Liver fibrosis
Contents:
Description:
Fibrosis of a liver is a gradual substitution of cells of a liver connecting fabric. At fibrosis of a cell of a liver are not recovered. The disease develops rather slowly, and passes the first five years asymptomatically.
Liver Fibrosis symptoms:
Symptoms of fibrosis of a liver are shown in 5-6 years after an onset of the illness:
- bleeding from gullet veins
- expansion of a spleen
- increase in the sizes of a liver
- thrombocytopenia.
Inborn fibrosis of a liver is observed preferential at children of post-natal and early age. The reason is not established. At the same time significant increase in a liver, sometimes stony density is noted. Esophageal and gastric bleedings owing to a rupture of varicose veins of a gullet which are observed more often at children are characteristic 3 years are more senior and can be a cause of death.
Fibrosis of a liver begins in a liver and in system of a portal vein, and develop in the following sequence:
1. Considerably the spleen increases
2. There is varicosity of veins of a gullet and bleeding from them
3. There is anemia, a leukopenia, thrombocytopenia.
At the same time, symptoms of cirrhosis are absent. However, the bounded function of a liver arising at fibrosis can promote developing of cirrhosis, liver failure and portal hypertensia that often demands transplantation of a liver.
Liver Fibrosis reasons:
Today classify several groups of origins of fibroses of a liver. It is heredity and inborn fibrosis, long alcoholic, drug and toxic poisoning of an organism, viral chronic hepatitis, obesity and diabetes, long deficit of some vitamins and mineral substances.
Treatment of Fibrosis of a liver:
At the disposal of the clinical physician very few effective ways of treatment of fibrosis of a liver. Now correction of a hepatic fibrogenesis can be carried out in several directions:
* treatment of a basic disease for the purpose of elimination of a causative factor of fibrosis;
* "activation braking" of PZK;
* reduction of activity of inflammatory process in a liver;
* activation of mechanisms of a fibroliz for destruction of excess of proteins of VKM.
Elimination of an etiological factor of pathological process serves in a liver to an important component of the therapy directed to reduction of processes of fibrosing. The refusal of alcohol intake, narcotic and hepatotropic drugs, elimination of excess of iron, copper, a decompression at obstruction of bilious channels, etc. belong to the specified medical actions causal treatment of virus defeats (an interferona, inductors of interferon, a himiopreparata).
PZK mean blocking of processes of transformation of star-shaped cells in active miofibroblasta which triggers can be an oxidatic stress, endointoxication, disturbance of lipidic exchange by "braking" of activation and др for the purpose of braking of activation of star-shaped cells antioxidants (and - tocopherol, vitamin C) can be used under the influence of which in a liver the glutathione which is a part of the glutationperokidaza destroying active forms of oxygen collects. Besides, can be used phosphotidylsincaline, холестирамин, antibacterial drugs and др
For the purpose of braking of activation of PZK drugs with antiinflammatory activity - glucocorticoids, interferona (and, P), D-Penicillaminum, etc. can be used.
Activation of mechanisms of a fibroliz can be carried out by strengthening of degradation of proteins of BKM, K to the substances having similar effect alkaloids like cytochalasin B or colchicine, group E prostaglandins belong. Toxicity of these alkaloids interferes with their broad use in clinical practice. It is necessary to remember that exogenous PGE quickly collapse in an organism, without having managed to influence connecting tissue of a liver. Now researches on use as medicinal substances of cytokines and antagonists of their receptors are conducted. At fibrosis of a liver of a cell of Ito have hypersensitivity to growth cytokines (TGF-bb). However their sensitivity decreases under the influence of the factors stimulating regeneration of hepatocytes that confirms prospects of use of a growth factor in the prevention of development of fibrosing.
