Gipergomotsisteinemiya
Contents:
Description:
Gipergomotsisteinemiya - multifactor process with involvement of genetic and not genetic mechanisms.
Gipergomotsisteinemiya's symptoms:
Gomotsistein is formed of methionine by transmethylene reactions. Enzymes цистотионин - beta синтетаза and a metilentetragidrofolatreduktaz (MTHFR) in the presence of cofactors - a pyridoxine and cyanocobalamin and as substrate, folic acid serve key in a metabolic way of transformation of a gomotsistein. As a result of a mutation of genes activity of these enzymes decreases and broken a metabolic way of transformation of a gomotsistein, and its content in plasma increases.
Decrease in food of maintenance of a pyridoxine, cyanocobalamin and folic acid causes a gipergomotsisteinemiya not only in homozygous carriers, but also people without mutation of a gene have MTHFR.
The normal maintenance of a gomotsistein is equal in plasma to 5-16 µmol/l. Increase in level of a gomotsistein to 100 µmol/l is followed by a gomotsisteinuriya.
Gipergomotsisteinemiya and defects of development of the central nervous system of an embryo are well studied and explain as well as why treatment by folic acid allows to reduce their emergence. Gipergomotsisteinemiya is connected with such obstetric pathology as usual early losses of pregnancy, the early beginning of a gestosis, placental detachment, a delay of pre-natal development. At the same time I. Martinelli and соавт. (2000) did not find communication of late death of a fruit with a gipergomotsisteinemiya.
Believe that the gipergomotsisteinemiya can cause damage to an endothelium because of disturbance of redoxreactions, increases in level of free radicals and decrease in level of nitrogen oxide due to influence on activation of coagulative factors (a fabric factor and a factor of XII) and/or blood coagulation inhibitors.
Gipergomotsisteinemiya's reasons:
The reasons of a gipergomotsisteinemiya can be hereditary and acquired. Hereditary factors can be divided into deficit of enzymes and deficit of transport.
Gipergomotsisteinemiya's treatment:
Saturation by folic acid (not less than 4 mg/days), cyanocobalamin and a pyridoxine is enough.
