Cirrhosis-Hepatic Encephalopathy (Hepatic Dysfunction)

Siroz – Hepatik Ensefalopati (Karaciğer Fonksiyon Bozukluğu)

What is Hepatic Encephalopathy & How is it Treated with Stem Cell?

Hepatic encephalopathy is a complex neuropsychiatric syndrome seen in patients with significant hepatic dysfunction. Significant liver dysfunction includes acute liver failure, large portosystemic shunts and cirrhosis. Hepatic encephalopathy results from inadequate liver function and/or impaired liver perfusion leading to the accumulation of hypothetical intestinal neuroactive toxins.

The diagnosis of hepatic encephalopathy is clinical and the diagnosis is based on the definition of definite liver dysfunction, ruling out other causes of encephalopathy and grading of the severity of hepatic encephalopathy. The care of hepatic encephalopathy requires a simultaneous approach in four groups:

  1. Supportive measures for the patient with a change in mental status,
  2. Ruling out other causes of encephalopathy,
  3. Identification and treatment of facilitating factors,
  4. Administration of empirical treatment.

Hepatic encephalopathy can be studied in three groups depending on the underlying mechanism:

  1. Acute Liver Failure Associated Hepatic Encephalopathy; ALFA-HE: It is rarely seen with a sudden aggravation in chronic liver disease, however, it usually accompanies pure acute liver failure. It expresses hepatic encephalopathy that has developed due to hepatocellular insufficiency without portosystemic shunt.
  2. Encephalopathy associated with major portosystemic shunt without a liver disease: There is hepatic encephalopathy without definable liver dysfunction. In such patients, encephalopathy is often indistinct. Liver biopsy specimens are typically either normal or have very mild histopathological changes.
  3. Encephalopathy in patients with chronic liver disease or cirrhosis: They usually have cirrhosis – hence chronic liver dysfunction – as well as well-developed portosystemic collateral circulation. This group is the most common group. Two abnormalities leading to hepatic encephalopathy in people with chronic liver disease are hepatic insufficiency and circulatory ‘bypass’ of the liver.

The decline in hepatic function is probably the main factor; circulatory bypass works as a secondary and facilitator. This view is supported by the low incidence of hepatic encephalopathy in people with no apparent liver disease, although with portosystemic shunts. Type C Hepatic encephalopathy includes both Type A and Type B hepatocellular insufficiency and portosystemic shunt elements as well as presentation forms including those of Type A and Type B.

A patient with type C hepatic encephalopathy may present with the following:

  1. Acute hepatic encephalopathy: This may come up with a single episode as well as with multiple episodes separated from each other by intervals in which the mental state is normal.
  2. Chronic hepatic encephalopathy: In this condition, changes in the mental state have been added to the underlying abnormality. The patient returns to an abnormal baseline at best between the episodes; there may be cases where the patient cannot even return to an abnormal baseline among some of the epizodes.
  3. Sub-clinic hepatic encephalopathy: The mental state is never completely impaired, however, there are subclinical changes that can be demonstrated by neuropsychiatric tests.

Stem Cell Treatment Method

Stem cells have the ability to turn into liver cells when they touch damaged liver cells so they are used in the treatment of liver disorders. In this way, they may slow the progression of the disease, completely stop it and make it regress. The success rate of the treatment is proportional to the patient’s age, the duration of the disease and the patient’s condition. If the disease has severely progressed, treatment may need to be applied more than once. However, since there are problems of blood clotting in the later stages of cirrhosis; it may not be possible to perform liposuction and other techniques while obtaining stem cells from a patient. Therefore, in the case of liver failure; if possible, stem cells should be provided at the beginning of the disease and also some of them should be stored. In the treatment, ultrasound-guided injection of stem cells directly into the patient’s vessel leading to the liver. This disease can be treated in our GenCell stem cell therapy clinic in Kiev, Ukraine.

Method of administration:

The number of cells to be administered is determined according to the age and weight of the patient. Treatment is carried out using mesenchymal stem cells (derived from the patient’s own adipose tissue or bone marrow) or fetal stem cells. The treatment of the patient is decided according to the condition of the patient. It can be performed in 3 sessions 45 days apart or in 3 consecutive days. They can be administered intravenously (by vascular access) and a certain amount of injection to a vessel leading to the liver is performed. Fetal stem cells are generally preferred as fat removal is not possible in patients with severe cirrhosis.

The treatment protocol is completely adjusted according to the patient’s condition and a different protocol may be applied for each patient. 

Success Rate in Treatment

In the case of cirrhosis onset and the early diagnosis of hepatic failure, over 95% success rate is achieved, and this rate decreases to 20% when the disease progresses.

Scientific Studies:

  1. Tsuji, M., & Shintaku, H. (2018). Clinical Trial of Autologous Cord Blood Cell Therapy for Neonatal Hypoxic Ischemic Encephalopathy (HIE). In Cell Therapy for Perinatal Brain Injury(pp. 1-15). Springer, Singapore.
  2. Cotten, C. M., Murtha, A. P., Goldberg, R. N., Grotegut, C. A., Smith, P. B., Goldstein, R. F., … & Rattray, B. (2014). Feasibility of autologous cord blood cells for infants with hypoxic-ischemic encephalopathy. The Journal of pediatrics164(5), 973-979.
  3. Nabetani, M., Shintaku, H., & Hamazaki, T. (2018). Future perspectives of cell therapy for neonatal hypoxic–ischemic encephalopathy. Pediatric research83(1-2), 356.

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