Zinc supplementation and amino acid-nitrogen metabolism in patients with advanced cirrhosis

Abstract

Zinc deficiency is common in cirrhosis and has been tent is common in patients with advanced cirrhosis, involved in the altered nitrogen metabolism. In this particularly of alcohol origin, 2 but the biochemical basis study, we measured the effects of zinc supplementation for zinc deficiency is still unknown. Several factors, on the dynamics of amino acid-derived urea synthesis such as poor dietary intake, impaired intestinal absorpin cirrhosis with mild or latent encephalopathy. The he-tion, and excessive urinary losses may be responsible patic conversion of amino acids into urea was studied in for reduced whole-body zinc content. rent hepatic encephalopathy, zinc levels after zinc for hepatocellular failure and encephalopathy, served as controls. Plasma zinc levels were reduced in all pa-supplementation and artificially induced zinc defitients and returned to normal after oral zinc. The ala-ciency correlated closely with mental state and electronine-stimulated urea nitrogen synthesis rate in relation encephalography tracings. 4 In a randomized doubleto a-amino-N concentration-the functional hepatic ni-blind trial, zinc sulfate oral supplements increased to trogen clearance-increased by 25% after zinc supple-normal plasma zinc levels of cirrhotic patients and sigmentation, i.e., more urea was produced at any a-amino-nificantly improved mild encephalopathy of the chronic N concentration. Basal and alanine-induced glucagon type.5 During treatment, ammonia levels decreased, decreased by 50%, and the ammonia response to alanine and plasma urea concentration increased. The results decreased by 30%. Psychometric tests improved, as did routine and dynamic liver function tests and the Child-were not confirmed in a short-term crossover study Pugh score. Also, the plasma concentration of lipid per-with zinc acetate supplements, which failed to normaloxides was reduced by zinc. No significant changes were ize plasma zinc levels. 6 Also episodes of acute encephaobserved in the control group. Our data indicate that lopathy after gastrointestinal hemorrhage have been long-term oral zinc speeds up the kinetics of urea forma-successfully treated with zinc. 7 In cirrhotic rats, zinc tion from amino acids and ammonia. Changes in the hor-supplementation was shown to increase the hepatic ac- be the biochemical basis for the beneficial effects of zinc on mental state in humans. Zinc is considered an essential trace element for sevThe liver plays a pivotal role in amino acid/protein eral metabolic processes, exerting a protective action disposition. Most of the amino acid nitrogen that is not on liver cell activity and possibly preventing cellular used for protein synthesis is converted by hepatocytes damage caused by oxidative stress.1 Reduced zinc con-into urea, which is irreversibly lost in the urine. The process may be quantified, after standardization for to study the effects of disease, hormone, drugs, and Received March 2, 1995; accepted December 11, 1995. dietary manipulations on the dynamics of amino acidSupported by a gr...

Zinc as a Rescue Therapy for Acute Liver Failure: Report of 3 Cases

“…The acute effects involve two mechanisms: protection of protein sulfhydryls or reduction of -OH formation from H2O2 through the antagonism of redox-active transition metals, such as iron and copper [19]. These properties has led to the theory that zinc may be capable of reducing cellular injury that might have a component of sitespecific oxidative damage such as post ischemic tissue damage [19] and also there are some hopeful experiences in management of advances liver cirrhosis and hepatic encephalopathy [20].…”

“…Based on these properties of Zinc, It has been evaluated in a varieties of chronic liver disease with inconsistent results [20][21][22]. In this article we report the results of treatment with Zinc as a salvage therapy in addition to conservative ICU care and its usage as a bridge until definite diagnosis and management of acute liver failure if any at all.…”

Therapeutic Effectiveness of Nutrition Therapy in Pediatric Patients with Chronic Liver Diseases Awaiting Liver Transplantation

“…The pre-transplant daily nutritional support, equal to 130-150% of the basal energy expenditure (Alonso, 2008;Greer, Lehnert, Lewindon, Cleghorn, & Shepherd, 2003;Novy, & Schwarz, 1997;Shepherd, 1996;Ramaccioni, Soriano, Arumugam, & Klish, 2000;Heubi, Helman, Melvin, & Shulman, 2002;Campos, Matias, & Coelho 2002;Falcão & Tannuri, 2002), consisted of the supply of a lipid emulsion of long-chain triglyceride/medium-chain triglyceride in a ratio of 3:2, liposoluble vitamins, and micronutrients (Johnson, Young, Cotter, Lin, & Rowe, 1990;Lai & Chen, 2000;Marchesini, Fabbri, Bianchi, Brizi, & Zoli, 1996). Oral intake was the administration route of preference.…”

Minimal Hepatic Encephalopathy (MHE)

“…66,67 Psychometric test batteries that shall be used for the diagnosis of MHE ought to examine exactly the fields of cognition: visual perception, visuo-spatial orientation, visual construction, concentration, attention and memory. 29 The small number of neuropsychological tests represent the cerebral disfunction of MHE. The number connection test (NCT) is the most widely used test in the psychometric assessment of cirrhotic patients.…”