Hemochromatosis

Summarized by Plex Health
Last Updated: 02 May 2022
enhanced mr imaging of the shoulder, and sternoclavicular and acromioclavicular joint arthritis in primary hemochromatosis. "enhanced mr imaging of the shoulder, and sternoclavicular and acromioclavicular joint arthritis in primary hemochromatosis.", by Farpour F, Phan SJ, Burns J, Tehranzadeh J. Fig1: a Hemochromatosis of the shoulder. AP radiograph of the left shoulder shows linear chondrocalcinosis (linear calcification) (arrow) of the hyaline articular cartilage surface of the humeral head. There is small calcification at the acromioclavicular...

Hemochromatosis is a disease in which way too much iron accumulates in your body. You absorb more iron than you require if you have hemochromatosis. The added iron can damage your body organs. Secondary hemochromatosis is usually the result of another thing, such as anemia, thalassemia, liver disease, or blood transfusions. If you do, you may have joint pain, tiredness, basic weak point, fat burning, and stomach pain. Your doctor will detect hemochromatosis based on your clinical and family histories, a physical exam, and the arise from treatments and tests. Without therapy, hemochromatosis can cause iron overload, a buildup of iron that can harm many components of the body, including your liver, heart, pancreatic, endocrine glands, and joints. Doctors diagnose hemochromatosis based on blood tests to inspect degrees of iron and particular proteins in the blood and to examine for gene mutations that generally cause hemochromatosis. In some cases, physicians may use a liver biopsy to verify iron overload exists. An approximated one million people in the United States have genetic hemochromatosis. Normally humans draw out needed iron from food using the intestines. In a person with HH, the mechanism for regulating iron absorption is faulty and the body takes in excessive iron. Nonetheless, not all people that have two altered duplicates develop symptoms and signs of HH. People who inherit only one duplicate of the mutated genetics are providers, but usually have no symptoms, or have very mild symptoms since one appropriate copy of the gene shows up to sufficiently regulate iron absorption. "Silent" service providers, without symptoms of the disease, can still pass on the defect to their children If two parents are silent service providers, each child has a 25 percent chance of acquiring two copies of the faulty gene, and will most likely develop the disease.

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PubChem - CovalentUnitCount

(Table source)
CIDMolecularFormulaMolecularWeightCanonicalSMILESIsomericSMILESInChIInChIKeyIUPACNameXLogPExactMassMonoisotopicMassTPSAComplexityChargeHBondDonorCountHBondAcceptorCountRotatableBondCountHeavyAtomCountIsotopeAtomCountAtomStereoCountDefinedAtomStereoCountUndefinedAtomStereoCountBondStereoCountDefinedBondStereoCountUndefinedBondStereoCountCovalentUnitCount
160727835C15H20Cl2N8S2447.4CC1=NC=C(C(=N1)N)CNC2=CC=C(S2)Cl.C1=C(C(=NC=N1)N)SCN.ClCC1=NC=C(C(=N1)N)CNC2=CC=C(S2)Cl.C1=C(C(=NC=N1)N)SCN.ClInChI=1S/C10H11ClN4S.C5H8N4S.ClH/c1-6-13-4-7(10(12)15-6)5-14-9-3-2-8(11)16-9;6-2-10-4-1-8-3-9-5(4)7;/h2-4,14H,5H2,1H3,(H2,12,13,15);1,3H,2,6H2,(H2,7,8,9);1HMGUXAZHHEJVOOL-UHFFFAOYSA-N5-(aminomethylsulfanyl)pyrimidin-4-amine;5-[[(5-chlorothiophen-2-yl)amino]methyl]-2-methylpyrimidin-4-amine;hydrochloride446.0629404446.0629404195331051052700000003
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