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Physiology and Inflammation Driven Pathophysiology of Iron Homeostasis-Mechanistic Insights into Anemia of Inflammation and Its Treatment.

Nutrients
January 1, 1970
Lukas Lanser et al. (4 authors)
Journal ArticleReviewHuman Study
Study Details

Study Goal

The researchers aimed to evaluate the role of iron metabolism in anemia of inflammation (AI) and discuss therapeutic approaches, including iron supplementation and emerging treatments.

Results Summary

The study found that AI is caused by iron retention in macrophages, reduced erythrocyte half-life, and cytokine-mediated inhibition of erythropoiesis. Treatment of the underlying inflammatory disease often normalizes hemoglobin, but iron supplementation or erythropoietin therapy may be needed if unresolved.

Population

Patients with inflammatory disorders and associated anemia.

Effective Dosage

Not specified

Duration

Not specified

Interactions

None mentioned

Extracted Claims (5)
InterventionDirectionEndpointPopulationDosageImpactClaim #
treatment of the underlying inflammatory disease
increase
hemoglobin levels
patients with anemia of inflammation
normalization
mostly results in normalization
#1
iron supplementation therapy
neutral
anemia of inflammation
patients where underlying disease and/or anemia are not resolved
-
may be considered
#2
treatment with erythropoietin stimulating agents
neutral
anemia of inflammation
patients where underlying disease and/or anemia are not resolved
-
may be considered
#3
blood transfusions
neutral
life-threatening anemia
patients with anemia of inflammation
-
are an emergency treatment
#4
new treatments with hepcidin-modifying strategies and stabilizers of hypoxia inducible factors
neutral
anemia of inflammation
ill patients
-
emerge
#5
Abstract

Anemia is very common in patients with inflammatory disorders. Its prevalence is associated with severity of the underlying disease, and it negatively affects quality of life and cardio-vascular performance of patients. Anemia of inflammation (AI) is caused by disturbances of iron metabolism resulting in iron retention within macrophages, a reduced erythrocyte half-life, and cytokine mediated inhibition of erythropoietin function and erythroid progenitor cell differentiation. AI is mostly mild to moderate, normochromic and normocytic, and characterized by low circulating iron, but normal and increased levels of the storage protein ferritin and the iron hormone hepcidin. The primary therapeutic approach for AI is treatment of the underlying inflammatory disease which mostly results in normalization of hemoglobin levels over time unless other pathologies such as vitamin deficiencies, true iron deficiency on the basis of bleeding episodes, or renal insufficiency are present. If the underlying disease and/or anemia are not resolved, iron supplementation therapy and/or treatment with erythropoietin stimulating agents may be considered whereas blood transfusions are an emergency treatment for life-threatening anemia. New treatments with hepcidin-modifying strategies and stabilizers of hypoxia inducible factors emerge but their therapeutic efficacy for treatment of AI in ill patients needs to be evaluated in clinical trials.

Medical Subject Headings (MeSH)
AnemiaErythropoiesisHomeostasisHumansInflammationIronNutritional Physiological Phenomena
Study Links
Quality Scores
SafetyNot Assessed
Efficacy70/10
Quality80/10
Citation Metrics
Total Citations66
Citations/Year16.5
Relative Citation Ratio5.74
NIH Percentile94.4%
Research Impact Scores
APT Score0.75
Weight Score0.95
Normalized Score0.64
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