Can Anorexia Nervosa Cause Elevated Liver Function Tests?
Yes, anorexia nervosa (AN) can definitively cause elevated liver function tests through multiple mechanisms, occurring both during severe malnutrition and paradoxically during refeeding. 1, 2, 3
Mechanisms of Liver Enzyme Elevation in Anorexia Nervosa
During Severe Malnutrition (Pre-Refeeding)
Elevated LFTs can occur in severely malnourished AN patients before refeeding begins through:
Ischemic hepatitis from liver hypoperfusion - The most dramatic mechanism, where severe malnutrition creates a predisposing state for acute liver injury when combined with hemodynamic compromise (marked dehydration, hypotension, bradycardia, hypothermia). 1, 2
Direct starvation-induced hepatocyte injury - Prolonged severe malnutrition itself causes liver cell death and transaminase elevation, which paradoxically improves with careful refeeding and weight restoration. 3, 4
Acute liver failure-like presentation - In severely undernourished AN patients (BMI ~10), an ALF-like condition can develop without morphologic evidence of hepatocyte necrosis, which resolves completely with adequate refeeding. 5
During Refeeding
Excessive glucose deposition - Rapid caloric repletion causes fat and glucose deposition in hepatocytes, leading to transaminase elevation during the refeeding process. 4
Refeeding syndrome manifestations - Metabolic disturbances during nutritional rehabilitation can contribute to hepatic dysfunction. 4
Clinical Recognition and Monitoring
Key Clinical Features Suggesting Liver Hypoperfusion
Monitor for hemodynamic compromise that predisposes to ischemic hepatitis:
Laboratory Patterns
Dramatic transaminase elevations can occur (not just mild elevations), sometimes reaching levels consistent with acute liver failure. 2, 6
Rapid normalization of LFTs with rehydration and gradual nutritional support confirms the diagnosis and distinguishes this from other causes of liver injury. 1, 2
In severely malnourished patients (BMI ~10), LFTs may be markedly abnormal before refeeding and then paradoxically improve as caloric intake increases and weight gain progresses. 3
Clinical Management Approach
Initial Assessment
When encountering elevated LFTs in AN patients, determine:
Timing relative to nutritional status - Are elevations occurring during severe malnutrition or during refeeding? 3, 4
Hemodynamic stability - Assess for signs of hypoperfusion (dehydration, hypotension, bradycardia, hypothermia) that suggest ischemic hepatitis. 1, 2
Exclude other etiologies - Rule out viral hepatitis, drug-induced liver injury, and other causes of acute hepatitis before attributing to AN. 6
Therapeutic Intervention
Volume support with gradual (not rapid) nutritional rehabilitation results in normalization of LFTs when liver dysfunction is AN-related. 2
Frequent LFT monitoring during medical stabilization and refeeding is essential, as elevations can occur at multiple time points. 2, 3
Avoid excessive caloric repletion initially, as this can worsen hepatic fat deposition and transaminase elevation. 4
Critical Clinical Pitfalls
Do not assume elevated LFTs in AN always represent refeeding syndrome. Elevations can occur before refeeding begins due to severe malnutrition itself or acute hypoperfusion, and these actually improve with careful nutritional support. 3
Recognize that small insults can cause exaggerated liver inflammation in malnourished patients. Once other etiologies are excluded, this represents a benign clinical event not associated with adverse outcomes or higher mortality. 6
Monitor hemodynamic parameters closely - acute liver failure can result from sudden liver hypoperfusion in severe AN, requiring immediate volume support. 2
Prognosis
When LFT elevations are directly attributable to AN (after excluding other causes), the prognosis is favorable with appropriate nutritional rehabilitation. Complete normalization occurs with rehydration and gradual refeeding, confirming the reversible nature of AN-related hepatic dysfunction. 1, 2, 3