Effects of low dose zinc supplementation on biochemical markers in non-alcoholic cirrhosis: a randomized clinical trial

ABSTRACT

The present study aimed to evaluate the effects of low dose zinc [Zn] supplementation on biochemical markers and underlying disease status in non-alcoholic cirrhotic patients. We enrolled 60 cirrhotic patients in a double-blind, placebo-controlled, randomized clinical trial. All patients in the interventional group [n = 30] received long-term, low dose Zn supplementation [50 mg elemental Zn sulfate daily]. The control group [n = 30] received placebo [starch]. Child-Pugh scores and biochemical markers were assessed for both interventional and control groups at the first day and the end of the 90th day of the interventional period. A per-protocol analysis was performed after excluding all participants who did not receive or complete the randomized intervention. The mean differences of quantitative variables between and within groups were evaluated by independent samples t-test and paired-samples t-test, respectively. SPSS version 13.00 was used for statistical analysis. In the initial evaluation, 16 [53.30%] patients from the interventional group had a Child-Pugh score of 5-8 and 14 [46. 70%] had a score of 9-12. In the control group 18 [60.00%] had a Child-Pugh score of 5-8 and 12 [40.00%] scored 9-12. After three months the mean Child-Pugh score in the interventional group showed a significant improvement [from 6.56 +/- 0.21 to 5.72 +/- 0.22, P = 0.001] whereas in the control group despite no significant decline, the mean Child-Pugh score increased slightly [from 6.25 +/- 0.27 to 6.67 +/- 0.31, P = 0.14]. Zn supplementation significantly decreased copper [Cu; P = 0.01] and creatinine [Cr; P < 0.0001] levels. In this study, we determined that low dose Zn supplementation could prevent deterioration of clinical status of cirrhosis and prevent excess Cu accumulation in non-alcoholic cirrhotic patients. Zn supplementation produces metabolic effects and trends towards improvements in liver function, hepatic encephalopathy, and nutritional status