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Diagnosis and management of hereditary hemochromatosis: lifestyle modification, phlebotomy, and blood donation.

Hematology Am Soc Hematol Educ Program

December 2024

Department of Medicine, University of Verona and EuroBloodNet Referral Center for Iron Disorders, Azienda Ospedaliera Universitaria Integrata Verona, Verona, Italy.

The term hemochromatosis refers to a group of genetic disorders characterized by hepcidin insufficiency in the context of normal erythropoiesis, iron hyperabsorption, and expansion of the plasma iron pool with increased transferrin saturation, the diagnostic hallmark of the disease. This results in the formation of toxic non-transferrin-bound iron, which ultimately accumulates in multiple organs, including the liver, heart, endocrine glands, and joints. The most common form is HFE-hemochromatosis (HFE-H) due to p.

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Ferritin is one of the most requested blood tests in both primary and inpatient care, and high values occur frequently. One of the greatest challenges in the investigation of hyperferritinemia is to determine if there is a presence of iron overload. Patient history (chronic liver disease, excessive alcohol consumption, hereditary factors), clinical features (metabolic syndrome, acute or chronic inflammation, infection, malignancy) and biochemical tests (ferritin, transferrin saturation, hemoglobin, liver enzymes, CRP/SR, phosphatidyl ethanol, lipid profile, glucose) facilitate the determination of the cause of hyperferritinemia.

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Ferroptosis is a newly discovered form of cell death caused by the peroxidation of fragile fatty acids in cell membranes, which combines with iron to increase reactive oxygen species and disable mitochondria. Ferroptosis has been linked to aging-related conditions, including type 2 diabetes, cardiovascular disease, and nonalcoholic fatty liver disease (NAFLD). Pentadecanoic acid (C15:0), an odd-chain saturated fat, is an essential fatty acid with the primary roles of stabilizing cell membranes and repairing mitochondrial function.

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Research advances on molecular mechanism and natural product therapy of iron metabolism in heart failure.

Eur J Med Res

April 2024

Department of Cardiology, Changde Hospital, Xiangya School of Medicine, Central South University, Hunan, China.

Article Synopsis
  • The progression of heart failure (HF) is complex, influenced by iron metabolism, where both deficiencies and excesses of iron can lead to myocarditis and contribute to HF development.
  • Iron ions serve as vital cofactors for proteins essential in myocardial energy metabolism, making iron toxicity and abnormal iron levels important for diagnosing and treating HF.
  • Recent studies suggest that iron chelators, antioxidants, and natural compounds can effectively regulate iron levels and protect heart tissue, offering new treatment strategies targeting ferroptosis in heart failure.
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Kidney tubules are mostly responsible for pathogenesis of diabetic kidney disease. Actively reabsorption of iron, high rate of lipid metabolism and exposure to concentrated redox-active compounds constructed the three main pillars of ferroptosis in tubular cells. However, limited evidence has indicated that ferroptosis is indispensable for diabetic tubular injury.

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