However, this minimal period of abstinence is sometimes waived if the patient is deemed too ill to survive beyond 6 months without a liver transplant. One study showed that recovery in decompensated alcoholic cirrhosis by alcohol abstinence can be predicted within 3 months of abstinence by the monitoring of clinical signs via the Child-Pugh scoring system serum bilirubin, albumin, international normalized ratio, ascites, and hepatic encephalopathy [ 50 ].
This study by Veldt et al. Yet, abstinence less than 12 months was recently identified as a significant risk factor for relapse in a large retrospective study of OLT recipients [ 50 ]. Finally, an increasing concern of late is the high risk for de novo malignancies in long-term survivors transplanted for ALD. Although posttransplantation lymphoproliferative disorder and nonmelanoma skin cancer remain the most common malignancies after liver transplantation, the incidence of esophageal cancer is significantly increased in patients with alcohol as the etiology of end-stage liver disease.
Duvoux et al. They also detected squamous cell carcinoma of the oropharynx or esophagus only in recipients transplanted for ALD. Risk factors undoubtedly include the cumulative effects of alcohol and, in most cases, smoking with posttransplant immunosuppression. Thus, regular ear, nose, and throat examinations appear justified in patients transplanted for ALD.
This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors.
Read the winning articles. Journal overview. Special Issues. Academic Editor: Deepak Amarapurkar. Received 22 Feb Accepted 12 May Published 12 Jul Abstract Alcoholic liver disease ALD is a spectrum ranging from simple hepatic steatosis to alcoholic hepatitis and cirrhosis. Introduction Alcohol is a major risk factor for chronic disease burden all over the world.
Discriminant Function The Maddrey discriminant function DF score remains the most commonly used predictive model and was developed to facilitate the assessment of response in a clinical trial of corticosteroids in patients with alcoholic hepatitis [ 6 ].
Lille Model The Lille model incorporates age, renal insufficiency, albumin, PT, bilirubin, and the evolution of bilirubin on day 7 to predict 6-month mortality in patients with severe alcoholic hepatitis who have received corticosteroid therapy [ 12 ]. Treatment of Alcoholic Liver Disease 3. General Management One of the first therapeutic goals of patient management in patients with ALD is to induce alcohol withdrawal.
Abstinence Abstinence is the cornerstone of therapy in the management of ALD. Nutrition Patients with ALD are malnourished for a number of reasons, including malabsorption, the induction of a catabolic state, and the replacement of calories with alcohol. Glucocorticoids Glucocorticoids are the most intensely studied and yet most hotly debated treatment for acute alcoholic hepatitis. Antitumor Necrosis Factor Alpha Treatment 3.
Etanercept A small, uncontrolled study evaluated the use of etanercept in 13 patients with moderate to severe alcoholic hepatitis. Antioxidant Cocktails Antioxidants have been tried in alcoholic hepatitis as oxidative stress is a key factor in its pathogenesis. S-Adenosyl Methionine S -Adenosyl methionine SAMe is a precursor of glutathione that theoretically might be protective in alcohol-induced liver injury.
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Naveau, S. Chollet-Martin, S. Menon, L. Stadheim, P. Kamath et al. Boetticher, C. Peine, P. Kwo et al. Phillips, H. Curtis, B. Portmann, N. There exist significant differences in the etiology of liver diseases between the East and West. HBV-activated immune response and immune pathology caused by liver cell inflammation and necrosis are the initiated factors of liver failure. Although a large number of studies reported that GC therapy is effective in liver failure 22 , 23 , GC therapy is only recommended for the treatment of early stages of liver failure, and there is little evidence to support its effectiveness.
However, with the arrival of nucleoside analogs NAs , more and more guidelines have recommended NAs to be used in patients with acute exacerbation of chronic HBV infection. The early combined use of NAs and GCs could be a good option to reverse the potential deterioration in patients with HBV-related liver failure.
A recent study reported that early combination therapy with corticosteroid and NAs induces rapid resolution of inflammation in ALF due to transient HBV infection However, Huang et al. The clinical stage of HBV-ACLF can be divided into four stages: early stage of ascending period, late stage of ascending period, platform period, and recovery period.
Immune injury is the major event in the early stage of ascending period. The pathogenesis in the late stage of ascending period is involved in ischemia, immune injury, and hypoxia injury During the platform period, body conditions achieve an immunosuppression state. Endotoxemia is an important factor during the initiation of liver injury. The sooner systemic inflammatory response syndromes SIRS occurred, the higher the mortality rate would be. GCs can inhibit inflammation, stabilize the liver cell membrane, and prevent further necrosis of liver cells Therefore, early application of GC therapy can inhibit immune responses.
The inhibition of systemic inflammation delays rapid progression and improves the survival rate of patients with ACLF. Zhao et al. The optimal time of intervention with GCs was within 14 days of the onset of symptoms. We consider that the efficacy of GC treatment is primarily associated with the timing of GC administration.
Meanwhile, the first-time physician, age, basic condition, and complications should also be considered for GC administration. However, until now, there has been a lack of accurate quantitative indicators for GC therapy. Therefore, it is particularly important for doctors to accumulate more and more clinical experience. Today, the ideal choices regarding GC type and does remains inconclusive. Kotoh et al. As a result, 13 patients were cured, 2 patients died, and 2 patients underwent LT without serious complications.
Fujiwara et al. It was found that the survival rate and liver regeneration in the GC-treated group showed a slim advantage, but there was no statistical difference, while patients with HBV infection and a poor basic condition had an unfavorable prognosis. When the efficacy of GCs therapy cannot be determined in clinic, it is required that possible side effects of GCs are kept within a controllable range based on the principle of safety.
GCs can significantly inhibit the presence of phagocytic cells to the antigen, promote the destruction and disintegration of lymphocytes, and develop the removal of lymphocytes from blood vessels so as to reduce the number of lymphocytes in circulation Small doses of GCs mainly inhibit cellular immunity, while high doses of GCs can suppress humoral immune function by inhibiting B cells and antibody production The number of liver surface glucocorticoid receptors GRs may be reduced in liver failure If greater doses of GCs are given, the GCs cannot play a role during the presence of receptor saturation, but may increase the incidence of side effects of GCs.
Therefore, patients with liver failure, especially those with cirrhosis, are not recommended to use high-dose GCs. Although GCs can increase the incidence of infection and upper gastrointestinal bleeding, as well as other complications, the side effects of GCs are controllable. Therefore, it is essential to screen and monitor the side effects during GCs therapy in patients with liver failure. The chemical essence of endotoxin is lipopolysaccharide [LPS, recognized by the pattern-recognition receptor toll-like receptor 4 TLR4 ] The liver cells are injured by delayed type hypersensitivity, oxidative stress, and apoptosis.
If the immune response cannot be suspended in time, it would lead to a vicious cycle, resulting in significant liver cell necrosis, apoptosis, and liver failure 38 — Heat shock proteins HSPs are well-known as protective proteins that make cells resistant to stress-induced cell damage.
As the most commonly used anti-inflammatory and immunosuppressive agents, GCs can inhibit macrophage phagocytosis and antigen treatment and suppress the production of inflammatory cytokines. Therefore, GCs have the theoretical basis for the treatment of liver failure. Aside from rapid non-genomic effects, GCs exert genomic effects by binding to the glucocorticoid receptor GR , a member of the nuclear receptor family of transcription factors Upon ligand binding, the GR translocates to the nucleus, where it acts either as a monomeric protein that affects transcription with other transcription factors or as a homodimeric transcription factor, which binds glucocorticoid response elements GREs in promoter regions of GC-inducible genes Some reports have clearly showed that GR dimer-dependent transactivation is essential in the anti-inflammatory activities of GR 47 — Emerging studies have shown that GCs have a two-way regulation for inflammatory and immune responses The basal state of the immune system and the type of exposure to GCs are significant factors influencing the effects of GCs For instance, while chronic exposure to GCs seems to be immunosuppressive, acute exposure increases the peripheral immune response Hermoso et al.
Besides, some studies indicated that GCs can work synergistically with pro-inflammatory mediators to enhance the defense mechanisms to ensure removal and clearance of pathogens in the hepatic acute-phase response 58 , All these results provide a potential explanation for the controversial actions of GC therapy in liver failure. More studies are required to characterize the liver-specific effects of the anti- and pro- inflammatory roles of GR signaling.
It is accepted that a pro-inflammatory environment can negatively affect GR sensitivity 64 , The mechanisms contributing to reduced GC responsiveness are heterogeneous as they involve various cytokines and cell types. The mechanisms of GCR are still unclear. As GCR occurs in many inflammatory diseases, it is widely considered that GCR is a heterogeneous phenomenon with multiple underlying mechanisms Some of these involve problems with the GR protein itself, but many others are independent from GR and involved in mutations in GR-induced genes and problems with chaperones or cofactors In addition to the non-genomic and genomic actions of GCs, GR signaling also relies on the existence of post-translational modifications PTMs and multiple receptor isoforms.
Sepsis is a common complication of ACLF, which is an acute systemic inflammatory disease However, GCs are hardly useful in sepsis Thus, sepsis is considered a GCR disease. GCR is an essential problem in sepsis and leads to: lack of transport and removal of bile acids in the liver, resulting in cholestasis; increased production and reduced removal of L-lactate, resulting in lactic acidosis; GCs having no anti-inflammatory effects.
Our previous study proposed that the diagnostic criteria of sepsis are not suitable for patients in HBV-ACLF with sepsis, because patients with underlying chronic liver disease and cirrhosis may have deranged clinical parameters Therefore, it is essential to establish compatible diagnostic criteria for sepsis in patients with ACLF. We argue that when sepsis occurs during the process of liver failure GCs are not recommended for patients. The idea of using GCs during acute liver failure has circulated for so many years, but, so far, no meaningful work has provided conclusive evidence of its therapeutic efficacy, except in the field of autoimmune etiology.
More results should be confirmed using a larger randomized clinical trial to in order to arrive at better definitions in terms of treatment schedules according to different clinical settings. Meanwhile, due to the complicated pathophysiology of liver failure, the exploration of immunological manifestations with different etiology and different clinical staging of patients with liver failure is needed urgently. This is a prerequisite for the feasibility and safety of GC applications.
With an in-depth study, we can find the accurate timing, dosage, and clinical indicators of GC therapy for the clinical management of liver failure, so that clinicians can make timely treatment options so as to obtain the greatest benefits for patients. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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European Association for the Study of the Liver. EASL clinical practice guidelines: drug-induced liver injury. Acute liver failure induced by idiosyncratic reaction to drugs: challenges in diagnosis and therapy. Hepatotoxicity associated with antiepileptic drugs. Acta Neurol Scand. Efficacy of short-term dexamethasone therapy in acute-on-chronic pre-liver failure.
Hepatol Res. Arterial steroid injection therapy can inhibit the progression of severe acute hepatic failure toward fulminant liver failure. Early combination therapy with corticosteroid and nucleoside analogue induces rapid resolution of inflammation in acute liver failure due to transient hepatitis B virus infection. Intern Med. Dynamic changes of clinical features that predict the prognosis of acute-on-chronic hepatitis B liver failure: a retrospective cohort study.
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