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Iron overload (also known as haemochromatosis or hemochromatosis) is the abnormal and increased accumulation of total iron in the body, leading to organ damage. [1] The primary mechanism of organ damage is oxidative stress, as elevated intracellular iron levels increase free radical formation via the Fenton reaction.
Symptoms that emerge early on in the disease are generally less severe, and may include conditions such as fatigue, weakness, skin discoloration, loss of sex drive and joint pain. Late in the disease, people may experience liver disease as well as disease to other major organs as excess iron is deposited over time.
The symptoms of type 4B hemochromatosis tend to be more severe. They resemble the symptoms of hemochromatosis types 1, 2, and 3. Plasma iron concentration is elevated, and symptoms include joint pain, diabetes, and arrhythmia. Liver iron deposition tends to be greater in type 4B than in type 4A. [5]
Iron is a mineral that is crucial for optimal health and well-being. Found naturally in many foods and dietary supplements, it is a key component of hemoglobin, the part of red blood cells ...
“Those who are iron deficient likely feel weakness, headaches, fatigue, pale, and/or have joint pain,” says Eric Ascher, DO, a family medicine physician at Lenox Hill Hospital.
Since the liver is a primary storage area for iron and naturally accumulates excess iron over time, it is likely to be damaged by iron overload. Toxins may accumulate in the blood and eventually affect mental functioning due to increased risk of hepatic encephalopathy. Together, they can increase the risk of liver cancer to one in three persons.
Iron poisoning typically occurs from ingestion of excess iron that results in acute toxicity. Mild symptoms which occur within hours include vomiting, diarrhea, abdominal pain, and drowsiness. [1] In more severe cases, symptoms can include tachypnea, low blood pressure, seizures, or coma. [2]
Iron metabolism disorders may involve a number of genes including HFE and TFR2. [ 1 ] Hepcidin is the master regulator of iron metabolism and, therefore, most genetic forms of iron overload can be thought of as relative hepcidin deficiency in one way or another [1] .
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