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Blood cell HbA1c measured by enzymatic assay show higher than whole blood HbA1c in patients with iron deficiency anemia.
Diabetol Int
January 2025
Department of Clinical Laboratory, New Tokyo Hospital, Chiba, Japan.
In Japan, most HbA1c measurements by enzymatic assays or immunoassays represent the HbA1c levels in the blood cell fraction obtained after centrifugation of the blood samples. The present study investigated that the blood cell enzymatic HbA1c assay (EA-HbA1c) was compared with whole blood HbA1c in patients with iron deficiency anemia (IDA). Study 1: EA-HbA1c levels using blood cell samples (blood cell EA-HbA1c) and high-performance liquid chromatography (HPLC)-HbA1c levels using whole blood samples (whole blood HPLC-HbA1c) were measured in 15 IDA patients with Hb < 8 g/dL and transferrin saturation (TSAT) < 20%, and the correlations between the blood cell EA-HbA1c/whole blood HPLC-HbA1c ratio (%) and various IDA indicators [mean corpuscular hemoglobin concentration (MCHC), TSAT, and logarithmically transformed ferritin (log-FER)] were examined.
View Article and Find Full Text PDFRationale and design of the FAIR-HF2-DZHK05 trial: Ferric carboxymaltose assessment of morbidity and mortality in patients with iron deficiency and chronic heart failure.
Eur J Heart Fail
January 2025
Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Aims: While it is widely accepted that intravenous (IV) iron improves functional capacity, symptoms, and cardiovascular outcomes in patients with heart failure (HF) with reduced ejection fraction (HFrEF) diagnosed with iron deficiency (ID), three recently published cardiovascular outcome trials (AFFIRM-AHF, IRONMAN and HEART-FID) of IV iron supplementation in HF failed to demonstrate a significant benefit on their respective primary endpoints. Dosing of IV iron after the initial correction of baseline ID - by design or as a result of trial circumstances - was relatively low (i.e.
View Article and Find Full Text PDFIron Overload in Histidine-to-Aspartic Acid Substitution at 63 (H63D) Gene Heterozygous Hereditary Hemochromatosis With Erythrocytosis: A Case Report.
Cureus
December 2024
Internal Medicine, National Hospital of Sri Lanka, Colombo, LKA.
Hereditary hemochromatosis occurs due to genetic mutations, namely, cysteine-to-tyrosine substitution at amino acid 282 (C282Y) and histidine-to-aspartic acid substitution at 63 (H63D) mutations. The role of H63D mutation in hemochromatosis is less clear, and its penetrance is low even in homozygotes. Therefore, iron overload in H63D heterozygotes is extremely rare and scarcely reported.
View Article and Find Full Text PDFBackground And Aims: Red blood cell transfusions are often used to treat iron-deficient patients in the emergency department (ED), while treatment with intravenous (IV) iron is preferred, as it increases hemoglobin concentration rapidly and durably. We aim to evaluate the incidence of iron deficiency anemia, frequency of blood transfusion and iron supplementation, and factors associated with blood transfusion in the ED.
Methods: We conducted a retrospective cohort study of adult patients presenting to the St.
Introduction: The aim of this study was to define the relationships between factors other than transferrin saturation (TS) to mean corpuscular volume (MCV) and macrocytosis (MCV > 100 fL) in p.C282Y (rs1800562) homozygotes.
Methods: We studied white post-screening participants with p.
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