However it is just a speculation and not our focus prognostic value in HBVACLF

In brief, the aims of the present study were to determine the serum sphingolipid composition in a population of patients with chronic HBV infection, paying special attention to differential sphingolipid metabolites among disease stages, and to further explore novel prognostic markers in HBV-ACLF. AbMole BioScience kinase inhibitors sphingolipids are extensively involved HBV infection pathways and have a significant influence on the life of hepatocytes. This study was designed to examine changes in the serum sphingolipidome of patients with chronic HBV infection, and is the first to demonstrate the utility of serum sphingolipidomic profiling to identify novel prognostic biomarkers of 3-month mortality in patients with HBV-ACLF. Because perturbations in the levels of certain compounds may initiate a cascade of changes in the levels of multiple lipids, which is called the “ripple effect”, metabolic homeostasis of sphingolipids is key for maintaining the physical health of an organism. To our knowledge, this is the first study to perform serum sphingolipidomic profiling in patients with chronic HBV infection. In the training cohort, multivariate analysis identified potential biomarkers that could discriminate CHB patients from CTRL subjects and HBV-ACLF patients from CHB patients. In the validation cohort, however, all of the potential biomarkers that discriminated CHB patients from HBV-ACLF patients were confirmed, whereas those that potentially differentiated CTRL subjects from CHB patients were screened out. These results suggested that the ripple effect is more significant in patients showing disease progression. These results allowed us to speculate on the role played by sphingolipids in disease progression. Because the liver plays an essential role in the metabolism of sphingolipids, it is not surprising that liver diseases are associated with major changes in serum sphingolipid concentrations. Progression of HBV-ACLF ultimately leads to increased hepatocyte apoptosis and/or necrosis, which is a hallmark of liver failure. Cellular debris released by necrotic or apoptotic hepatocytes into the circulation may also cause substantial changes in serum sphingolipid composition. Thus, the use of cell death-related sphingolipids to indicate HBVACLF status might represent a novel prognostic marker that can be used to better identify patients that require a liver transplant. On the other hand, sphingolipids are extensively involved in the function of the immune system. Increasing evidence suggests that non-HBV-specific inflammation of the liver is likely responsible for the hepatic pathology observed in patients with CHB. Perhaps the most interesting finding from the present study is that decreasing dhCer concentrations can serve as an independent predictor of 3-month mortality in patients with HBVACLF. The mechanism underlying the association between serum dhCer concentrations and death in ACLF patients is unclear. However, inflammation in an HBV-infected liver is mediated by cytokines, which are regulated by sphingolipids. The specific cause of this association requires further study. On the other hand, liver failure of other etiologies such as alcohol, acetaminophen, drug-induced hepatitis and autoimmune hepatitis and shock etc. may also have similar associations with serum sphingolipidome.

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