Interpret the following laboratory results—electrolytes Na 142 mmol/L, K 4.5 mmol/L, Cl 106 mmol/L, CO₂ 29 mmol/L, anion gap 7; renal function BUN 15 mg/dL, creatinine 0.79 mg/dL, eGFR 82 mL/min/1.73 m², BUN/creatinine ratio 19; calcium 9.6 mg/dL; liver panel AST 111 U/L, ALT 47 U/L, alkaline phosphatase 103 U/L, total protein 7.1 g/dL, albumin 4.6 g/dL, globulin 2.5 g/dL, bilirubin 0.6 mg/dL—what is the clinical interpretation and recommended next steps?

Laboratory Interpretation: Predominantly Hepatocellular Pattern with Elevated AST

Primary Finding: Disproportionate AST Elevation

The most significant abnormality is an AST of 111 U/L (approximately 2.4 times the upper limit of normal) with a relatively modest ALT elevation of 47 U/L, creating an AST:ALT ratio of 2.4:1, which strongly suggests alcohol-related liver injury as the primary diagnostic consideration. 1

Critical Pattern Recognition

AST:ALT Ratio Analysis

• An AST:ALT ratio >2:1 is highly characteristic of alcoholic liver disease, distinguishing it from most other causes of hepatocellular injury where ALT typically exceeds AST 1
• The absolute AST level of 111 U/L represents mild-to-moderate hepatocellular injury (not severe, which would be >1000 U/L) 1
• This pattern warrants direct questioning about alcohol consumption, including quantity, frequency, and recent binge drinking episodes 1

Supporting Laboratory Findings

• Alkaline phosphatase 103 U/L is within normal limits, ruling out significant cholestatic or biliary obstruction 1
• Total bilirubin 0.6 mg/dL is normal, indicating preserved hepatic excretory function and arguing against advanced liver disease 1, 2
• Albumin 4.6 g/dL is normal-to-high, confirming intact hepatic synthetic capacity and excluding chronic liver disease with cirrhosis 2, 3
• Total protein 7.1 g/dL is normal, further supporting adequate hepatic function 2

Electrolyte and Renal Assessment

Anion Gap Interpretation

• Anion gap of 7 mmol/L is at the lower end of the modern reference range (5-12 mmol/L using ion-selective electrodes) 4
• This low-normal anion gap does NOT indicate metabolic acidosis and is within expected parameters 4
• The bicarbonate (CO₂) of 29 mmol/L is normal-to-high, confirming no metabolic acidosis 1

Renal Function

• eGFR 82 mL/min/1.73m² indicates normal kidney function (>60 is normal) 1
• BUN 15 mg/dL and creatinine 0.79 mg/dL are both normal 1
• BUN/creatinine ratio of 19 is within normal range (10-20), indicating adequate hydration and no prerenal azotemia 1

Electrolytes

• Sodium 142, potassium 4.5, chloride 106, and calcium 9.6 are all within normal limits 5, 6
• No electrolyte abnormalities requiring intervention 5

Mandatory Next Steps

Immediate Clinical Assessment

1. Obtain detailed alcohol history: Quantify daily/weekly consumption in standard drinks, assess for binge drinking patterns, and screen for alcohol use disorder using validated tools (AUDIT-C) 1
2. Medication and supplement review: Document all prescription medications, over-the-counter drugs, herbal supplements, and vitamins taken in the past 3 months to exclude drug-induced liver injury 7
3. Physical examination: Look specifically for stigmata of chronic liver disease (spider angiomata, palmar erythema, hepatomegaly, splenomegaly) and signs of alcohol use disorder 1

Essential Laboratory Workup

If alcohol history is positive or unclear, obtain: 1, 7

• Hepatitis serologies: Hepatitis B surface antigen, hepatitis C antibody, hepatitis A IgM
• Autoimmune markers: Antinuclear antibody (ANA), anti-smooth muscle antibody (ASMA), anti-mitochondrial antibody (AMA) to exclude autoimmune hepatitis
• Iron studies: Serum iron, ferritin, transferrin saturation to exclude hemochromatosis
• Prothrombin time/INR: To assess hepatic synthetic function more sensitively than albumin alone 7, 2
• GGT (gamma-glutamyl transferase): Elevated GGT with this AST:ALT pattern further supports alcohol-related injury 1

Imaging Consideration

• Abdominal ultrasound is indicated if hepatomegaly is detected on examination, if there is concern for fatty liver disease, or if transaminases remain elevated after 4-6 weeks 1
• Ultrasound can identify hepatic steatosis, cirrhosis, and exclude biliary obstruction 1

Monitoring Protocol

Short-Term Follow-Up

• Repeat liver enzymes in 2-4 weeks if alcohol cessation is achieved or other hepatotoxins are removed 1, 7
• Expected pattern: AST should normalize faster than ALT if alcohol-related, typically within 2-6 weeks of abstinence 1
• Weekly monitoring is NOT required for this degree of elevation unless symptoms develop or synthetic function deteriorates 1

Red Flags Requiring Urgent Hepatology Referral

• AST or ALT rising above 500 U/L 7
• Development of jaundice (bilirubin >2 mg/dL) 7
• Prolonged PT/INR (>1.5) indicating impaired synthetic function 7, 2
• Persistent elevation beyond 3 months despite removal of hepatotoxins 7
• Development of ascites, encephalopathy, or other signs of hepatic decompensation 7

Critical Pitfalls to Avoid

1. Do not assume transaminase elevations will spontaneously resolve without identifying and removing the causative agent (alcohol, medications, or other hepatotoxins) 7
2. Do not overlook non-alcoholic causes even with a classic AST:ALT ratio—viral hepatitis and autoimmune hepatitis must be excluded with serologic testing 1, 7
3. Do not delay investigation beyond 3 months if liver enzymes remain abnormal, as this indicates chronic liver disease requiring comprehensive evaluation 7
4. Do not rely solely on albumin to assess liver disease severity—it can be normal in acute or early chronic liver disease and is affected by non-hepatic conditions 2, 3

Clinical Bottom Line

This laboratory pattern most likely represents alcohol-related hepatocellular injury given the AST:ALT ratio >2:1 with preserved synthetic function. The immediate priority is obtaining an accurate alcohol history, excluding viral and autoimmune hepatitis with serologic testing, and establishing a monitoring plan with repeat liver enzymes in 2-4 weeks. 1, 7 If alcohol use is confirmed, counseling for cessation and consideration of addiction medicine referral is essential. 1