В настоящее время в терапии цирроза печени разрабатывается несколько направлений, в
том числе направленные на устранение причинного фактора, коррекцию иммуновоспалительных изменений, воздействие на процесс апоптоза и др. Одним из перспективных методов управления обратным развитием фиброзных изменений ткани печени является применение обогащенной тромбоцитами плазмы (ОТП). В серии экспериментов, выполненных нами на крысах,
было продемонстрировано значительное улучшение морфофункционального состояния печени у животных с индуцированным фиброзом. Однако возможность регресса не всегда реализуется при значительных нарушениях архитектоники органа вследствие отсутствия адекватной
васкуляризации. Значительный потенциал в ангиогенном направлении терапии цирроза имеют
системное использование цитокинов, клеточная терапия с применением аутологичных ранних
гемопоэтических предшественников и использование ОТП.
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 CСl
4-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.
