Guideline Summary for Alcoholic Hepatitis

Diagnosis

• Alcoholic hepatitis should be suspected in patients with a history of heavy alcohol consumption (>40 g/day for women, >50–60 g/day for men) for more than 6 months who present with recent‑onset jaundice (bilirubin > 3 mg/dL), AST > 50 IU/L but < 400 IU/L, and an AST/ALT ratio > 1.5 after exclusion of other etiologies. 1
• Typical clinical features include progressive jaundice, fever (often without infection), malaise, tender hepatomegaly, weight loss, and signs of decompensation such as ascites and encephalopathy. 2
• The majority of patients have underlying cirrhosis at the time of diagnosis. 1
• Additional laboratory abnormalities that support the diagnosis are neutrophilia, prolonged INR, hypoalbuminemia, and thrombocytopenia in severe cases. 2
• Imaging should be performed to rule out biliary obstruction, but iodinated contrast agents should be avoided because they markedly increase the risk of acute kidney injury. 1
• Serologic testing must exclude viral hepatitis, severe autoimmune liver disease, and Wilson disease. 3
• Blood, urine, and ascitic fluid cultures should be obtained on admission regardless of the presence of fever, as infection is a common precipitant. 1
• Liver biopsy is not required for diagnosis but is useful when diagnostic uncertainty exists (≈10–20 % of cases); a transjugular approach is preferred to minimize bleeding risk. 3
• Histologic hallmarks include macrovesicular steatosis, neutrophilic infiltrates, hepatocyte ballooning, Mallory‑Denk bodies, megamitochondria, cholestasis, and fibrosis. 1

Severity Assessment

• Calculate Maddrey’s Discriminant Function (MDF) and/or MELD score at presentation to guide treatment decisions. 1
• MDF > 32 identifies severe alcoholic hepatitis and predicts a 28‑day mortality of 20–30 %. 1
• MELD > 20 predicts a high 90‑day mortality; MELD > 26 warrants evaluation for liver transplantation. 1
• Alternative prognostic tools (ABIC category C, Glasgow score ≥ 9) also identify patients at high short‑term mortality risk. 1
• Without specific therapy and continued alcohol use, 90‑day mortality ranges from 40 % to 50 %. 1
• Systemic inflammatory response syndrome (SIRS) on admission markedly increases the risk of multi‑organ failure and mortality. 1
• Early acute kidney injury is a frequent manifestation of multi‑organ failure; nephrotoxic drugs (including diuretics) should be avoided. 1

Management

Hospitalization & Supportive Care

• Patients with severe disease (MDF > 32 or MELD > 20) require inpatient care for enforced abstinence, infection screening, and nutritional optimization. 1
• Absolute abstinence from alcohol is the cornerstone of therapy and is essential for long‑term survival. 1
• Brief alcohol‑intervention counseling during hospitalization reduces subsequent alcohol intake by roughly 40 g/week. 4
• Pharmacologic relapse‑prevention (e.g., naltrexone or acamprosate) should be considered in conjunction with counseling. 5

Nutritional Support

• Provide 35–40 kcal/kg/day with protein 1.2–1.5 g/kg/day (increase to 1.5 g/kg/day in critically ill patients); adequate nutrition is a major determinant of survival. 1
• If oral intake is not possible, initiate enteral feeding via nasogastric tube; parenteral nutrition alone is insufficient. 1
• Normal‑to‑high protein diets are safe and do not increase the risk of hepatic encephalopathy. 4

Infection Management

• Systematic infection screening must be completed before any immunosuppressive therapy is started. 1
• Maintain a high index of suspicion for infection because fever and leukocytosis are unreliable in this population. 1

Pharmacologic Therapy for Severe Disease

• In the absence of contraindications (active infection, hepatitis B, tuberculosis, gastrointestinal bleeding), initiate prednisolone 40 mg daily (or methylprednisolone 32 mg daily) for 28 days. 1
• Evaluate response on day 7 using the Lille score; discontinue steroids if there is no improvement. 2
• Contraindications to corticosteroids include active infection, hepatitis B, tuberculosis, and active gastrointestinal bleeding. 1
• Adding intravenous N‑acetylcysteine (NAC) for the first 5 days to prednisolone significantly lowers 1‑month mortality (8 % vs 24 %) and reduces infection rates (19 % vs 42 %). 4
• Pentoxifylline 400 mg three times daily may be used when steroids are contraindicated, although evidence for steroids is stronger. 1

Management of Complications

• Ascites: Use diuretics cautiously; over‑use increases the risk of acute kidney injury. 1
• Encephalopathy: Treat with standard regimens; high‑protein diets remain safe. 4
• Acute Kidney Injury: Avoid nephrotoxic agents, maintain careful fluid balance, and refrain from iodinated contrast. 1
• Variceal Bleeding: Perform urgent endoscopy and manage according to standard variceal‑bleeding protocols. 4

Liver Transplantation

• Patients with MELD > 26 who fail to respond to medical therapy should be evaluated for liver transplantation, which can be life‑saving. 1
• Transplant candidacy requires careful patient selection and demonstrated insight into the disease. 1

Non‑Severe Disease (MDF < 32, MELD < 20)

• Supportive care and enforced abstinence are sufficient; routine pharmacologic therapy is not required. 5
• Monitor bilirubin trends during hospitalization to gauge clinical improvement. 5

Common Pitfalls

• Failing to screen for infection before starting corticosteroids markedly increases mortality. 1
• Aggressive diuretic use precipitates acute kidney injury and multi‑organ failure. 1
• Continuing corticosteroids beyond day 7 in non‑responders (based on Lille score) wastes resources and raises infection risk. 2
• Providing less than approximately 20 kcal/kg/day of nutrition significantly reduces survival. 4
• Relying on fever or leukocytosis alone to diagnose infection leads to missed infections in this immunocompromised population. 1

Evidence‑Based Assessment and Monitoring of Alcohol‑Related Liver Injury After Recent Cessation

Laboratory Interpretation

• The AST = 139 U/L and ALT = 345 U/L yield an AST/ALT ratio of ≈0.4, which is atypical for alcoholic hepatitis (the ratio is usually > 1.5). This pattern suggests concurrent non‑alcoholic injury, recent alcohol cessation with ongoing inflammation, or a mixed etiology. 6
• After recent alcohol cessation, AST levels can fall by roughly 48 % within 5 days; therefore the current transaminase elevation most likely reflects resolving inflammation rather than active severe alcoholic hepatitis. 7

Monitoring After Sustained Abstinence

• Repeat the full liver panel (AST, ALT, GGT, alkaline phosphatase, bilirubin, albumin, INR, platelets) 1–2 weeks after confirmed abstinence; values should demonstrate measurable improvement. 8
• When AST remains > 2 × the upper limit of normal, liver‑stiffness measurements (e.g., FibroScan) may be falsely elevated, so non‑invasive fibrosis testing should be postponed until transaminases normalize. 8

Non‑Invasive Fibrosis Assessment

• Transient elastography (FibroScan) values < 8–10 kPa reliably exclude advanced fibrosis, whereas values > 12–15 kPa indicate advanced fibrosis or cirrhosis; however, active inflammation can artificially raise stiffness, so testing should be deferred until biochemical inflammation subsides. 8
• Serum‑based scores such as FIB‑4 or Forns’ index have a high negative predictive value (95–97 %) for ruling out advanced fibrosis and can be calculated from routine laboratory results. 8
• Patented biomarker panels (e.g., FibroTest, ELF test, FibroMeter) provide greater diagnostic accuracy than non‑patented scores but require specialized testing. 9

Required Diagnostic Workup

• To enable prognostic scoring (Maddrey Discriminant Function, MELD), obtain the missing laboratory values: total and direct bilirubin, INR/PT, albumin, creatinine, complete blood count with platelets, and γ‑glutamyl transferase (GGT). 6