Effect of Pancreatic Enzymes on Zinc Absorption in Cystic Fibrosis

Easley, David; Krebs, Nancy F.; Jefferson, Mary; Miller, Leland V.; Erskine, Jamie; Accurso, Frank J.; Hambidge, K. Michael

doi:10.1097/00005176-199802000-00003

Cited by 50 publications

(24 citation statements)

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“…The mean fractional absorption was approximately half that for normal infants fed a cow milkbased, iron-fortified formula (0.22 Ϯ 0.04) (20). We have observed significant improvement in fractional zinc absorption with pancreatic enzyme replacement in older children (21). Such an effect was not evident in these infants for either feeding type, but the apparent lack of benefit may be related to the small number of infants on enzymes and to the finding that Figure 1.…”

Section: Discussionmentioning

confidence: 70%

Abnormalities in Zinc Homeostasis in Young Infants with Cystic Fibrosis

et al. 2000

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Low plasma zinc concentrations have been reported in approximately 30% of young infants with cystic fibrosis identified by newborn screening. The objective of this study was to examine zinc homeostasis in this population by application of stable isotope methodology. Fifteen infants with cystic fibrosis (9 male, 6 female; 7 breast-fed, 8 formula-fed) were studied at a mean (ϮSD) age of 1.8 Ϯ 0.7 mo. On d 1, 70 Zn was administered intravenously, and 67 Zn was quantitatively administered with all human milk/formula feeds during the day. Three days later, a 3-d metabolic period was initiated, during which time intake was measured and complete urine and fecal collections were obtained. Fractional zinc absorption, total absorbed zinc, endogenous fecal zinc, and net absorbed zinc were measured; fecal fat excretion was also determined. Fractional absorption was significantly higher for the breast-fed infants (0.40 Ϯ 0.21) compared with the formula-fed group (0.13 Ϯ 0.06) (p ϭ 0.01), but with the significantly higher dietary zinc intake of the formula-fed group, total absorbed zinc was higher for those receiving formula (p ϭ 0.01). In 11 infants with complete zinc metabolic data, excretion of endogenous zinc was twofold greater for the formula-fed infants (p Ͻ 0.05); net absorption (mg zinc/d) was negative for both feeding groups: Ϫ0.04 Ϯ 0.52 for breast-fed; Ϫ0.28 Ϯ 0.57 for formula-fed. Endogenous fecal zinc losses correlated with fecal fat excretion (r ϭ 0.89, n ϭ 9, p ϭ 0.001), suggesting interference with normal conservation of endogenously secreted zinc. These findings indicate impaired zinc homeostasis in this population and suggest an explanation for the observations of suboptimal zinc status in many young infants with cystic fibrosis prior to diagnosis and treatment. The prevalence of zinc deficiency in individuals with cystic fibrosis has been an area of some uncertainty. Young infants, because of their rapid rates of growth, have relatively high physiologic zinc requirements. There have been several reports of young infants with cystic fibrosis presenting with signs and symptoms of severe zinc deficiency (1-3). Previous observations from the Colorado Newborn Screening Program suggested that zinc status was frequently suboptimal by 6 wk of age in infants found to have cystic fibrosis. Nearly 30% of subjects were found to have plasma zinc concentrations below the normal range, consistent with moderate zinc deficiency. In the same infants, treatment with pancreatic enzymes was associated with significant increases in plasma zinc concentrations (4). To investigate the potential underlying perturbations, we undertook detailed studies of zinc metabolism in these infants by the application of zinc stable isotope methodology.The objectives were to examine fractional absorption and fecal excretion of endogenous zinc according to type of feeding and degree of fat malabsorption. METHODS Study design.This was a cross-sectional study of zinc homeostasis in young infants with cystic fibrosis who were identified by newborn ...

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Section: Discussionmentioning

confidence: 70%

Abnormalities in Zinc Homeostasis in Young Infants with Cystic Fibrosis

et al. 2000

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“…In this population it is reflected by their higher H Z-score and serum cholesterol values. The group of Hambidge showed a decreased fractional absorption of Zn in PI CF and its increase by pancreatic enzyme supplementation (2). The faecal Zn loss correlated with faecal fat loss (32).…”

Section: Discussionmentioning

confidence: 95%

“…Since in our healthy controls (1) 12.6 % has a serum Zn concentration below the lower cut-off of the NHANES II study (3), they could be considered as a population at risk for Zn deficiency. Therefore it is interesting to have a closer look at populations with diseases known to cause increased Zn losses such as CF (2,32). Especially since the data on prevalence of Zn deficiency in the CF population are inconsistent (32)(33)(34)(35)(36).…”

Section: Discussionmentioning

confidence: 99%

Serum Zinc Concentrations in Cystic Fibrosis Patients Aged Above 4 Years: A Cross-sectional Evaluation

Biervliet

Velde

et al. 2007

Biol Trace Elem Res

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Aim: Assess the risk of zinc (Zn) deficiency in the older cystic fibrosis (CF) population. Method:Cross sectional investigation of all CF patients above the age of 4 followed at the Ghent university centre between 2002 and 2003. Data on age, weight and height z-score, pancreatic and pulmonary functions, chronic pseudomonas infection and CF transmembrane conductance regulator (CFTR) mutations were collected. Serum Zn, vitamin A, E, retinol binding protein (RBP), albumin, sedimentation rate, total IgG and cholesterol were determined. Serum Zn was compared with a local healthy control group (1) and with literature data (3). Results: 101 patients (median age 16 years) were included. There was no difference in serum Zn concentration between CF patients and controls. In CF patients no difference in serum Zn concentration between pancreatic sufficient or insufficient patients was seen. Serum Zn was not associated to nutritional status or height Z-score. A significant association serum Zn to serum albumin (p< 0.0005) and to vitamin A (p< 0.01) was seen. No associations of serum Zn to serum vitamin E, RBP, cholesterol or CFTR were present. There is a significant association serum Zn -forced vital capacity (p<0.01). Serum Zn was not associated to inflammatory parameters or chronic pseudomonas infection. Conclusion: Comparison of CF patients with local controls revealed no significant differences. However, since persisting steatorrhoea increases Zn loss (2) and 12.6% of our population has a serum Zn below the P 2.5 value of the NHANES II study (3), there could remain an increased risk of Zn deficiency in some CF patients. Further on the association with pulmonary function needs more investigation.

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“…Stable isotope studies have demonstrated lower absorption in infants and adolescents, especially without enzyme replacement therapy [53], and fecal excretion of endogenous zinc was observed in infants to significantly correlate with fecal fat excretion [54]. For infants and children <2 years of age who are not growing despite apparently adequate nutritional intake, a 6-month trial of zinc supplementation (1 mg zinc/kg/day) has been recommended [55].…”

Section: Acquired Zinc Deficiencymentioning

confidence: 99%

Update on Zinc Deficiency and Excess in Clinical Pediatric Practice

Krebs¹

2013

Ann Nutr Metab

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The critical importance of adequate zinc status to human health, including normal growth and development, is indisputable. The high prevalence of zinc deficiency on a global basis and its importance to public health have been well documented through large-scale randomized controlled zinc supplementation trials. Similar evidence in the clinical setting, however, is much less widely available due to the nonspecific features of zinc deficiency and to the lack of sensitive biomarkers to detect zinc deficiency, especially that of a mild degree of severity. The current understanding of zinc homeostasis indicates that the primary determinants of zinc absorption are the amount of zinc ingested and dietary phytate, the latter having a major effect on zinc bioavailability. In normal as well as in many pathologic conditions, the gastrointestinal tract is the major site of zinc losses resulting from secretion of endogenous zinc into the lumen and subsequent excretion in the feces. The amount excreted is dependent on host status, the amount reabsorbed, and sometimes the presence of pathophysiologic conditions, including diarrhea and steatorrhea. Assessment in the clinical setting dictates that the clinician obtain a careful medical and diet history, recognize clinical presentations in which zinc adequacy may be compromised, and link this risk with nonspecific but plausible manifestations of deficiency. Examples discussed in this article include primary zinc deficiency due to dietary inadequacy (older breastfed infants or toddlers without zinc-rich complementary foods); genetically based deficiency (acrodermatitis enteropathica, acquired zinc deficiency of lactogenic origin), and acquired secondary deficiency in low birth weight and prematurity, gastrointestinal and hepatic disease, and cystic fibrosis. Evidence for efficacy of zinc therapy with pharmacologic doses for two conditions, Wilson's disease and viral upper respiratory infections, is also discussed.

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Effect of Pancreatic Enzymes on Zinc Absorption in Cystic Fibrosis

Abstract: These results indicate that fractional absorption of zinc is impaired by pancreatic insufficiency in patients with cystic fibrosis, and is improved by exocrine pancreatic enzyme replacement.

Cited by 50 publications

References 5 publications

Abnormalities in Zinc Homeostasis in Young Infants with Cystic Fibrosis

Abnormalities in Zinc Homeostasis in Young Infants with Cystic Fibrosis

Serum Zinc Concentrations in Cystic Fibrosis Patients Aged Above 4 Years: A Cross-sectional Evaluation

Update on Zinc Deficiency and Excess in Clinical Pediatric Practice

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