The safety of modern intravenous iron infusions in patients with rheumatoid arthritis – a review of the literature

Ooi, Michael; Hibbs, Stephen; Chen, Frederick

doi:10.1080/16078454.2020.1730557

Cited by 8 publications

(5 citation statements)

References 11 publications

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“…However, importantly, oral supplementary strategies for functional iron deficiency remain more or less unsatisfactory, since iron absorption and export require FPN, which is degraded upon hepcidin production in response to inflammation. In addition, although parenteral iron supplementation appears to be safe in case of stimulated erythropoiesis, it was recently shown that at least the intravenous route of iron administration can even aggravate inflammation [21,22]. Accordingly, our data also argue against iron supplementation in inflammatory arthritis, but rather suggest a positive role of enteral iron restriction.…”

Section: Discussionmentioning

confidence: 56%

Low Iron Diet Improves Clinical Arthritis in the Mouse Model of Collagen-Induced Arthritis

Scholz,

Xie,

Arsiwala

et al. 2024

Preprint

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Background: In response to inflammation, the absorption of nutritional iron is restricted. Multiple inflammation-related signaling pathways can lead to ferroptosis, an iron-dependent mechanism of programmed cell death. Since the pathophysiological significance of the presence and uptake of iron in chronic inflammation is still unknown, we tested the effect of a low iron diet on the clinical course of arthritis in the mouse model of collagen-induced arthritis (CIA). Methods: Six- to eight-week-old male DBA/1 mice were fed either a normal or a low iron diet starting three weeks before arthritis induction. From day four after the collagen-booster made on day 25, the development of arthritis was regularly monitored until the end of the experiment (day 34), using a standard clinical arthritis score. The complete blood count was determined as well as Fe2+, Fe3+, oxidized and reduced glutathione (GSH and GSSG) and malondialdehyde (MDA) in whole paw tissue by ELISA. Quantitative PCR was performed from whole paw tissue for glutathione peroxidase 4 and other key regulator genes of iron metabolism and ferroptosis. We used nonparametric tests to com-pare markers of iron metabolism and ferroptosis as well as nonlinear regression models for longitu-dinal data for signs of arthritis. Results: Mice fed a low iron diet showed a significantly less severe course of arthritis compared to mice fed a normal iron diet (p

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Section: Discussionmentioning

confidence: 56%

Low Iron Diet Improves Clinical Arthritis in the Mouse Model of Collagen-Induced Arthritis

Scholz,

Xie,

Arsiwala

et al. 2024

Preprint

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“…The second peak occurs later when over 90% of low MW iron preparation has been taken up by macrophages, representing indirect ferroportin-mediated iron efflux from macrophages that fully saturates transferrin (Pathway II) [4] . Previous studies suggested that parenteral iron infusions mostly with iron dextran could exacerbate joint pain, synovitis, and arthralgia in patients with rheumatoid arthritis [5] . Accordingly, injection of iron dextran or sucrose led to significant exacerbation of joint inflammation along with iron deposition in the synovium of rats with adjuvant arthritis.…”

Section: Discussionmentioning

confidence: 99%

Rhabdomyolysis after Intravenous Ferric Gluconate: A Case Report

Botti

Piperno

Cianflone

et al. 2022

European Journal of Case Reports in Internal Medicine

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Patients with severe iron deficiency, malabsorption or intolerance to oral iron are frequently treated with intravenous iron replacement. We report the case of a 42-year-old woman with non-erosive oligoarticular arthritis with antiparietal cell antibodies and iron deficiency anemia secondary to menorrhagia and unresponsive to oral iron preparations. She was treated with an intravenous infusion of ferric gluconate. After the first infusion of 125 mg (in 250 mL saline), she developed transient pain in her knee and wrist joints. When the dose was subsequently halved, the patient showed no adverse symptoms in the next four infusions and had normalized hemoglobin levels and iron indices. However, after a subsequent 125 mg ferric gluconate infusion she developed severe leg pain, muscular and joint stiffness, and functional impairment of her hands, right foot, and ankle. Laboratory tests showed a progressive increase in creatine kinase, transaminase, and C-reactive protein that normalized several days after the infusion. Although rhabdomyolysis is not reported among endovenous iron-induced adverse events, our findings suggest that intravenous iron infusions might have increased free iron generation promoting oxidative joint and muscular injury, which would explain the joint pain and stiffness, and rhabdomyolysis. Greater attention should be paid to the more frequent cases of myalgia occurring after iron infusion, which may underlie a rhabdomyolytic event requiring clinical observation.

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“… 144 Due to the resistance of FLS to ferroptosis and the redistribution of iron, iron supplementation in RA patients with iron deficiency anemia may lead to exacerbation of RA. 145 …”

Section: Ferroptosis and Rheumatoid Arthritismentioning

confidence: 99%

“…144 Due to the resistance of FLS to ferroptosis and the redistribution of iron, iron supplementation in RA patients with iron deficiency anemia may lead to exacerbation of RA. 145 Targeting ferroptosis has already shown positive effects in RA. Icariin can promote the SLC7A11-GSH-GPX4 axis to alleviate ferroptosis and lipopolysaccharide-induced synovitis.…”

Section: Ferroptosis and Rheumatoid Arthritismentioning

confidence: 99%

Targeting Ferroptosis in Bone-Related Diseases: Facts and Perspectives

Chen,

Han,

Wang

et al. 2023

JIR

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Ferroptosis is a new cell fate decision discovered in recent years. Unlike apoptosis, autophagy or pyroptosis, ferroptosis is characterized by iron-dependent lipid peroxidation and mitochondrial morphological changes. Ferroptosis is involved in a variety of physiological and pathological processes. Since its discovery, ferroptosis has been increasingly studied concerning bone-related diseases. In this review, we focus on the latest research progress and prospects, summarize the regulatory mechanisms of ferroptosis, and discuss the role of ferroptosis in the pathogenesis of bone-related diseases, such as osteoporosis (OP), osteoarthritis (OA), rheumatoid arthritis (RA), and osteosarcoma (OS), as well as its therapeutic potential.

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The safety of modern intravenous iron infusions in patients with rheumatoid arthritis – a review of the literature

Cited by 8 publications

References 11 publications

Low Iron Diet Improves Clinical Arthritis in the Mouse Model of Collagen-Induced Arthritis

Low Iron Diet Improves Clinical Arthritis in the Mouse Model of Collagen-Induced Arthritis

Rhabdomyolysis after Intravenous Ferric Gluconate: A Case Report

Targeting Ferroptosis in Bone-Related Diseases: Facts and Perspectives

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