo-Tf and apo-hemopexin are also known to be made locally in the retina. Free Fe is cytotoxic, promotes oxidation/lipid peroxidation, has been implicated as a risk factor in cardiac disease, and is itself associated with age-related macular degeneration (ARMD), the leading cause of blindness in aging western societies. The authors evaluated Fe overload serum markers and dietary intake in patients with atrophic ARMD. After obtaining informed consent, an Fe panel consisting of serum Fe, total Fe binding capacity (TIBC), and ferritin was performed on 75 veterans (70 men, five women) with an average age of 75 years with a diagnosis of atrophic ARMD by combined criteria of International Retinal Classification and psychophysical/symptom abnormalities. Tf saturation was calculated by dividing serum Fe concentration by TIBC. Dietary iron with and without supplementation and vitamin C intake were determined for 86 patients using the Harvard School of Public Health/Department of Nutrition Food Frequency Questionnaire. Statistically significant correlations (P <0.1) were found between serum and dietary Fe (r = -.26), between serum Fe and serum ferritin (r =.34), and between dietary Fe and dietary vitamin C (r =.30). The data on mostly male geriatric veterans with atrophic ARMD indicate that single time-point assessment of systemic Fe status and dietary Fe is not useful. However, serial multiple-year data, correlating Fe markers with disease, may still be important. Also, because Fe transport proteins do not cross the blood-retina barrier, the local cellular toxic effects of Fe must also be considered.
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“Retinal iron levels increase with age [1322], iron is significantly implicated in AMD [1323-1329], and iron chelation may help to reverse the process [1330].”
From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [1324]
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Metadata
- Authors
- Richer, S., Rudy, D., Statkute, L., Karofty, K., & Frankowski, J.
- Venue
- American Journal of Therapeutics
- Published
- 2002-01
- Volume
- 9
- Issue
- 1
- Pages
- 25-28
- ISSN
- 1075-2765 (ISSN-L)
- OpenAlex
- W2064117025
- Cited by
- 17
- References
- 12
- Citations by year
- 2020: 1 · 2016: 1 · 2013: 1 · 2012: 2
- FWCI
- 0.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Aeronautics Research Mission Directorate
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- age-related macular degeneration, iron overload, serum iron, transferrin saturation, ferritin, iron intake, vitamin C intake, iron supplementation, atrophic macular degeneration, veterans, iron transport proteins, blood-retinal barrier, oxidative stress
- MeSH terms
- Aged, Aged, 80 and over, Antioxidants, Ascorbic Acid, Diet Surveys, Female, Ferritins, Humans, Iron, Macular Degeneration, Male, Risk Factors, Transferrin, Lutein, Biomarkers, Randomized Controlled Trials as Topic, Dietary Supplements
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