Association between Zinc Deficiency and Hepatic Encephalopathy in Outpatients with Cirrhosis at Phrapokklao Hospital.

Abstract

BACKGROUND: Zinc is an essential micronutrient that serves as a component of more than 300 enzymes. Zinc homeostasis is primarily regulated by the liver. Therefore, patients with liver disease, particularly cirrhosis, experience disrupted zinc homeostasis, which leads to zinc deficiency. Zinc deficiency impairs the enzymatic activity involved in the urea cycle, resulting in elevated blood ammonia levels. Consequently, zinc deficiency is considered one of the contributing factors to hepatic encephalopathy in cirrhotic patients. Treating zinc deficiency alongside other etiologies may help reduce the occurrence of hepatic encephalopathy, improve quality of life, and decrease mortality.

OBJECTIVES: To study plasma zinc deficiency between patients with liver cirrhosis who had hepatic encephalopathy and those without hepatic encephalopathy.

METHODS: Outpatients with liver cirrhosis at Phrapokklao Hospital, with and without hepatic encephalopathy, underwent blood tests to assess plasma zinc levels, liver function tests, renal function tests, and inflammatory markers, including ESR and C-reactive protein.

RESULTS: A total of 41 patients were enrolled, 6 of whom had hepatic encephalopathy, and 35 who did not. All patients in the hepatic encephalopathy group had a Child-Pugh score of Class B, whereas nearly all patients in the non-hepatic encephalopathy group had a Child-Pugh score of Class A (97.1%), with only one patient classified as Class B. No patients with Child-Pugh Class C were included in this study. Zinc deficiency was found in all patients with hepatic encephalopathy, compared with 22.9% in those without hepatic encephalopathy, a difference that was statistically significant (p=0.001).

CONCLUSIONS: Patients with liver cirrhosis and hepatic encephalopathy had a significantly higher prevalence of zinc deficiency than those without hepatic encephalopathy.