Dysgeusia-Driven Nutritional Decline in Cirrhosis: A Case of Autoimmune Hepatitis and Primary Biliary Cholangitis
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Updated: Jan 13, 2026

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury
Published on: October 21, 2017
Newton Rahming1, Stephan Corcho2, Oluwasegun Olowe2
1Surgery, Caribbean Medical University, Willemstad, CUW.
Abstract:
Dysgeusia, or altered taste perception, is characterized by metallic, sweet, sour, or bitter sensations that can significantly impair oral intake and contribute to malnutrition, particularly in patients with chronic illness. This report describes a 75-year-old woman with decompensated cirrhosis secondary to autoimmune hepatitis and primary biliary cholangitis (PBC), who presented with a persistent metallic taste and an unintentional 25-pound weight loss over three months. Dysgeusia began shortly after the initiation of mycophenolate mofetil (MMF) and led to reduced caloric intake, early satiety, and progressive sarcopenia. Laboratory evaluation demonstrated pancytopenia, hypoalbuminemia, and hyperbilirubinemia, consistent with decompensated cirrhosis. Zinc levels were normal (82 mcg/dL), and the patient remained compliant with supplementation, making isolated zinc deficiency an unlikely cause of her symptoms. Longitudinal assessment demonstrated parallel declines in weight, nutritional intake, and hepatic synthetic function. Imaging and alpha-fetoprotein (AFP) testing excluded hepatocellular carcinoma, and no acute complications of cirrhosis were identified. The overall clinical picture suggested that dysgeusia-associated malnutrition, likely exacerbated by medication exposure in the context of portal hypertension, contributed substantially to hepatic decompensation. This case underscores the overlooked impact of taste disturbances in cirrhotic patients and highlights the importance of early identification, medication review, and nutritional intervention to mitigate malnutrition-related complications.
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