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June 4, 2008
Letter to the Editor

Denture cream
An unusual source of excess zinc, leading to hypocupremia and neurologic disease

August 26, 2008 issue
71 (9) 639-643

Abstract

Background: Chronic, excess zinc intake can result in copper deficiency and profound neurologic disease. However, when hyperzincemia is identified, the source often remains elusive. We identified four patients, one previously reported, with various neurologic abnormalities in the setting of hypocupremia and hyperzincemia. Each of these patients wore dentures and used very large amounts of denture cream chronically.
Objective: To determine zinc concentration in the denture creams used by the patients as a possible source of excess zinc ingestion.
Methods: Detailed clinical and laboratory data for each patient were compiled. Tubes of denture adhesives were analyzed for zinc content using dynamic reaction cell-inductively coupled plasma-mass spectrometry. Patients received copper supplementation. Copper and zinc levels were obtained post-treatment at varying intervals.
Results: Zinc concentrations ranging from about 17,000 to 34,000 μg/g were identified in Fixodent and Poli-Grip denture creams. Serum zinc levels improved in three patients following cessation of denture cream use. Copper supplementation resulted in mild neurologic improvement in two patients who stopped using denture cream. No alternative source of excess zinc ingestion or explanation for hypocupremia was identified.
Conclusion: Denture cream contains zinc, and chronic excessive use may result in hypocupremia and serious neurologic disease.

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Letters to the Editor
28 October 2008
Denture cream: An unusual source of excess zinc, leading to hypocupremia and neurologic disease
Marco Spinazzi, University of Padova
Mario Armani

We read with interest the article by Nations et al. describing four additional cases of copper deficiency myeloneuropathy in association with hyperzincemia and chronic use of denture creams containing zinc. [1]

We previously reported a patient with copper deficiency myeloneuropathy and zinc excess associated with over 15 years using a similar denture cream. [2] The daily amount of zinc oxide applied with the adhesive was about 150 mg. Even though there are no data on zinc bioavailability from this source, we agree with Nations et al. that these findings prompt important safety concerns on the chronic use of denture creams containing zinc.

Considering the potential detrimental effects to those exposed to these agents and the severe disability caused by copper deficiency myeloneuropathy, urgent verification is warranted. Even though many denture creams contain zinc, others do not. Those without zinc may contain polymethylvinyl ether/maleic acid and partial salts of sodium, calcium, magnesium. Therefore, clinicians treating patients with copper deficiency myeloneuropathy should ask patients about composition and usage before inferring a cause-effect mechanism.

Some patients with copper deficiency myeloneuropathy show evidence of zinc overload with elevated urine but not plasma zinc. [2-3] We observed persistent hyperzincuria with normal serum zinc in our patient for several years after she discontinued use of the denture cream. The underlying mechanism is unknown, but one hypothesis is that chronic zinc intoxication could have increased body zinc storage requiring long-term renal excretion of zinc or--less likely--a different, unknown mechanism of zinc overload. Therefore, we suggest that follow-up of all the patients after zinc denture cream discontinuation should always include 24-hour urine testing in addition to serum zinc levels.

Moreover, the apparently limited prevalence of myeloneuropathy among denture cream users may suggest that unless an abuse of the denture cream occurs, as in some of the patients described by Nations et al. [1], additional factors could combine with zinc excess to precipitate the profound copper deficiency observed in this condition. Interestingly, many of the reported cases of copper deficiency myeloneuropathy showed evidence of both zinc excess and previous gastric surgery, malnutrition, or other malabsorption syndromes. [2-3]

It is possible that copper deficiency has a multifactorial genesis that should be specifically investigated, since some predisposing conditions may be subclinical (i.e., celiac disease) but increase the risk of recurrence of micronutrients deficiencies.

References

1. Nations SP, Boyer PJ, Love LA, et al. Denture cream. An unusual source of excess zinc, leading to hypocupremia and neurologic disease. Neurology 2008;71:639-643.

2. Spinazzi M, De Lazzari F, Tavolato B et al. Myelo-optico-neuropathy in copper deficiency occurring after partial gastrectomy. Do small bowel bacterial overgrowth syndrome and occult zinc ingestion tip the balance? J Neurol 2007;254:1012-1017.

3. Kumar N, Gross JB Jr, Ahlskog JE. Copper deficiency myelopathy produces a clinical picture like subacute combined degeneration. Neurology 2004;63:33-39.

Editor's Note: The authors of the article were offered the opportunity to respond but declined.

Disclosure: The authors report no disclosures.

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Published In

Neurology®
Volume 71Number 9August 26, 2008
Pages: 639-643
PubMed: 18525032

Publication History

Published online: June 4, 2008
Published in print: August 26, 2008

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Authors

Affiliations & Disclosures

S. P. Nations, MD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
P. J. Boyer, MD, PhD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
L. A. Love, MD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
M. F. Burritt, PhD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
J. A. Butz, BA
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
G. I. Wolfe, MD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
L. S. Hynan, PhD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
J. Reisch, PhD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.
J. R. Trivedi, MD
From the Departments of Neurology (S.P.N., L.A.L, G.I.W., J.R.T.) and Clinical Sciences (L.S.H., J.R.), University of Texas Southwestern Medical Center, Dallas; the Department of Pathology (P.J.B.), University of Colorado Health Sciences Center; and the Department of Laboratory Medicine and Pathology (M.F.B., J.A.B.), Mayo Clinic, Rochester, MN.

Notes

Address correspondence and reprint requests to Dr. Sharon P. Nations, Department of Neurology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8897 [email protected]

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