Hemochromatosis
Original Editors - Jill Heil & Jillian Redlinger from Bellarmine University's Pathophysiology of Complex Patient Problems project.
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Definition/Description[edit | edit source]
Hemochromatosis, also known as bronze diabetes or iron storage disease, is an autosomal recessive hereditary disorder characterized by excessive iron absorption by the small intestines[1]. Individuals with hemochromatosis lack an effective way to remove excess iron, and the iron begins to accumulate with subsequent development of fibrosis in the liver, pancreas, skin, heart, and other organs[2]. Excess iron accumulation in the body promotes oxidation and causes tissue injury, fatigue, arthralgia or arthritis, and skin changes. Complications can include hepatomegaly, diabetes, impotence (males), pulmonary involvement, and cardiac myopathy[2].
Prevalence[edit | edit source]
• In one of every 200-300 people there is a genetic abnormality found, but there can also be an excessive amount of iron intake that can cause Hemochromatosis. (symptoms and remedies)
• Occurs 5-10 times more often in men than women; this is due to women losing blood through menstuation and pregnanacy.(diff diagnosis)
• Symptoms occur in men >50 years and are rarely symptomatic before 30 years of age. (diff diagnosis)
• Women experience symptoms around age 60. (diff diagnosis)
• It is the most common autosomal recessive disorder in people of Northern European descent (http://emedicine.medscape.com/article/177216-clinical#a0256)
• If an individual has hemochromatosis, their brothers and sisters have a 1 in 4 chance (25%) of having two HFE gene mutations and their children have about a 1 in 20 chance (5%) of having two HFE gene mutations. (http://www.cdc.gov/ncbddd/hemochromatosis/families.html)
Characteristics/Clinical Presentation[edit | edit source]
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Associated Co-morbidities[edit | edit source]
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Medications[edit | edit source]
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Etiology/Causes[edit | edit source]
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Differential Diagnosis[edit | edit source]
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