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%. Several trials and models exist to determine the severity of alcoholic hepatitis, to ascertain which patients would likely benefit from a pharmacological approach. A liver biopsy should be done with care as these patients may have coagulopathy and thrombocytopenia. A liver biopsy is not always required but is useful for excluding other disorders.
Ultrasound 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. Carbohydrate-deficient transferrin is the most reliable marker of chronic alcoholism. This is the opposite of what is seen in other liver disorders. Liver tests may show elevation of AST, whereas ALT is usually in the normal range. All patients should have had an abdominal imaging study to exclude biliary obstruction and liver diseases such as hepatocellular carcinoma and liver abscess. The diagnosis of alcoholic hepatitis is a clinical one with supporting laboratory findings of AH. Recent studies indicate that patients with specific intestinal dysbiosis have been increasingly susceptible to alcoholic liver disease and AH. 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 the accumulation of neutrophils, macrophages, and systemic clinical features of alcohol injury. 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). This promotes lipogenesis by inhibiting the oxidation of triglycerides and fatty acids.Īnother known mechanism of alcohol-induced liver injury is the translocation of endotoxins in the form of lipopolysaccharides (LPS), from the intestines into the hepatocytes. Īlcohol undergoes an oxidative metabolic pathway in the hepatocytes, leading to a reduced ratio of the nicotinamide adenine dinucleotide (NAD) to NADH. Acute binge drinking is likely the trigger for AH in patients with a history of chronic, heavy alcohol abuse. Clinical jaundice is a poor prognostic factor. 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). 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. Even shorter durations of alcohol abuse could lead to AH. AH can occur in patients with any stage of alcoholic liver disease.Īlthough 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. AH, on the other hand, is characterized by a 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. 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. ASH is a diagnosis based on liver histology, while AH is a clinical diagnosis. 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. While using the terminology alcoholic hepatitis, it is important to understand the difference between alcoholic steatohepatitis (ASH) and alcoholic hepatitis (AH).