Journal of Practical Hepatology ›› 2022, Vol. 25 ›› Issue (1): 74-78.doi: 10.3969/j.issn.1672-5069.2022.01.019

• Liver cirrhosis • Previous Articles     Next Articles

Serum ammonia level changes and its correlation to cognitive impairment in patients with hepatitis B cirrhosis and hepatic encephalopathy

Li Yanle, Liu Xiaoyu, Yao Jianning, et al   

  1. Department of Gastroenterology, First Affiliated Hospital, Zhengzhou University, Zhengzhou 450000,Henan Province, China
  • Received:2021-03-08 Published:2022-01-12

Abstract: Objective The aim of this study was to investigate serum ammonia level changes and itscorrelation to cognitive impairment (CI) in patients with hepatitis B cirrhosis and hepatic encephalopathy (HE). Methods There were 94 patients with hepatitis B liver cirrhosis and HE encountered in our hospital between March 2018 and September 2020, the cognitive impairment was estimated by Montreal cognitive assessment scale (MoCA) and homeostasis model assessment-insulin resistance (HOMA-IR) wascalculated. The Logistic regression model was applied to analyze the risk factors impacting cognitive impairment, and the area under receiver operating characteristic (AUC) was used to predict the occurrence of hepatic coma. Results There were 32 cases of hepatic coma out of 94 patients (34.0%) in our series; the blood ammonia level in patients with hepatic coma was (120.7±18.2) μmol/L, significantly higher than [(76.4±18.3)μmol/L,P<0.05], and the total score of MoCA was (13.7±1.2), significantly lower than [(18.2±2.9), P<0.05] in patients with mild to moderate CI; the scores of visuospatial executive ability, naming, attention, language, abstraction, delayed memory and orientation were (1.5±0.6),(1.6±0.7),(2.1±1.0),(1.7±0.6),(0.9±0.3),(2.0±0.8)and (4.9±0.8), all significantly lower than [(2.7±1.0),(2.2±0.9),(3.4±1.2),(2.5±0.7),(1.5±0.4),(4.4±1.1) and (5.4±1.0),respectively, P<0.05] in patients with mild to moderate CI; there was a significant negative correlation between serum ammonia levels and total MoCA scores in patients with hepatitis B cirrhosis and HE (r=-0.511, P<0.001); the Logistic multivariate analysis showed that blood ammonia (β=-0.529,95% CI=0.432-0.803, P<0.001), serum high sensitivity C-reactive protein levels (β= -0.345,95% CI=0.518-0.968,P =0.030) and HOMA-IR (β=-0.761,95% CI=0.289-0.755, P=0.002) were the independent influencing factors for patients with hepatic coma; the performance of our established prediction model: P=1/[1+e(0.242+0.980X1+0.529X2+0.345X3+0.761X4)] was excellent with the AUC of 0.843 (SE=0.042,95%CI=0.760-0.926,P<0.001), and the sensitivity and specificity of 0.806 and 0.781, respectively in predicting the occurrence of hepatic coma. Conclusion The cognitive functions of patients with hepatitis B cirrhosis and HE is closely related to blood ammonialevels, and it might be helpful to predict the risk of hepatic coma by monitoring blood ammonia levels.

Key words: Liver cirrhosis, Hepatic encephalopathy, Blood ammonia, Cognitive impairment, Diagnostic trial