Effect of oral zinc in hepatic encephalopathy remains unclear: authors’ reply

Abstract

Sirs, We thank Coughlan and colleagues for their comments1 relating to our recently published paper.2 The first suggestion is that we overestimated any treatment effect on the quality of life, due to detection bias. Detection bias arises from the knowledge of patient assignment, and the blinding of patients prevented this type of bias. The self-completion version of the SF-36 is preferred because it eliminates observer bias; however, this version is not suitable for inpatients3 and an interview can improve the response rate. However, this study was not double-blind. Although treatment bias was unavoidable, detection bias by the observer was minimized because the observer was unaware of the treatment assignment. The second suggestion is that the assessment of hepatic encephalopathy (HE) was subjective and temporary, due to fluctuations in the patients’ condition. We assessed only those patients with recurrent episodic encephalopathy, and excluded those patients with a continuously altered mental state (persistent HE), because the responses of patients with persistent HE may not be reproducible. The third suggestion is the possibility that the HE improvements were caused by the potential neurological effect of l-carnosine, and not the zinc. However, we found that the improvements in HE were accompanied by a decrease in the blood ammonia level. Consequently, we concluded that the improvements in HE were due to the zinc supplementation because l-carnosine has no known effect on ammonia metabolism. Finally, we do agree that further, well-designed, double-blind, randomized controlled trials are needed to confirm our results. Declaration of personal and funding interests: None.