scholarly journals New horizons in iron deficiency anaemia in older adults

2020 ◽  
Vol 49 (3) ◽  
pp. 309-318 ◽  
Author(s):  
Jennifer Kirsty Burton ◽  
Luke C Yates ◽  
Lindsay Whyte ◽  
Edward Fitzsimons ◽  
David J Stott

Abstract Iron deficiency anaemia (IDA) is common in older adults and associated with a range of adverse outcomes. Differentiating iron deficiency from other causes of anaemia is important to ensure appropriate investigations and treatment. It is possible to make the diagnosis reliably using simple blood tests. Clinical evaluation and assessment are required to help determine the underlying cause and to initiate appropriate investigations. IDA in men and post-menopausal females is most commonly due to occult gastrointestinal blood loss until proven otherwise, although there is a spectrum of underlying causative pathologies. Investigation decisions should take account of the wishes of the patient and their competing comorbidities, individualising the approach. Management involves supplementation using oral or intravenous (IV) iron then consideration of treatment of the underlying cause of deficiency. Future research areas are outlined including the role of Hepcidin and serum soluble transferrin receptor measurement, quantitative faecal immunochemical testing, alternative dosing regimens and the potential role of IV iron preparations.

2014 ◽  
Vol 5 (4) ◽  
pp. 231-236 ◽  
Author(s):  
A T M Dilshad Chowdhury ◽  
Gaius Longcroft-Wheaton ◽  
Andrew Davis ◽  
David Massey ◽  
Patrick Goggin

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 498 ◽  
Author(s):  
Faisal Nuhu ◽  
Anne-Marie Seymour ◽  
Sunil Bhandari

Background: Mitochondrial dysfunction is observed in chronic kidney disease (CKD). Iron deficiency anaemia (IDA), a common complication in CKD, is associated with poor clinical outcomes affecting mitochondrial function and exacerbating oxidative stress. Intravenous (iv) iron, that is used to treat anaemia, may lead to acute systemic oxidative stress. This study evaluated the impact of iv iron on mitochondrial function and oxidative stress. Methods: Uraemia was induced surgically in male Sprague-Dawley rats and studies were carried out 12 weeks later in two groups sham operated and uraemic (5/6 nephrectomy) rats not exposed to i.v. iron versus sham operated and uraemic rats with iv iron. Results: Induction of uraemia resulted in reduced iron availability (serum iron: 31.1 ± 1.8 versus 46.4 ± 1.4 µM), low total iron binding capacity (26.4 ± 0.7 versus 29.5 ± 0.8 µM), anaemia (haematocrit: 42.5 ± 3.0 versus 55.0 ± 3.0%), cardiac hypertrophy, reduced systemic glutathione peroxidase activity (1.12 ± 0.11 versus 1.48 ± 0.12 U/mL), tissue oxidative stress (oxidised glutathione: 0.50 ± 0.03 versus 0.36 ± 0.04 nmol/mg of tissue), renal mitochondrial dysfunction (proton/electron leak: 61.8 ± 8.0 versus 22.7 ± 5.77) and complex I respiration (134.6 ± 31.4 versus 267.6 ± 26.4 pmol/min/µg). Iron therapy had no effect on renal function and cardiac hypertrophy but improved anaemia and systemic glutathione peroxidase (GPx) activity. There was increased renal iron content and complex II and complex IV dysfunction. Conclusion: Iron therapy improved iron deficiency anaemia in CKD without significant impact on renal function or oxidant status.


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