Abstract
Liver failure is characterized by rapid progression and high mortality. Excessive systemic inflammation is considered as the trigger of liver failure. Glucocorticoids (GCs) can rapidly suppress excessive inflammatory reactions and immune response. GCs have been applied in the treatment of liver failure since the 1970s. However, until now, the use of GCs in the treatment of liver failure has been somewhat unclear and controversial. New research regarding the molecular mechanisms of GCs may explain the controversial actions of GCs in liver failure. More results should be confirmed in a larger randomized clinical trial; this can aid the discovery of better definitions in terms of treatment schedules according to different clinical settings. Meanwhile, the timing and dosing of GCs in the treatment of liver failure should also be explored.
Highlights
Liver failure is a life-threatening clinical syndrome with heterogeneous etiology that can cause serious disorders, such as coagulation disorders, icteria, hepatic encephalopathy (HE), and ascites [1, 2]
As a “double-edged sword,” the timing, dosage, and clinical indication of GC therapy are the key points to better definitions in terms of treatment schedules according to different clinical settings in the future
GC-mediated activation of NLRP3, TLR2, and P2Y2R and the potentiation of LIF and tumor necrosis factor-α (TNF-α) regulated pro-inflammatory genes [58, 62]. All these results provide a potential explanation for the controversial actions of GC therapy in liver failure
Summary
Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology. Excessive systemic inflammation is considered as the trigger of liver failure. Glucocorticoids (GCs) can rapidly suppress excessive inflammatory reactions and immune response. GCs have been applied in the treatment of liver failure since the 1970s. Until now, the use of GCs in the treatment of liver failure has been somewhat unclear and controversial. New research regarding the molecular mechanisms of GCs may explain the controversial actions of GCs in liver failure. More results should be confirmed in a larger randomized clinical trial; this can aid the discovery of better definitions in terms of treatment schedules according to different clinical settings. The timing and dosing of GCs in the treatment of liver failure should be explored
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