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With primary hemochromatosis (PHC), a person is born having received from both parents a gene that carries bad information (autosomal recessive inheritance).

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True, the patient does not know about this for a long time, accumulating this chemical element from day to day. For example, if 5 mg of iron from dietary intake remains in the body daily, then the first symptoms will appear after about gabapentin pills online. Secondary hemochromatosis (SHCH) is formed at some stage, as a result of neurontin pills.

And then it doesn’t matter for what reason the malabsorption occurred, the fact is that iron accumulates in large quantities in vital organs (heart, liver, individual endocrine glands, joints) and thus interferes with their normal functioning. Hereditary or primary hemochromatosis.

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As it turned out, hereditary hemochromatosis (NH) is not a rare disease at all. This was thought earlier, when population genetic analysis on a modern scale was not available. The assumption of the genetic origin of primary hemochromatosis was confirmed in the 70s of the last century, when the major histocompatibility complex (MHC) was actively studied, and antigens of the HLA leukocyte system were discovered one by one. The gene that controls the concentration of Fe in the body is located on the short arm of chromosome 6, next to the A (A3) locus of the HLA complex. As a result, certificates were obtainedevidence of an associative relationship between hemochromatosis and genes of the major histocompatibility system.

Primary hemochromatosis is always hereditary, it appears in the population along with the birth of a new (homozygous) member, but it will manifest itself only after 2-3 decades.

It has now been reliably established that the prevalence of a defective recessive gene (hemochromatosis gene), which carries distorted information about metabolism, accompanied by increased absorption of iron, is not so small - up to 10% among all residents.

Four varieties of primary hemochromatosis are designated.

Hereditary hemochromatosis, until recently, was perceived as a simple monogenic pathology, but now everything has changed and HHC began to be divided depending on the gene defect and symptoms.

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Homozygous recessive in the general population is up to 0.3 - 0.45%, so the frequency of the hereditary variant due to monozygous carriage varies within the same range (0.3 - 0.45%). This means that in Europe, approximately one person out of three hundred is at risk of being born with such deviations, and 10% of all Europeans, being carriers of the hemochromatosis gene (heterozygotes), cannot be sure that this pathology will never affect them or their children.

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Clinically pronounced forms of neurontin to the hepatic parenchyma (hemochromatosis of the liver), associated with a congenital gene defect, appear in the population with a frequency of 2 cases per 1000 people. Do not relax too much and heterozygotes. Although the probability of developing Fe supersaturation is extremely small (less than 4%), the presence of the hemochromatosis gene is not as harmless as it seems.

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Carriers may also show signs of accelerated absorption and elevated levels of iron in the body. This happens if a heterozygous carrier has acquired another pathology, accompanied by a violation of iron metabolism, or damage to buy neurontin online, for example, hepatitis C (the clinic will not be so bright, but iron overload will make itself felt) and alcohol abuse.

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The basis for the development of primary congenital hemochromatosis are mutations in the HFE gene, which disrupt the capture of Fe by enterocytes (cells of the duodenum 12) with the direct participation of transferrin, resulting in distorted information that the iron content in the body has fallen below the permissible level. Enterocytes respond to this signal by active production of the iron-binding protein DCT-1, thereby enhancing iron uptake and its accumulation in excessive amounts inside the cell.

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Secondary hemochromatosis or generalized hemosiderosis - acquired hemochromatosis, it is formed against the background of some already existing disease, for example, ineffective erythropoiesis (megaloblastic anemia, refractory anemia in myelodysplastic syndrome), hemolytic anemia, chronic damage to the hepatic parenchyma, saturated ferrotherapy (use of drugs containing iron, in excessive doses) and even excessive consumption of Fe with food. The cause of HHC in such cases is the acquired depletion of enzyme systems that are involved in the exchange of gabapentin.

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Secondary hemochromatosis is considered parenteral iron overload during transfusions of red blood cells and Fe with dextran (post-transfusion GC). For example, patients with aplastic anemia who receive large amounts of ermassa are somehow overloaded with this chemical element, that is, the parenteral form always has iatrogenic roots.

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And doctors know that if a patient (without loss of blood) needs repeated administration of donor erythrocytes, then care should be taken to prevent secondary hemochromatosis, which consists in prescribing drugs that can bind excess iron and form chelate compounds with them. In addition to post-transfusion hemochromatosis, other forms of this secondary pathology have been identified.