In a 56-year-old female with chronically elevated liver function tests and ultrasound demonstrating hepatic steatosis and asymptomatic cholelithiasis without biliary obstruction, what is the appropriate treatment and management plan?

Management of Chronic Elevated LFTs with Hepatic Steatosis and Asymptomatic Cholelithiasis

For this 56-year-old woman with hepatic steatosis and asymptomatic gallstones, focus management on the underlying fatty liver disease through lifestyle modification and metabolic risk factor control, while monitoring the gallstones expectantly without surgical intervention. 1

Immediate Diagnostic Workup

Complete the evaluation for chronic liver disease causes beyond simple steatosis:

• Obtain fasting lipid panel, hemoglobin A1c, and assess for metabolic syndrome components (obesity, diabetes, hypertension, dyslipidemia), as NAFLD prevalence increases to 70% with obesity and 90% with diabetes 1
• Measure alcohol consumption history using validated questionnaires, calculating AST:ALT ratio (>2 suggests alcohol-induced disease, <1 suggests metabolic disease-related fatty liver) 1
• Test for chronic hepatitis B surface antigen, hepatitis C antibody, and hepatitis E if immunosuppressed 1
• Screen for hereditary hemochromatosis with serum ferritin and transferrin saturation 1
• Check alpha-1 antitrypsin phenotype, ceruloplasmin (Wilson disease), and antinuclear antibodies/smooth muscle antibodies (autoimmune hepatitis) 1
• Exclude drug-induced liver injury by reviewing all medications, supplements, and herbal products 1

Assess Disease Severity and Fibrosis Risk

Determine whether simple steatosis has progressed to steatohepatitis or fibrosis, which fundamentally changes prognosis:

• Calculate noninvasive fibrosis scores (FIB-4 or NAFLD fibrosis score) using age, AST, ALT, and platelet count 1
• Perform liver stiffness measurement using transient elastography (FibroScan) or shear wave elastography to detect significant fibrosis (≥F2) or cirrhosis 1, 2
• If elastography shows liver stiffness >8 kPa or noninvasive scores suggest advanced fibrosis, refer to hepatology for consideration of liver biopsy to distinguish NASH from simple steatosis and stage fibrosis accurately 1

The distinction between simple steatosis (70-75% of NAFLD cases) and NASH (25-30% of cases) is critical because only NASH progresses to cirrhosis and hepatocellular carcinoma. 1

Primary Treatment Strategy for Hepatic Steatosis

Implement aggressive lifestyle modification as the cornerstone of NAFLD management:

• Target 7-10% body weight loss through caloric restriction (500-1000 kcal/day deficit) combined with 150-200 minutes weekly of moderate-intensity aerobic exercise 1
• Refer to registered dietitian for Mediterranean diet counseling, which reduces hepatic fat independent of weight loss 1
• Screen for and aggressively treat components of metabolic syndrome: optimize glycemic control in diabetes (target HbA1c <7%), treat dyslipidemia with statins (which are safe in NAFLD), and control hypertension 1

No FDA-approved pharmacologic therapy exists specifically for NAFLD/NASH, so lifestyle intervention remains the only evidence-based treatment. 1

Management of Asymptomatic Cholelithiasis

Adopt expectant management without prophylactic cholecystectomy:

• Asymptomatic gallstones require no surgical intervention, as only 10-15% of patients develop symptoms over 10-15 years, and prophylactic cholecystectomy carries greater risk than observation 3
• Educate the patient to recognize biliary colic symptoms (episodic right upper quadrant or epigastric pain lasting 30 minutes to several hours, often postprandial) and acute cholecystitis signs (persistent pain, fever, positive Murphy's sign) 3
• If biliary symptoms develop, obtain repeat ultrasound to assess for gallbladder wall thickening, pericholecystic fluid, or common bile duct dilation, then refer for laparoscopic cholecystectomy 3

The presence of gallstones does not explain chronically elevated LFTs unless biliary obstruction is present, which this ultrasound excludes (CBD 3mm, no ductal dilation). 1, 4

Surveillance and Monitoring Protocol

Establish a structured follow-up schedule to detect disease progression:

• Repeat liver function tests (AST, ALT, alkaline phosphatase, bilirubin) every 3-6 months initially, then annually once stable 1
• Perform annual liver ultrasound to monitor for development of cirrhosis features (nodular contour, splenomegaly) or hepatocellular carcinoma if advanced fibrosis is present 1
• Repeat liver stiffness measurement annually if baseline elastography shows any fibrosis (≥F1), as progression occurs in 20-30% of NASH patients over 5 years 1, 2
• Screen for hepatocellular carcinoma with ultrasound and alpha-fetoprotein every 6 months if cirrhosis develops 1

Critical Pitfalls to Avoid

Do not perform liver biopsy routinely in all NAFLD patients, as it is reserved for cases where noninvasive testing suggests advanced fibrosis, alternative diagnoses remain possible despite workup, or clinical trials require histologic endpoints 1

Do not attribute all elevated LFTs to "fatty liver" without excluding other treatable causes, particularly autoimmune hepatitis, Wilson disease (in patients <40 years), and hemochromatosis, which require specific therapies 1

Avoid prophylactic cholecystectomy for asymptomatic gallstones, as surgical risks outweigh benefits in the absence of symptoms, and fatty liver disease itself does not increase gallstone complication rates 3

Do not assume ultrasound-detected steatosis equals NASH, since ultrasound cannot distinguish simple steatosis from steatohepatitis or detect mild steatosis (<33% hepatic fat content), and only NASH carries risk of progressive fibrosis 1, 2, 5

Recognize that hepatic steatosis on ultrasound has 84.8% sensitivity and 93.6% specificity only for moderate-to-severe fat deposition (>30%), with sensitivity dropping to 53-65% for mild steatosis, so negative ultrasound does not exclude early NAFLD 1