The fibrosis of the liver is partly reversed. The main directions of anti-fibrotic therapy are aimed to eliminate the cause, correction of immune-inflammatory changes, etc.
One of the promising methods for managing the reverse development of liver fibrosis is the local application of platelet-rich-plasma (PRP). In a series of our studies on rats, significant improvement of the morpho-functional status of the liver in animals with CСl4-induced chronic hepatitis-fibrosis after the introduction of PRP was demonstrated. The effect of PRP is explained both by stimulation of processes of angiogenesis and anti-inflammatory action. It was shown platelets induced the migration and adhesion of progenitor cells to sites that were subsequently modeled as neoangiogenic, and this fact could explain the differentiation of multipotent cells in the precursors of endothelial cells.
The most patients suffer from the clinical manifestations of cholestatic syndrome and portal hypertension. So, the question is to change the antifibrose paradigm for angiogenic in the case of already developed cirrhosis of the liver, that is, primarily to influence portal hypertension in order to mitigate its manifestations, seems to be relevant. Mechanically this is reminiscent of invasive transujugular porto-caval shunting, with its main negative effect of hepatic encephalopathy due to the “evasion” of ammonia from incorporation into non-toxic urea, and aromatic amino acids — from catabolism in hepatocytes.
Perspective directions in this respect may be: systemic use of cytokines (recombinant erythropoietin, granulocyte colony stimulating factor, interleukin-2); the use of autologous CD133+ cells (early hematopoietic precursors with endothelial progenitor activity) intraparally or in the hepatic artery; the use of the PRP. It is expected that the use of these therapeutic agents will lead to active angiogenesis in the areas of necrosis and fibrotic transformation, and, along with the growth vessels, the processes of differentiation of stem and progenitor cells in endothelial hepatocyte precursors with reproduction of normal cytoarchitectonics of the liver will occur along with the growth vessels.