Zinc-induced copper deficiency: a report of three cases initially recognized on bone marrow examination.

Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75390-9072, USA.
American Journal of Clinical Pathology (Impact Factor: 2.51). 02/2005; 123(1):125-31.
Source: PubMed

ABSTRACT Copper deficiency is a rare cause of sideroblastic anemia and neutropenia that often is not suspected clinically. The morphologic findings in bone marrow, while not pathognomonic, are sufficiently characteristic to suggest the diagnosis, leading to further testing to establish the correct diagnosis. Excess zinc ingestion is among the causes of copper deficiency. We present 3 cases of zinc-induced copper deficiency in which the diagnosis first was suggested on the basis of bone marrow examination. The first patient was a 47-year-old man with a debilitating peripheral neuropathy that had progressed during the previous 18 months, mild anemia, and severe neutropenia. The second was a 21-year-old man receiving zinc supplementation for acrodermatitis enteropathica in whom moderate normocytic anemia and neutropenia developed. The third patient was a 42-year-old man with anemia, severe neutropenia, and a peripheral neuropathy that had progressed during 8 months. The bone marrow findings in all cases suggested copper deficiency, which was confirmed by further laboratory testing and determined to be due to zinc excess. The morphologic features, clinical manifestations, differential diagnosis, and pathogenetic mechanisms are discussed.

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    • "It is noteworthy that deficiency of individual multivalent cations (such as iron) has a profound effect on how the brain barrier systems transport other cations (such as copper) between the blood, brain interstitial fluid and CSF3132. Interestingly, disruption of homeostasis of individual multivalent cations may affect the amount of other multivalent cations32333435; for instance it was shown that excess zinc ingestion is among the causes of copper deficiency34. As another example, systemic iron levels altered the transport of copper across the brain barriers; more specifically, in an iron-deficient rat model, a considerable increase (+55%) of copper levels in the CSF, brain parenchyma and the choroid plexus was observed, while no effect was detected on CSF iron levels31. "
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    Scientific Reports 10/2013; 3:2782. DOI:10.1038/srep02782 · 5.58 Impact Factor
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    • "Zinc is one of the most abundant divalent metals in living organisms (2.3 g of zinc for an average person) and it is an essential cofactor of many metabolic enzymes and a group of transcription factors [2]. Unlikely, this essential trace element in the form of inorganic salt onerously invites fatal organ failure and induces the copper deficiency [3]. Therefore, demand is on the rise for selective recognition of zinc ions in biological systems enabling accurate and timely diagnosis. "
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    • "The clinical and radiological picture is usually indistinguishable from subacute combined degeneration due to vitamin B12 (cobalamin) deficiency (SCD) [40, 44], and the syndrome is thought to represent the human counterpart of swayback or enzootic ataxia, a copper deficiency myelopathy (CDM) occurring in ruminants [3]. Other, less frequently reported and less clearly causally related neurological associations of acquired copper deficiency include isolated peripheral neuropathy [20, 86], motor neuron disease [84], myopathy [46], cerebral demyelination [65, 74], cognitive dysfunction [58, 77] and optic neuropathy [20, 74]. "
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