Mesenchymal stem cell (MSC) transplantation may be an alternative to liver transplantation for patients with end-stage liver disease. A 24-year-old patient with Hepatic Encephalopathy due to alcoholic liver cirrhosis underwent UCMSC transplantation because there were no donors available for liver transplants involving adult deceased and living individuals. The patient was given allogeneic Umbilical cord-derived MSCs, which were then cultured following accepted practices. Subsequently,
the UCMSCs were infused through the intravenous route 3 times at the interval of 30 days. Serum bilirubin, globulin, and ammonia levels were improved after the infusion and the morphology of the liver and spleen had also improved.
One impact of neurotoxins that enter the bloodstream and travel to the brain is hepatic encephalopathy (HE) [1]. Hepatic encephalopathy (HE) can be caused by several variables, including inlammation, toxins, necrotic liver, blood ammonia levels, and systemic inlammatory response syndrome (SIRS) [2]. A small amount of ammonia remains in the hepatic vessels under normal circumstances because the liver effectively excretes the ammonia produced by the body through the urea cycle and glutamine synthesis. The liver’s capacity to expel ammonia from the hepatic veins is lost in
Acute Liver Failure, and the hepatic vein’s ammonia content rises. Through glutamine synthesis, the muscles and brain start the detoxiication process from ammonia. As a result, these two tissues are regarded as glutamine-releasing and ammonia-scavenging organs [3].
Hyperammonemia is often associated with hepatic encephalopathy (HE) and cirrhosis (LC). Decreased detoxiication capacity of the liver caused hyperammonemia [4]. Infections with urease-producing bacteria, high- protein diets, malignancies, sarcopenia, renal failure, gastrointestinal bleeding, gastric bypass, and organ transplantation can all cause high ammonia levels and noncirrhotic encephalopathy [5,6].
Many different organs, including the liver, brain, kidneys, muscles, and gastrointestinal tract, are involved in ammonia metabolism. Therefore, malnourishment, persistent multiorgan dysfunction, and low non-cerebral function reserves may be indicated by hyperammonemia [4]. Several neoteric investigations have demonstrated the link between hyperammonemia and unfavorable outcomes in people with clinically stable severe chronic liver disease or cirrhosis.
These outcomes include hospitalization, liver-related repercussions (LRCs), progression to LC, and mortality [6,7]. Previous studies found that ammonia was directly associated with LC-grade, organ failure such as the liver, kidney, and brain, and is an independent risk factor for 28-day death [7,8]. These indings provided evidence that ammonia levels are not only clinically relevant in assessing HE severity but may also be a prognostic biomarker for identifying patients at high risk of poor outcomes.
Due to their low concentration of class I MHC molecules and lack of expression of class II major histocompatibility complex (MHC) antigens, MSCs are almost immune-privileged. Furthermore, MSCs lack the co-stimulatory molecules—such as CD80, CD86, and CD40—that are necessary for immune recognition, which is the foundation for their allogeneic use [9]. As a result, MSCs from both autologous and allogeneic donors have been used in clinical settings.
This study aimed to evaluate the safety and eventual eficacy of umbilical cord- derived mesenchymal stem cell transfusion in patients with hepatic encephalopathy due to advanced liver cirrhosis.
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