Evaluation of treatment with zinc acetate hydrate in patients with liver cirrhosis complicated by zinc deficiency

Abstract

Aim: In Japan, no zinc preparation had been approved for therapeutic purposes before March 2017. Zinc acetate hydrate was recently approved for the treatment of hypozincemia. We evaluated the efficacy and safety of treatment with zinc acetate hydrate.Methods: A total of 97 patients with cirrhosis complicated by hypozincemia were treated with zinc acetate hydrate, and their serum zinc normalization rates; factors contributing to normalization; changes in blood ammonia levels; branched-chain amino acids-to-tyrosine ratios; levels of albumin, hemoglobin, alkaline phosphatase, serum copper, and iron; incidence of adverse events; improvement in subjective symptoms; and serum zinc levels taken at 3 months post-treatment were determined.Results: The cumulative serum zinc normalization rates, when normalization was defined as achievement of a serum zinc level ≥80 μg/dL, after 2, 4, and 6 months of treatment were 64.9%, 80.3%, and 82.5%, respectively. Multivariate analysis identified an albumin level of ≥3.3 g/dL and branched-chain amino acids to tyrosine ratio of ≥3.46 as factors contributing to zinc normalization within 3 months of treatment. Treatment resulted in a significant decrease in blood ammonia and serum copper levels, and significant increases in branched-chain amino acidsto-tyrosine ratios and alkaline phosphatase levels. Seven (7.2%) patients prematurely discontinued treatment due to hypocupremia. By the end of treatment, subjective symptoms had resolved in 46.2% of patients. By 3 months post-treatment, serum zinc levels had reverted to levels close to those at baseline.Conclusions: Treatment with zinc acetate hydrate resulted in normalization of serum zinc levels at a high rate. The main reasons for discontinuation of treatment included hypocupremia.

Administration of zinc to preterm infants with hypozincemia does not reduce serum copper concentrations in most cases: a single-center retrospective observational study

“…The administration of zinc acetate dihydrate was previously predicted to reduce serum copper concentrations [ 7 ]; however, in the present study on preterm infants, there were more cases in which serum copper concentrations did not decrease. Since significant differences were observed in PMA and serum zinc concentrations before the start of administration between the groups with and without decreased serum copper concentrations, we proposed the following three mechanisms.…”

“…A decrease in copper concentrations has been reported as adverse effects of zinc administration [ 7 ]. The intestinal absorption of zinc and copper is performed by transporters in small intestinal epithelial cells.…”

Zinc Administration and Improved Serum Markers of Hepatic Fibrosis in Patients with Autoimmune Hepatitis

“…In this study, patients took 150 mg of polaprezinc (containing 34 mg of elemental zinc) every day. In contrast, there have been reports of copper deficiency with the long-term administration of polaprezinc and zinc acetate [61][62][63], as well as reports that caution should be exercised when using zinc acetate rather than polaprezinc [64]. In this study involving polaprezinc, there were no cases of serum copper below baseline levels and no adverse physical findings, such as anemia or neurological symptoms, were observed, including in preexcluded subjects because of their insufficiency of taking polaprezinc.…”

Low Levels of Serum Zinc Associate with Malnutrition Risk Assessed by the Royal Free Hospital-Nutritional Prioritizing Tool in Cirrhosis

“…It has been suggested that zinc deficiency in cirrhosis is influenced by multifaceted factors. Poor dietary intake, maldigestion/malabsorption through gastrointestinal tract, hypoalbuminemia, excess excretion in the urine, and nutritional deficiency have been documented as possible mechanisms [2,24]. Moreover, anorexia can be induced by the intestinal mucosal atrophy due to zinc deficiency along with decrease in digestive juice secretion and impaired gastrointestinal motility [25].…”

“…Last, it is suggested that zinc ions generally bind to albumin, whereas a decrease in albumin can result in the formation of non-albuminbound zinc ions, which are excreted into the urine [32]. Therefore, cirrhotics tend to have low levels of serum albumin, and thus, are at increased risk of zinc deficiency [24,33]. To avoid this influence, we have established two multivariate models, and each incorporating index relevant Given high malnutrition risk closely relevant to zinc deficiency, and its intimate overlap with sarcopenia, we suppose it may be beneficial to combine zinc and BCAA supplementation therapy.…”