Alcoholic hepatitis

Objectives
• INTRODUCTION
• CLINICAL MANIFESTATIONS
• INVESTIGATIONS AND DIAGNOSIS
• ASSESSING DISEASE SEVERITY
• DIFFERENTIAL DIAGNOSIS
• MANAGEMENT AND PROGNOSIS

INTRODUCTION
• Excessive alcohol consumption is associated with a range of
hepatic manifestations, including
• Alcoholic fatty liver disease (with or without steatohepatitis),
• Alcoholic hepatitis, and
• Cirrhosis.

What is the amount of alcohol intake that puts
an individual at risk for alcoholic hepatitis?

Alcoholic hepatitis typically occurs after more than 10 years of
regular heavy alcohol use; average consumption in one study
was 100 g/day (the equivalent of 10 drinks per day)

Is alcohol intake related to Gender?

Laboratory tests
• Moderate elevations of the AST and ALT (typically less than
300 int. unit/L, rarely higher than 500 int. unit/L)
• An AST:ALT ratio ≥2
• An elevated serum bilirubin
• An elevated gamma-glutamyl transferase (GGT)
• A leukocytosis with a predominance of neutrophils
• An elevated international normalized ratio (INR)
• In addition, patients may have low serum albumin and
prealbumin levels due to malnutrition and decreased synthesis

Hematologic abnormalities
• Common in moderate to severe alcoholic hepatitis.
• Moderate leukocytosis (<20,000/microL) is a frequent finding
• Macrocytosis suggests longstanding disease and may reflect poor
nutritional status, cobalamin or folate deficiency, toxicity of alcohol,
and/or increased lipid deposition on red cell membranes
• Thrombocytopenia can result from primary bone marrow
hypoplasia (which can be due to alcohol and is usually brief) and/or
splenic sequestration due to portal hypertension and an enlarged
spleen ("hypersplenism")

Imaging tests
• Abdominal imaging (ultrasound, computed tomographic scan,
magnetic resonance imaging)
• fatty change in the liver, evidence of underlying cirrhosis, or
ascites. Transabdominal ultrasound may also reveal parallel
tubular structures in the liver, thought to represent the dilated
hepatic artery adjacent to a portal vein radical.
• Doppler flow studies of the hepatic artery may reveal an
elevated peak systolic velocity or an increase in vessel
diameter.
• Transient elastography may be useful in determining the
likelihood of cirrhosis.

DIAGNOSIS
• The diagnosis is mainly CLINICAL.
• Clinical and laboratory features and heavy alcohol use (typically
>100g per day for more than 20 years)
• patient presents with jaundice,+/- Ascites, moderately elevated
aminotransferases (typically <300 int. unit/mL and rarely higher
than 500 int. unit/mL), an AST:ALT ratio ≥2, an elevated serum
bilirubin (>5 mg/dL or 86 micromol/L), and an elevated INR.
• Rule out other common causes of acute hepatitis
●Anti-hepatitis A IgM
●Hepatitis B surface antigen, anti-hepatitis B core IgM
●Anti-hepatitis C virus (HCV) antibodies, hepatitis C RNA
●Biliary obstruction /Budd-Chiari syndrome using ultrasound with
Doppler

Is liver biopsy always needed?
• Although alcoholic hepatitis can be suspected on the basis of clinical and
biochemical clues, liver biopsy remains the gold standard diagnostic tool.
• It confirms the clinical diagnosis of alcoholic hepatitis in about 85% of all
patients and in up to 95% when significant hyperbilirubinemia is present.
• However, whether a particular patient needs a biopsy is not always clear.
The American Association for the Study of Liver Diseases (AASLD)
recommends biopsy in patients who have a clinical diagnosis of severe
alcoholic hepatitis for whom medical treatment is being considered and in
those with an uncertain underlying diagnosis.
• In addition to confirming the diagnosis and staging the disease,
liver biopsy has prognostic value.

Assessing disease severity
• The Maddrey discriminant function (MDF) and the Model for
End-stage Liver Disease (MELD) score are the most commonly
used to help identify patients who are more likely to benefit from
pharmacologic therapy.
• Other validated scores include the
• Glasgow alcoholic hepatitis score,
• the ABIC score (which includes age, serum bilirubin,
international normalized ratio, and serum creatinine), and
• the Lille score (which is used to determine if a patient is
responding to treatment)

MANAGEMENT
• Treatment considerations for all patients —
• Consultation with a gastroenterologist is recommended
• Alcohol abstinence is the cornerstone of treatment of alcoholic hepatitis.
• treatment of withdrawal.
• Hydration(use albumin rather than crystalloid for patients with prerenal azotemia and
underlying cirrhosis).
• Treat complications such as infections or conditions related to complications of
cirrhosis and portal hypertension such as hepatic encephalopathy, ascites, or
variceal bleeding.
• Renal failure and acute kidney injury
• Ulcer prophylaxis
• Discontinue nonselective beta blockers — In patients with severe alcoholic hepatitis,
the use of nonselective beta blockers has been associated with an increased risk of acute
kidney injury (AKI).
• Screen for infection. Patients with alcoholic hepatitis should be screened for infection, as about
25% of those with severe alcoholic hepatitis have an infection at admission.
• Vitamin E, silymarin, propylthiouracil, colchicine, and oxandrolone (anabolic steroid) have also
been studied, but with no convincing benefit.

Nutrition —
• Most patients with severe alcoholic hepatitis are malnourished and
require nutritional support.
• The goal of nutritional support is to provide adequate calories and
protein, in addition to vitamin (eg, thiamine, folate, and
pyridoxine) and mineral (eg, phosphate, magnesium)
repletion. vitamin K is usually given to patients with a prolonged
prothrombin time, even though this regimen is often ineffective
because the coagulopathy is reflection of underlying liver failure
than vitamin K deficiency. Oral vitamin K is not well absorbed; a
parenteral route of administration is preferred for these patients.
• Protein intake is well tolerated and should not be restricted in
patients with alcoholic hepatitis. In patients who develop
encephalopathy associated with protein feeding, the use of
branched-chain amino acids may be helpful.

Mild to moderate alcoholic hepatitis:
• Abstinence from alcohol is the mainstay of treatment in patients
with mild to moderate alcoholic hepatitis (Maddrey discriminant
function [MDF] <32) (calculator 1).
• general supportive care (eg, nutritional support and
hydration) treatment with glucocorticoids is not
recommended in patients with mild to moderate alcoholic
hepatitis. While glucocorticoids may provide a short-term
survival benefit in alcoholic hepatitis, patients with mild to
moderate disease have a relatively favorable prognosis, and
therefore, potential benefits do not outweigh potential harm.

Severe alcoholic hepatitis
• Glucocorticoids
• Indications and contraindications — In addition to general
supportive care, we suggest treatment with glucocorticoids (40 mg
per day) for patients with severe alcoholic hepatitis (DF ≥32
(calculator 1)).
• provided there are no contraindications to its use (eg, active
bacterial or fungal infection or chronic hepatitis C virus or
hepatitis B virus infection)
• Prednisolone is preferred over prednisone because the latter
requires conversion to prednisolone (the active form) in the liver, a
process that may be impaired in alcoholic
hepatitis. Methylprednisolone 32 mg daily by intravenous route is
used for patients who cannot take oral.

• For patients who respond to treatment, we
continue prednisolone for 28 days, and finish therapy with a 16-day
prednisolone taper (we decrease the dose by 10 mg per day
every four days until a dose of 10 mg per day is reached, at
which point we decrease it by 5 mg per day every three days).
• Response and early termination of treatment — For patients who
receive glucocorticoids, the duration of treatment is 28 days.
However, we stop therapy if fail to show signs of improvement after
one week (ie, those who fail to have improvement in their bilirubin
or MDF) (calculator 1).
• The Lille score is another method to determine if patients with
alcoholic hepatitis are responding to glucocorticoid therapy.

Pentoxifylline
• Pentoxifylline is an alternative to glucocorticoids for patients who
have contraindications to glucocorticoids or who are at risk for
sepsis or for failing to follow up after discharge.
• some authorities favor pentoxifylline because it may provide more
benefit for certain subgroups of patients (those with renal failure)
compared with glucocorticoids.
• Pentoxifylline is given as 400 mg three times per day (400 mg once
per day in patients with a creatinine clearance <30 mL per minute).
• A bilirubin less than 5 mg/dL may be an appropriate time to stop
therapy. Pentoxifylline should be stopped earlier in patients who
develop dyspepsia that limits oral intake.
• Pentoxifylline inhibits tumor necrosis factor (TNF) synthesis, which is
increased in patients with alcoholic hepatitis.

Liver transplantation
• — Patients with severe alcoholic hepatitis who fail to respond to
treatment with glucocorticoids or pentoxifylline may require liver
transplantation.
• Liver transplantation for alcoholic liver disease has been a topic of
great medical and social controversy.
• Many countries require 6 months of abstinence from alcohol before
placing a patient on the liver transplant list, posing a major obstacle to
patients with alcoholic hepatitis, as almost all are active drinkers at the
time of presentation and many will die within 6 months.
• Refractory patients — Patients with severe alcoholic hepatitis who
do not respond to supportive care, nutritional therapy, and
pharmacologic therapy, who are not candidates for liver
transplantation, and who have multiple (≥four) organ failures, may
be considered for palliative therapy

PROGNOSIS
• Mortality — Mortality rates among patients who do not receive
pharmacologic therapy (eg, prednisolone) for alcoholic hepatitis are
variable.
• In patients with severe alcoholic hepatitis (typically defined by a
Maddrey discriminant function ≥32 (calculator 1)), short-term
mortality rates are high (approximately 25 to 45 % at one month)
• patients with mild to moderate alcoholic hepatitis have lower
short-term mortality rates (<10 percent at one to three months)
• In one study, the primary causes of death were
hepatic failure (55 percent), gastrointestinal bleeding (21
percent), and sepsis (7 percent)

■ REFERENCES
• CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 82 • NUMBER 4
• The American Journal of Medicine - "The Green Journal"
• © 2021 UpToDate.

Alcoholic hepatitis

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