Europeans consume ≈ 1 - 20 mg of Fe, which comes (in the form of furosemide) with food. In 24 hours, 1-2 mg of the element enters the body through the gastrointestinal tract and the same amount leaves it. In patients who receive less iron, have hereditary hemochromatosis, or suffer from a pathology that occurs with impaired erythropoiesis, the amount of absorbed Fe increases by ≈ 3 times. The absorption process is very active and it is carried out in the small intestine (upper section).
However, all the processes described above go exactly like this if everything is in order in the body with the exchange of iron. But with hemochromatosis, there is an excessive accumulation of iron, and it ceases to fit into the ferritin form. Iron-containing protein molecules begin to break down, forming hemosiderin, the content of which naturally increases during GC, so hemochromatosis is often called hemosiderosis.
It is hard for the transport protein to overload with iron, because it is forced to take not 1/3 of the iron, but more, reaching full saturation. However, this does not helpdies, since iron still remains and then it begins to move independently (without transferrin) in the form of various compounds with low molecular weight chelators, that is, traps for Fe.
This shape allows this chemical element to easily pass into the cell, regardless of whether it is needed there or not. A cell saturated with iron cannot create obstacles for the entry of a new portion of the metal, which naturally becomes superfluous.
Excessive accumulation of iron can be suspected based on complaints and clinical symptoms. The fact that a male person may develop hereditary hemochromatosis can be judged by such signs as liver enlargement, asthenia, arthralgia, changes in the activity of transferases (AlT, AST), however, their indicators very rarely have significant deviations from the norm when manifest variants of HCH, even if all the symptoms of liver cirrhosis are present.
At the first stage of the diagnostic search, the doctor sends the patient for an ultrasound examination (ultrasound) and magnetic resonance imaging (MRI), in parallel prescribes laboratory tests. And since all the tests performed indicate the development of HC, then a liver biopsy will be useful, which can finally dispel doubts about the diagnosis. At the initial stage, in young patients, excessive accumulation of Fe will be noticeable only in the cells of the hepatic parenchyma (hepatocytes) and the periportal region. In elderly people, deposits are also noticeable in hepatocytes, and in Kupffer cells, and in cells of the bile ducts. Cirrhosis of the liver with HC is small-nodular (micronodular).
Taking as a basis changes in the liver and detecting the growth of connective tissue (cirrhosis), differential diagnosis should be carried out. Again, a histological examination (biopsy) will help in this, because the replacement of the hepatic parenchyma with connective tissue in case of hepatitis or alcohol abuse will have slightly different signs.
Hepatocellular carcinoma against the background of hemochromatosis can be suspected if the patient's condition has noticeably worsened recently, the liver has greatly increased, and the level of the tumor marker, α-fetoprotein, has increased. Treatment begins with a revision of the diet. All foods that contain iron should be excluded from the diet.
Of the medications, deferoxamine is considered the main one, which forms a complex with Fe and helps this element leave the body. Effective in GC bloodletting, they reduce the size of the liver and spleen, pigmentation, improve liver enzymes, and in some cases facilitate the treatment of diabetes. Often, extracorporeal treatment (hemosorption, plasmapheresis) is carried out simultaneously, which also helps to remove excess iron from the body.
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