Alcoholic Hepatitis


Article Author:
Niraj Shah


Article Editor:
Savio John


Editors In Chief:
Hela KCHIR
Joseph Lee
Savio John


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
7/31/2019 12:52:29 AM

Introduction

Excessive alcohol consumption could result in alcoholic, fatty liver disease or steatosis, alcoholic hepatitis (AH), and eventually cirrhosis. Alcoholic hepatitis is a severe syndrome of alcoholic liver disease (ALD), characterized by rapid onset of jaundice, malaise, tender hepatomegaly, and with subtle features of systemic inflammatory response. The recent worsening profile and trends of patients with AH related hospitalizations in the United States suggest its importance in the current realm of clinical practice with its subsequent management.[1][2][3][4]

Alcoholic hepatitis usually progresses to cirrhosis if drinking is continued. For those who discontinue alcohol, the hepatitis returns to normal within a few months but the cirrhosis that has already occurred does not reverse

Etiology

The National Institute on Alcohol Abuse and Alcoholism (NIAAA), Alcoholic Hepatitis Consortia defines AH to include the following:

  • The onset of jaundice within 60 days of heavy alcohol consumption (more than 50 g/day) for a minimum of 6 months
  • with serum bilirubin more than 3 mg/dL
  • elevated aspartate aminotransferase (AST) to 50 U/L to 400 U/L 
  • AST: ALT (alanine aminotransferase) ratio of more than 1.5, and
  • No other cause of acute hepatitis. 

While using the terminology alcoholic hepatitis, it is important to understand the difference between alcoholic steatohepatitis (ASH) and alcoholic hepatitis (AH). About 20% to 40% of those who drink alcohol in heavy amounts and have fatty liver eventually develop liver inflammation, which is known as ASH. ASH is a diagnosis based on liver histology, while AH is a clinical diagnosis. The typical features of ASH on liver biopsy are steatosis, hepatocyte ballooning, infiltration of neutrophils, Mallory-Denk hyaline inclusions and zone 3 perivenular injury with pericellular fibrosis or chicken-wire pattern of fibrosis. AH, on the other hand, is characterized by history of chronic heavy alcohol consumption until at least 3 to 4 weeks before the onset of jaundice, fever, tachycardia, tachypnea, hepatomegaly, leukocytosis with neutrophilia, and an AST: ALT elevation greater than 1.5:1 with the absolute value of AST/ALT typically never exceeding 500 U/L. AH can occur in patients with any stage of alcoholic liver disease.

Although the amount of alcohol ingested is the most important risk factor for the development of chronic liver disease, the progression to alcohol-induced chronic liver disease is neither dose-dependent nor is the correlation with the quantity of alcohol consumed and liver injury linear. Even shorter durations of alcohol abuse could lead to AH. A typical patient would be between 40 to 60 years of age with a history of more than 100 g/day of alcohol consumption for a decade, in whom you have ruled out other causes of acute hepatitis. Risk factors include a high BMI (body mass index), female sex, and having a genetic variant of patatin-like phospholipase domain-containing protein 3 (PNPLA3). Clinical jaundice is a poor prognostic factor. Acute binge drinking is likely the trigger for AH in patients with a history of chronic, heavy alcohol abuse.[5][6][7][8]

Epidemiology

Approximately two-thirds of adults in the United States drink alcohol, while 7.2% suffer from alcohol use disorder (AUD). Excessive alcohol intake is the third leading preventable cause of death in the United States. A 10-year survey, from 2001 through 2011 from 211 hospitals revealed a 0.08% to 0.09% admissions related to alcoholic hepatitis.

Pathophysiology

Alcohol undergoes an oxidative metabolic pathway in the hepatocytes, leading to a reduced ratio of the nicotinamide adenine dinucleotide (NAD) to NADH. This promotes lipogenesis by inhibiting oxidation of triglyceride and fatty acids.

Another known mechanism of alcohol-induced liver injury is the translocation of endotoxins in the form of lipopolysaccharides (LPS), from the intestines into the hepatocytes. In the hepatic Kupffer cells, the LPS binds to CD 14 and toll-like receptor 4 to release a barrage of reactive oxygen species (ROS). The ROS activates the release of cytokines such as tumor necrosis factor alpha (TNF alpha), interleukin-8, monocyte chemotactic protein 1 (MCP-1) and platelet-derived growth factor (PDGF), all of which leads to accumulation of neutrophils, macrophages and systemic clinical features of alcohol injury.

Recent studies indicate patients with specific intestinal dysbiosis been increasingly susceptible to alcoholic liver disease and AH.

Histopathology

A liver biopsy is generally not required, except in uncertain cases to delineate the etiology of the hepatic injury. The classical histological features include steatosis, hepatocellular ballooning representing steatohepatitis, cholestasis, chicken-wire fibrosis, cirrhosis in severely ill patients, neutrophilic and lymphocytic infiltration, and Mallory-Denk bodies.

History and Physical

The clinical presentation ranges from mild to severe. A mild clinical presentation would be a patient presenting with fever, right upper quadrant pain or discomfort and elevations in aminotransferases that normalizes with sobriety. While a severe presentation would include jaundice, ascites, hepatic encephalopathy, and coagulopathy.

The physical exam may reveal tachycardia, tachypnea, fever, enlarged liver and signs of portal hypertension. Spider angiomas, proximal muscle wasting, and gynecomastia are seen in severe cases of liver cirrhosis.

Evaluation

The diagnosis of AH is a clinical one with supporting laboratory findings of AH. All patients should have had an abdominal imaging study to exclude biliary obstruction and liver diseases such as hepatocellular carcinoma and liver abscess.

Liver tests may show elevation of AST, whereas ALT is usually in the normal range. This is the opposite of what is seen in other liver disorders. Carbohydrate-deficient transferrin is the most reliable marker of chronic alcoholism.

US is the first imaging test of choice to assess patients with alcoholic hepatitis; it can be used to exclude gallstones and other biliary tract disorders. A liver biopsy is not always required but is useful for excluding other disorders. A liver biopsy should be done with care as these patients may have coagulopathy and thrombocytopenia.

Several trials and models exist to determine the severity of alcoholic hepatitis, to ascertain which patients would likely benefit from a pharmacological approach. In 1977, the Maddrey discriminant factor (MDF), included serum total bilirubin and prothrombin time to segregate patients with a 28-day mortality risk of greater than 50%. These patients had an MDF greater than 32 and were deemed to benefit from steroid therapy. Subsequent scoring systems included the model for end-stage liver disease (MELD) score, the ABIC score (including the age, bilirubin, international normalized ratio and the creatinine score), the Glasgow AH score (including the age, bilirubin, international normalized ratio, blood urea nitrogen and the peripheral white blood count) and the Lille score. The Lille score obtains data from the beginning and end of the first week of steroid therapy to assess response and subsequent need for further steroid therapy. A histological scoring system for the prognosis of patients with alcoholic hepatitis has also been proposed. Various combinations of scoring systems have been studied to predict outcomes accurately, and the combination of the MELD and the Lille score is one. [9][10][11][12]

Recent studies indicate that CRP is a good marker of alcoholic hepatitis.

Treatment / Management

Abstinence along with adequate nutritional support remains the cornerstone of management of patients with AH. An addiction specialist could help individualize and enhance the support required for abstinence. About 10% to 20% of patients with AH are likely to progress to cirrhosis annually, and 10% of the individuals with AH have regression of liver injury with abstinence.

Patients with AH are subdivided into mild-moderate AH or severe AH. Patients with an MDF greater than 32, MELD score greater than 20, ABIC score category C, or a Glasgow AH score of 9 predicts higher mortality with a diagnosis of severe AH. Patients with severe AH with or without hepatic encephalopathy are considered candidates for a short course of prednisolone (40 mg/day for 28 days). Prednisolone is preferred to prednisone as it does not require metabolism in the liver for its therapeutic efficacy. For patients unable to take it orally, methylprednisolone, 32 mg intravenously daily, is an option. However, failure to respond to steroids within a week evident by a Lille score of greater than 0.45 indicates lack of response to steroids which should be discontinued, thereafter. For patients with a Lille score of less than 0.45 (Lille responders), prednisolone should be continued for another three weeks. Glucocorticoids alter the expression of anti-inflammatory genes, thus promoting its anti-inflammatory role. Contraindications to steroid use include any active gastrointestinal (GI) bleeding, severe pancreatitis, uncontrolled diabetes, active infection or renal failure. Such patients may be managed with pentoxifylline (400 mg orally, three times a day for 28 days). Hepatorenal syndrome is one of the major causes of death in patients with AH. Patients with acute kidney injury or hepatorenal syndrome respond poorly to corticosteroid therapy. Patients with bacterial infection may be treated with corticosteroids after the infection has been appropriately controlled with antibiotics. Response to prednisolone is graded as complete if Lille score is less than 0.16, partial if Lille score is between 0.16 and 0.56), or null if Lille score is greater than 0.56. A Lille score of more than 0.45 after 1 week of corticosteroid therapy is associated with 75% mortality at 6 months.[13]

Many recent trials, including the STOPAH trial and meta-analysis of the use of steroids and Pentoxifylline, reveal only short-term (28-day) mortality improvements with not much difference of 6-month, or 1-year mortality. In STOPAH trial, however, patients with less severe AH were included, and most patients were recruited with a clinical diagnosis of AH. Thus it is possible that patients with decompensated alcoholic cirrhosis may have received a diagnosis of AH, which significantly alters the result of the trial. Anti-TNF (tumor necrosis factor) agents like Infliximab and Etanercept have been used with no proven survival benefits. Anti-TNF agents may even increase the incidence of infections and death.

Patients with AH are prone to infections, especially when on steroids. This is in particularly important as it might lead to a poor prognosis, acute renal injury, and multi-organ dysfunction. Patients with AH are at risk of alcohol withdrawal. Lorazepam and oxazepam are the preferred benzodiazepines for prophylaxis and treatment of alcohol withdrawal. Daily caloric intake should be documented in patients with AH, and nutritional supplementation (preferably via mouth or NG tube) should be considered if oral intake is less than 1200 kcal in a day.

Both pentoxifylline and prednisolone are recommended for severe alcoholic hepatitis but long term benefits remain questionable.

Liver transplantation could be considered for patients not responsive to steroids and with a MELD of greater than 26. However, varied barriers including fear of recidivism, organ shortage, and social and ethical considerations exist. A survey of liver transplant programs conducted in 2015 revealed only 27% of the programs offering a transplant to AH patients. Of the 3,290 liver transplants performed 1.37% were on AH patients. The six months, one year and 5-year survival was 93%, 93%, and 87% respectively, the outcomes of which are comparable to patients with similar MELD scores. The recidivism rates are similar (17%) to patients transplanted for alcohol-related cirrhosis.

If the patient has acute renal failure, nephrology should be consulted to rule out hepatorenal syndrome.

If the patient has changes in mental status, develops seizures or focal deficits, a neurologist should be consulted. In addition, if the patient has leucocytosis and fever and there is a concern for an infection, an infectious disease consult should be obtained.

Differential Diagnosis

The differential diagnosis of AH includes nonalcoholic steatohepatitis, acute or chronic viral hepatitis, drug-induced liver injury, fulminant Wilson’s disease, autoimmune liver disease, alpha-1 antitrypsin deficiency, pyogenic hepatic abscess, ascending cholangitis or decompensation associated with hepatocellular carcinoma.

Prognosis

Patients with severe alcoholic hepatitis with an MDF greater than 32 have a 30-day mortality of 30% to 50%. Forty percent of the patients with severe alcoholic hepatitis die within 6 months after the onset of the clinical syndrome. Jaundice and hepatic encephalopathy at the time of presentation indicate a poorer outcome.

Mild alcoholic hepatitis is a benign disease and reversible if one stops alcohol consumption.

To determine prognosis the following factors need to be considered:

  • Histologically proven alcohol hepatitis
  • Serum bilirubin greater than 2.5 mg/dl
  • Serum albumin less than 2.5 g/dl
  • Prothrombin time more than 5 seconds

Complications

  • Variceal hemorrhage
  • Hepatic encephalopathy
  • Coaguloapthy
  • Thrombocytopenia
  • Ascites
  • Spontaneous bacterial peritonitis
  • Iron overload

Postoperative and Rehabilitation Care

A diet consisting of 100g/d of protein should be recommended. This should be supplemented with multivitamins including folate and thiamine. Protein-energy malnutrition is very common in alcoholics and associated with high mortality when compared to patients with no malnutrition. Unless the patient has encephalopathy, protein should not be restricted.

Deterrence and Patient Education

Patients with Alcoholic hepatitis need long term follow up. Many can benefit from attending AA or a similar abuse treatment program.

Serology for viral hepatitis should be ordered and period surveillance for liver cancer is recommended.

Patients with alcoholic hepatitis should be immunized againist hepatitis A, hepatitis B, influenza A virus and pneumococcus.

Pearls and Other Issues

The combination of systemic illness, malnutrition, concurrent renal injury, infections, lack of response to glucocorticoids or pentoxifylline result in poorer outcomes in severe AH. Further understanding of the pathophysiology of alcohol-induced liver injury, early recognition, including complications and potentially better pharmacological approach could in future improve clinical outcomes in patients with severe AH. A better understanding of alcohol-related liver injury, inflammation, liver fibrosis, and liver regeneration and associated gut-barrier permeability and dysfunction, along with newer pharmacological breakthroughs to treat AH would likely improve our present management strategies.

Enhancing Healthcare Team Outcomes

Alcoholic hepatitis has repercussions beyond the liver and is best managed by an interprofessional team that includes physicians, physician assistants, and nurse practitioners. The primary care provider and nurse practitioner should educate patients on the harms of alcohol and if alcoholic hepatitis is suspected, quickly refer them to a gastroenterologist for further workup. The disorder can affect the functioning of multiple organs, and early diagnosis is important.

At every opportunity, the key to treatment is patient education about the health risks of alcohol.  Patients with severe alcoholic hepatitis with an MDF greater than 32 have a 30-day mortality of 30% to 50%. Forty percent of the patients with severe alcoholic hepatitis die within 6 months after the onset of the clinical syndrome. Jaundice and hepatic encephalopathy at the time of presentation indicate a poorer outcome.

Nurse practitioners, pharmacists, and primary care providers should urge patients to enter AA and take their family members; there is evidence that this program can help some alcoholics become sober. Other alcoholics may need mental health counseling and cognitive behavior therapy.

The combination of systemic illness, malnutrition, concurrent renal injury, infections, lack of response to glucocorticoids or pentoxifylline result in poorer outcomes in severe AH. Further understanding of the pathophysiology of alcohol-induced liver injury, early recognition, including complications and potentially better pharmacological approach could in future improve clinical outcomes in patients with severe AH. A better understanding of alcohol-related liver injury, inflammation, liver fibrosis, and liver regeneration and associated gut-barrier permeability and dysfunction, along with newer pharmacological breakthroughs to treat AH would likely improve our present management strategies. 

Those with end-stage liver should be referred to a transplant nurse to determine eligibility. The transplant nurse should assist in coordination for transplant and report findings to the clinical transplant surgeon and hepatologist managing the case. Due to the complexity of care, an interdisciplinary team of specialty-trained nurses and clinicians should coordinate the long-term care of these patients.[14] [Level V]


Interested in Participating?

We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.

Improve Content - Become an Author or Editor

This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.

Alcoholic Hepatitis - Questions

Take a quiz of the questions on this article.

Take Quiz
What is the typical enzymatic pattern of liver enzymes after intake of ethanol?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 37-year-old patient with alcohol use disorder presents with 2 weeks of stomach pain and fatigue. Physical findings are confusion, jaundice, normal bowel sounds, right upper quadrant tenderness without rebound or guarding, liver edge 7 cm below the costal margin at the midclavicular line, splenomegaly, and asterixis. Labs show a marked white blood cell count without left shift and elevated transaminases. The patient has a calculated Maddrey discriminant function of 48. An ultrasound of the liver shows hepatomegaly, increased echogenicity, gallstones, and no ascites. A chest x-ray and urinalysis are normal. Which of the following is false?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Which of the following is not a histologic finding in alcoholic hepatitis?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
Concerning alcoholic liver injury, which of the following is false?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 56-year-old white male with hypertension, gout and known heterozygous C282Y for hemochromatosis and fatty liver disease with F2 fibrosis on transient elastography 2 months ago, comes transferred from his family care provider to the emergency department for a recent history of alcohol abuse, jaundice, and ascites. He has completed a 12-week course of Harvoni for his GT1a HCV and has attained virological cure. He has also been taking 1 to 3 extra strength acetaminophen every week for his chronic back pain. He has a long history of alcohol abuse which has become worse since his divorce 5 years ago. On examination, he has spider naevi, palmar erythema, and asterixis. He is alert and oriented to time, place and person. Vitals include a blood pressure of 102/70 mmHg, pulse rate of 96/minute, respiratory rate of 18/minute and a temperature of 99.8 F. Initial blood test shows a hemoglobin of 12.9 and white count of 3.6 with no left shift. He has thrombocytopenia to 110,000. The INR is prolonged to 1.2. The creatinine is 1.4, urea 25, total bilirubin 4.0 micromol/l, ALT 132 IU/l, AST 280 IU/l, albumin 2.9, and alkaline phosphatase of 267 IU/l. A blood culture, baseline chronic liver disease workup, and chest x-ray have been ordered. What would be the likely etiology of the elevated transaminitis for this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 48-year-old male with a BMI of 24.5, with a past medical history of alcoholic hepatitis secondary to a 2-year history of alcohol abuse following social stressors, has failed a 4 week trial of prednisolone. He has no other medical history and is not on any medications. Presently his MELD is 35, he is jaundiced, and his renal injury workup is consistent with a hepatorenal physiology. He is a highly functional individual and successfully runs his own business. He has not abused alcohol since his admission 12 weeks back. What options are there for this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up
A 44-year-old obese (BMI 34.7) female with a recent diagnosis of fatty liver, hypertension, and prediabetes, presents with a 2-week history of jaundice, abdominal distension, pedal edema, and confusion. She gives a history of alcohol intake of up to half a bottle of vodka on a daily basis for the past 10 to 12 years. Her last drink was last week. She works as a secretary in a school and has been functional till last month. She is accompanied by her mother and sister. Over the last 2 days, she has been having fevers to 101F and has had a poor appetite with abdominal pain, nausea, and chills. On examination she is jaundiced with multiple spider naevi, palmar erythema, tender hepatomegaly and ascites. She is alert, but nauseous. Vitals include a blood pressure of 108/60 mmHg, pulse rate of 92/minute, respiratory rate of 15/minute and a temperature of 101.2F. Initial blood test shows normal hemoglobin and white count, with thrombocytopenia. The INR is prolonged to 1.6. The creatinine is 1.4, urea 37, total bilirubin 4.7 micromol/l, ALT 160 IU/l, AST 350 IU/l, albumin 2.9, and alkaline phosphatase of 172 IU/l. A blood culture, baseline chronic liver disease workup, and chest x-ray have been ordered. What would be the next most appropriate step for this patient?



Click Your Answer Below


Would you like to access teaching points and more information on this topic?

Improve Content - Become an Author or Editor and get free access to the entire database, free eBooks, as well as free CME/CE as it becomes available. If interested, please click on "Sign Up" to register.

Purchase- Want immediate access to questions, answers, and teaching points? They can be purchased above at Apps and eBooks.


Sign Up

Alcoholic Hepatitis - References

References

Im GY,Cameron AM,Lucey MR, Liver transplantation for alcoholic hepatitis. Journal of hepatology. 2019 Feb;     [PubMed]
Gustot T,Jalan R, Acute-on-chronic liver failure in patients with alcohol-related liver disease. Journal of hepatology. 2019 Feb;     [PubMed]
Mathurin P,Thursz M, Endpoints and patient stratification in clinical trials for alcoholic hepatitis. Journal of hepatology. 2019 Feb;     [PubMed]
Singal AK,Shah VH, Current trials and novel therapeutic targets for alcoholic hepatitis. Journal of hepatology. 2019 Feb;     [PubMed]
Gao B,Ahmad MF,Nagy LE,Tsukamoto H, Inflammatory pathways in alcoholic steatohepatitis. Journal of hepatology. 2019 Feb;     [PubMed]
Milosevic I,Vujovic A,Barac A,Djelic M,Korac M,Radovanovic Spurnic A,Gmizic I,Stevanovic O,Djordjevic V,Lekic N,Russo E,Amedei A, Gut-Liver Axis, Gut Microbiota, and Its Modulation in the Management of Liver Diseases: A Review of the Literature. International journal of molecular sciences. 2019 Jan 17;     [PubMed]
García-Carretero R,Barquero-Pérez O,Mora-Jiménez I,Soguero-Ruiz C,Goya-Esteban R,Rodríguez-Castro C,Ramos-López J, [Prevalence and clinical features of non-alcoholic steatohepatitis in a hypertensive population]. Hipertension y riesgo vascular. 2019 Jan 14;     [PubMed]
Urban SK,Mocan T,Sänger H,Lukacs-Kornek V,Kornek M, Extracellular Vesicles in Liver Diseases: Diagnostic, Prognostic, and Therapeutic Application. Seminars in liver disease. 2019 Jan 17;     [PubMed]
van Welzen BJ,Mudrikova T,El Idrissi A,Hoepelman AIM,Arends JE, A Review of Non-Alcoholic Fatty Liver Disease in HIV-Infected Patients: The Next Big Thing? Infectious diseases and therapy. 2019 Jan 3;     [PubMed]
Weiskirchen R,Weiskirchen S,Tacke F, Recent advances in understanding liver fibrosis: bridging basic science and individualized treatment concepts. F1000Research. 2018;     [PubMed]
Daswani R,Kumar A,Anikhindi SA,Sharma P,Singla V,Bansal N,Arora A, Predictors of 90-day mortality in patients with severe alcoholic hepatitis: Experience with 183 patients at a tertiary care center from India. Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology. 2018 Mar;     [PubMed]
Testino G,Leone S, Acute alcoholic hepatitis: a literature review and proposal of treatment. Minerva medica. 2018 Aug;     [PubMed]
Puoti C,Elmo MG,Ceccarelli D,Ditrinco M, Liver steatosis: The new epidemic of the Third Millennium. Benign liver state or silent killer? European journal of internal medicine. 2017 Dec;     [PubMed]
Magistri P,Marzi L,Guerzoni S,Vandelli M,Mereu F,Ascari F,Guidetti C,Tarantino G,Serra V,Guerrini GP,Ballarin R,Moscara M,De Maria N,Villa E,Di Benedetto F, Impact of a Multidisciplinary Team on Alcohol Recidivism and Survival After Liver Transplant for Alcoholic Disease. Transplantation proceedings. 2019 Jan - Feb     [PubMed]

Disclaimer

The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Transplant Hepatology. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Transplant Hepatology, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Transplant Hepatology, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Transplant Hepatology. When it is time for the Transplant Hepatology board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Transplant Hepatology.