Understanding Hepatitis: Alcoholic Vs. Toxic Hepatitis

Alcoholic hepatitis is a liver disease caused by heavy alcohol consumption. It is characterised by a history of chronic heavy alcohol consumption leading to jaundice, fever, tachycardia, tachypnea, hepatomegaly, leukocytosis with neutrophilia, and an AST:ALT elevation greater than 1.5:1. The progression of liver disease is not dependent on the amount of alcohol consumed, and even shorter periods of alcohol abuse could lead to alcoholic hepatitis. Women are more prone to the toxic effects of alcohol and are at a higher risk of developing liver fibrosis and alcoholic hepatitis compared to men. Acute alcoholic hepatitis is a specific clinical entity characterised by rapid decompensation of hepatic function. It is important to distinguish alcoholic hepatitis from other causes of acute liver injury such as drug-induced liver injury, viral hepatitis, autoimmune hepatitis, Wilsonian crisis, and cholangitis.

Alcoholic hepatitis and cirrhosis

Alcoholic hepatitis (AH) is a specific clinical entity characterised by the rapid decompensation of hepatic function. AH is typically diagnosed in adults between the ages of 40 and 50, although younger patients are increasingly being diagnosed with the disease, likely due to earlier heavy alcohol use and binge drinking behaviour. Women are more prone to the toxic effects of alcohol and are at a higher risk of developing liver fibrosis and AH compared to men. This is due to several factors, including lower gastric levels of alcohol dehydrogenase, higher gut permeability, and greater alcohol-mediated cytokine release from macrophages.

The exact incidence and prevalence of AH are unclear, as many patients have subclinical disease and are never diagnosed. However, one study reported a prevalence of approximately 20% in a cohort of 1604 alcoholics based on liver biopsy data. AH has been linked to excessive alcohol drinking over a prolonged period, typically more than two decades. However, it is now recognised that many patients diagnosed with AH report alcohol use over shorter periods. The amount of alcohol ingested is the most important risk factor for the development of chronic liver disease, and even shorter durations of alcohol abuse could lead to AH.

Alcoholic hepatitis is one of the stages of alcoholic liver disease (ALD), which covers a spectrum of disorders. The initial stage is the accumulation of fat in the liver cells, known as fatty liver or steatosis. If alcohol consumption continues, it can lead to alcoholic hepatitis, characterised by inflammation of liver cells. The outcome at this stage depends on the severity of the damage. Alcohol abstinence, nutritional support, treatment of infection, and prednisolone therapy can help treat alcoholic hepatitis. However, more severe cases can lead to liver failure.

The final and most advanced stage of ALD is alcoholic cirrhosis, which is irreversible. This stage is characterised by progressive hepatic fibrosis and nodules. With complete alcohol avoidance and time, the liver can sometimes heal some of the damage caused by alcohol, allowing individuals to return to a normal life. However, when liver tissue loss is severe enough to cause liver failure, most of the damage may be permanent. Treatment options for AH patients include steroids, with liver transplantation considered for patients unresponsive to steroids.

Heavy drinking and liver damage

The progression of ALD to AH is influenced by various factors, including the amount and duration of alcohol consumption, genetic predisposition, and individual differences in metabolism. Women are more prone to the toxic effects of alcohol due to lower gastric levels of alcohol dehydrogenase, higher gut permeability, and higher body fat content, resulting in higher blood alcohol concentrations.

Heavy drinking over many years significantly increases the risk of developing AH. Binge drinking, defined as consuming more than five drinks in a night for men or four for women, can also lead to AH if it occurs at least five times per month for six months or more. The exact incidence and prevalence of AH are unclear, as many cases may go undiagnosed, but one study reported a prevalence of approximately 20% in a cohort of 1604 alcoholics based on liver biopsy data.

The treatment for AH aims to address both the acute symptoms and the underlying cause of heavy drinking. Complete alcohol abstinence is crucial, as it allows the liver to heal and can lead to a return to normal life. Participation in an alcohol use disorder treatment program can help achieve this goal. Dietary changes, vitamins, salt limits, procedures to shrink swollen veins in the digestive tract, diuretics, and anti-inflammatory medications may also be recommended.

In severe cases of AH, medical interventions such as corticosteroid therapy or liver transplantation may be considered. However, barriers such as fear of recidivism, organ shortage, and social and ethical considerations exist. The prognosis for AH patients can vary, with survival rates ranging from 87% at five years to higher mortality rates associated with acute renal failure, infections, hepatic encephalopathy, coagulopathy, and ascites.

Alcohol-induced hepatitis symptoms

Alcoholic hepatitis is a type of alcoholic liver disease that occurs when a person consumes more alcohol than their liver can process. It is an inflammatory liver condition that results from frequent high alcohol consumption. The liver breaks down alcohol, and processing large amounts can damage liver cells, leading to swelling and scarring of the liver. Obese people, tobacco smokers, and women are at higher risk of alcoholic hepatitis.

There is no single specific sign or symptom of alcoholic hepatitis, but a combination of symptoms can help make the diagnosis with reasonable accuracy. Clinical jaundice, or yellowing of the skin and eyes, is one of the most common signs and is present in 40%-60% of cases. Hyperbilirubinemia, an elevated level of a substance called bilirubin in the blood, is present in almost every patient with alcoholic hepatitis and is considered a cardinal feature of the disease. Other symptoms include right upper quadrant pain, fever, tachycardia, and a tender enlarged liver.

In more severe cases, patients may experience delirium tremens, a state of confusion that may include visual hallucinations, agitation, convulsions, and fever. Hepatic encephalopathy, acute renal failure, infections, coagulopathy, and ascites have been strongly associated with mortality. Malnutrition is also common in patients with alcoholic hepatitis, with up to 90% of patients in one series presenting with this condition.

Alcoholic hepatitis usually develops over time with continued drinking, but severe alcoholic hepatitis can develop suddenly and quickly lead to liver failure and death. The condition can be reversed in the early stages by abstaining from alcohol, and treatment options include dietary changes, vitamin supplements, medications, and, in severe cases, a liver transplant. However, there is currently no cure for alcoholic hepatitis, and the main treatment option is to stop consuming alcohol.

Treatment for alcoholic hepatitis

Alcoholic hepatitis (AH) is a clinical syndrome characterised by acute-onset jaundice and liver enzyme abnormalities resulting from long-term heavy alcohol use. It is a specific clinical entity characterised by rapid decompensation of hepatic function. The treatment for alcoholic hepatitis depends on the severity of the disease.

For patients with moderate AH, treatment primarily consists of supportive care, including alcohol cessation and nutritional support. It is important to monitor caloric intake, and nutritional supplementation is recommended if oral intake is less than 1200 kcal in a day. Patients with AH are prone to infections, especially when on steroids, so broad-spectrum empiric antibiotics can be administered while awaiting culture results.

For patients with severe AH, corticosteroids are recommended. Oral corticosteroids such as prednisolone (40 mg per day) or methylprednisolone (32 mg per day) are typically administered. However, the benefits of corticosteroids are questionable, and treatment should be limited to 28 days. Corticosteroid use is associated with an increased risk of infections and gastrointestinal haemorrhage, and can be harmful if the patient has unclear diagnoses, less severe disease, or concomitant infections. Responsiveness to corticosteroid therapy should be evaluated using the Lille score on day 7 of treatment. If a patient does not respond to steroids within a week, evidenced by a Lille score of greater than 0.45, steroids should be discontinued. For patients with a Lille score of less than 0.45, prednisolone should be continued for another three weeks.

In cases where patients do not respond to steroids and have a MELD (Model for End-Stage Liver Disease) score of greater than 26, liver transplantation may be considered. However, there are various barriers to this, including fear of recidivism, organ shortage, and social and ethical considerations.

Liver disease diagnosis

Liver disease encompasses a wide range of conditions that affect the liver, including hepatitis. Hepatitis refers to inflammation of the liver, and it can be caused by various factors such as viruses, toxins, or autoimmune disorders. Toxic hepatitis and acute alcoholic hepatitis are both types of liver inflammation with distinct characteristics and causes.

Diagnosis of Liver Disease

The diagnosis of liver disease involves a comprehensive approach to assess liver function and identify any underlying conditions. Here are some common procedures used in the diagnosis of liver diseases:

• Liver Function Tests (LFTs): LFTs are blood tests that measure the levels of certain proteins and enzymes in the blood. These proteins and enzymes provide valuable information about liver function, inflammation, and damage. Alanine transaminase (ALT) and aspartate transaminase (AST) are enzymes mainly found in the liver and are commonly measured in LFTs.
• Imaging Techniques: Imaging tests, such as ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI), can provide visual information about the liver. These tests help doctors identify structural abnormalities, scarring, and signs of fatty liver disease. Ultrasound, for example, can measure liver stiffness, with increased stiffness indicating more extensive scarring.
• Liver Biopsy: A liver biopsy is a medical procedure where a small piece of liver tissue is removed to be examined under a microscope. It is often performed when other tests suggest liver dysfunction. The biopsy tissue is studied to confirm the presence and type of liver disease, aiding in treatment decisions.
• Specific Tests for Hepatitis: When evaluating suspected acute alcoholic hepatitis (AH), other causes of acute liver injury, such as drug-induced liver injury, viral hepatitis, and autoimmune hepatitis, should be ruled out. Liver, vascular, and biliary imaging may be used to exclude biliary or vascular disorders and hepatocellular carcinoma. Scoring models, such as the Maddrey discriminant function (DF), are used to assess the severity of AH and guide treatment decisions.
• Treatment Options: Liver disease treatment can sometimes be administered during diagnosis. For example, esophageal variceal banding is used to treat enlarged veins in the oesophagus, which may bleed due to increased liver blood pressure. Paracentesis involves draining fluid from the peritoneal cavity, where ascites, a complication of liver cirrhosis, can build up.

Toxic Hepatitis and Acute Alcoholic Hepatitis

Toxic hepatitis and acute alcoholic hepatitis are distinct conditions with some similarities and differences:

• Toxic Hepatitis: Toxic hepatitis refers to liver inflammation caused by exposure to toxins, including certain drugs, chemicals, or herbal supplements. It can occur when the liver is overwhelmed by toxins and unable to process them effectively.
• Acute Alcoholic Hepatitis (AH): AH is a specific type of alcoholic liver disease (ALD) characterised by rapid decompensation of hepatic function. It is caused by excessive alcohol consumption over a prolonged period, typically more than two decades. However, it has also been diagnosed in patients with shorter periods of alcohol abuse. AH typically presents with jaundice, fever, tachycardia, tachypnea, hepatomegaly, and leukocytosis with neutrophilia.

While toxic hepatitis can be caused by various toxins, acute alcoholic hepatitis is specifically linked to excessive alcohol consumption. Both conditions result in liver inflammation, but the underlying causes and specific clinical presentations differ.

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