ArticlePloS one2014
Profound morphological changes in the erythrocytes and fibrin networks of patients with hemochromatosis or with hyperferritinemia, and their normalization by iron chelators and other agents.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 68 citations in OpenAlex.
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- A Direct Relationship Between 'Blood Stasis' and Fibrinaloid Microclots in Chronic, Inflammatory, and Vascular Diseases, and Some Traditional Natural Products Approaches to Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Protein Susceptibility to Peroxidation by 4-Hydroxynonenal in Hereditary Hemochromatosis.International journal of molecular sciences · 2023Article
- The potential role of ischaemia-reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications.The Biochemical journal · 2022Review
- A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications.The Biochemical journal · 2022Review
- Metabolic Influences Modulating Erythrocyte Deformability and Eryptosis.Metabolites · 2021Review
- Peripheral blood mononuclear cells (PBMC) microbiome is not affected by colon microbiota in healthy goats.Animal microbiome · 2021Article
- Analyses of hemorrhagic diathesis in high-iron diet-fed rats.Journal of toxicologic pathology · 2021Article
- TanP: A Multifunctional Anionic Peptide FromFrontiers in molecular biosciences · 2021Article
- Functional Mammalian Amyloids and Amyloid-Like Proteins.Life (Basel, Switzerland) · 2020Review
- Covid-19: The Rollercoaster of Fibrin(Ogen), D-Dimer, Von Willebrand Factor, P-Selectin and Their Interactions with Endothelial Cells, Platelets and Erythrocytes.International journal of molecular sciences · 2020Review
- No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases.Biological reviews of the Cambridge Philosophical Society · 2018Review
- To What Extent Are the Terminal Stages of Sepsis, Septic Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome Actually Driven by a Prion/Amyloid Form of Fibrin?Seminars in thrombosis and hemostasis · 2018Review
- Lipopolysaccharide-binding protein (LBP) can reverse the amyloid state of fibrin seen or induced in Parkinson's disease.PloS one · 2018Article
- Lipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular co-morbidities.Scientific reports · 2017Article
- Red blood cell distribution width as a prognostic marker in patients with heart failure and diabetes mellitus.Cardiovascular diabetology · 2017Article
- The stabilizing effect of an oligomeric proanthocyanidin on red blood cell membrane structure of poorly controlled Type II diabetes.Nutrition & diabetes · 2017Article
- The effect of physiological levels of South African puff adder (Bitis arietans) snake venom on blood cells: an in vitro model.Scientific reports · 2016Article
- Highly Absorbent Antibacterial Hemostatic Dressing for Healing Severe Hemorrhagic Wounds.Materials (Basel, Switzerland) · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well-known that individuals with increased iron levels are more prone to thrombotic diseases, mainly due to the presence of unliganded iron, and thereby the increased production of hydroxyl radicals. It is also known that erythrocytes (RBCs) may play an important role during thrombotic events. Therefore the purpose of the current study was to assess whether RBCs had an altered morphology in individuals with hereditary hemochromatosis (HH), as well as some who displayed hyperferritinemia (HF). Using scanning electron microscopy, we also assessed means by which the RBC and fibrin morphology might be normalized. An important objective was to test the hypothesis that the altered RBC morphology was due to the presence of excess unliganded iron by removing it through chelation. Very striking differences were observed, in that the erythrocytes from HH and HF individuals were distorted and had a much greater axial ratio compared to that accompanying the discoid appearance seen in the normal samples. The response to thrombin, and the appearance of a platelet-rich plasma smear, were also markedly different. These differences could largely be reversed by the iron chelator desferal and to some degree by the iron chelator clioquinol, or by the free radical trapping agents salicylate or selenite (that may themselves also be iron chelators). These findings are consistent with the view that the aberrant morphology of the HH and HF erythrocytes is caused, at least in part, by unliganded ('free') iron, whether derived directly via raised ferritin levels or otherwise, and that lowering it or affecting the consequences of its action may be of therapeutic benefit. The findings also bear on the question of the extent to which accepting blood donations from HH individuals may be desirable or otherwise.
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Registered trials
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