Background And Objective: To ascertain the frequency of iron deficiency and iron overload in an adult Catalan population.
Subjects And Method: Multiple iron measurements, including transferrin saturation (TS) and serum ferritin (SF), were performed in a representative sample of 1,296 adults.
Results: The prevalence of iron deficiency was 5.6% (95% CI, 4.4 to 6.9)(SF below 12 microg/l), and 9.3% (95% CI, 7.7 to 10.9) had an iron overload(SF above 300 microg/l in men and SF above 200 microg/l in women). Iron deficiency was especially frequent in women 50 years old or younger (14.8%; 95% CI, 11.4 to 18.1),while in men of the same age it was 1.1% (95% CI, 0.1 to 2.1), yet 11.7% (95% CI, 8.7 to 14.7) had iron overload. In the population over 50 years there was an iron deficiency in 0.9% (95% CI, 0.0 to 1.8), and an iron overload in 15.1% (95% CI, 11.7 to 18.4). 1.6% (95% CI, 0.9-2.3) of all population and 3.9% (1.4-6.4) of men older than 50 years had an SF above 500 microg/l.
Conclusions: Iron overload is more prevalent than iron deficiency in Catalonia, particularly in men and people over 50 years. The causes and effects of the disorder should be investigated in order to carry out corrective measures in the future.
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http://dx.doi.org/10.1016/s0025-7753(04)74435-8 | DOI Listing |
Mol Med
January 2025
Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Background: Lysinuric protein intolerance is a rare autosomal disorder caused by mutations in the Slc7a7 gene that lead to impaired transport of neutral and basic amino acids. The gold standard treatment for lysinuric protein intolerance involves a low-protein diet and citrulline supplementation. While this approach partially improves cationic amino acid plasma levels and alleviates some symptoms, long-term treatment is suggested to be detrimental and may lead to life-threatening complications characterized by a wide range of hematological and immunological abnormalities.
View Article and Find Full Text PDFGene
January 2025
Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine/The First Affiliated Hospital, Shihezi University, Shihezi 832002 China; Department of Pathology, Central People's Hospital of Zhanjiang and Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang 524000 Guangdong, China. Electronic address:
Background: In-stent restenosis (ISR) is one of the most significant complications following percutaneous coronary intervention (PCI) in patients with coronary artery disease (CAD). Ferroptosis is a novel cell death mode characterized by iron overload and lipid peroxidation. However, the role of ferroptosis in vascular smooth muscle cells (VSMCs) regulating neointimal formation during restenosis remains unclear.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Radiology, China-Japan Friendship Hospital, Beijing, China.
Introduction: The link between overload brain iron and transcriptional/cellular signatures in Alzheimer's disease (AD) remains inconclusive.
Methods: Iron deposition in 41 cortical and subcortical regions of 30 AD patients and 26 healthy controls (HCs) was measured using quantitative susceptibility mapping (QSM). The expression of 15,633 genes was estimated in the same regions using transcriptomic data from the Allen Human Brain Atlas (AHBA).
Eur J Haematol
January 2025
Hematology, St. Paul's Hospital and The University of British Columbia, Vancouver, British Columbia, Canada.
Introduction: Iron overload (IOL) accumulates in myelodysplastic syndromes (MDS) from expanded erythropoiesis and transfusions. Somatic mutations (SM) are frequent in MDS and stratify patient risk. MDS treatments reversing or limiting transfusion dependence are limited.
View Article and Find Full Text PDFCureus
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.
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