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<meta name="robots" content="INDEX,FOLLOW,NOARCHIVE" /><meta name="citation_inbook_title" content="LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]" /><meta name="citation_title" content="Copper" /><meta name="citation_publisher" content="National Institute of Diabetes and Digestive and Kidney Diseases" /><meta name="citation_date" content="2017/10/30" /><meta name="citation_pmid" content="31643420" /><meta name="citation_fulltext_html_url" content="https://www.ncbi.nlm.nih.gov/books/NBK548090/" /><link rel="schema.DC" href="http://purl.org/DC/elements/1.0/" /><meta name="DC.Title" content="Copper" /><meta name="DC.Type" content="Text" /><meta name="DC.Publisher" content="National Institute of Diabetes and Digestive and Kidney Diseases" /><meta name="DC.Date" content="2017/10/30" /><meta name="DC.Identifier" content="https://www.ncbi.nlm.nih.gov/books/NBK548090/" /><meta name="description" content="Copper is an essential trace element that is included in some over-the-counter multivitamin and mineral supplements, even though copper deficiency is quite rare and supplementation is rarely needed. The amounts of copper found in typical supplements has not been associated with serum enzyme elevations or with clinically apparent liver injury. However, accidental or intentional copper overdose can cause an acute liver injury and chronic ingestion of excessive amounts of copper can result in copper overload and chronic liver injury." /><meta name="og:title" content="Copper" /><meta name="og:type" content="book" /><meta name="og:description" content="Copper is an essential trace element that is included in some over-the-counter multivitamin and mineral supplements, even though copper deficiency is quite rare and supplementation is rarely needed. The amounts of copper found in typical supplements has not been associated with serum enzyme elevations or with clinically apparent liver injury. However, accidental or intentional copper overdose can cause an acute liver injury and chronic ingestion of excessive amounts of copper can result in copper overload and chronic liver injury." /><meta name="og:url" content="https://www.ncbi.nlm.nih.gov/books/NBK548090/" /><meta name="og:site_name" content="NCBI Bookshelf" /><meta name="og:image" content="https://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-livertox-lrg.png" /><meta name="twitter:card" content="summary" /><meta name="twitter:site" content="@ncbibooks" /><meta name="bk-non-canon-loc" content="/books/n/livertox/Copper/" /><link rel="canonical" href="https://www.ncbi.nlm.nih.gov/books/NBK548090/" /><link rel="stylesheet" href="/corehtml/pmc/css/figpopup.css" type="text/css" media="screen" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books.min.css" type="text/css" /><link rel="stylesheet" href="/corehtml/pmc/css/bookshelf/2.26/css/books_print.min.css" type="text/css" media="print" /><style type="text/css">p a.figpopup{display:inline !important} .bk_tt {font-family: monospace} .first-line-outdent .bk_ref {display: inline} .body-content h2, .body-content .h2 {border-bottom: 1px solid #97B0C8} .body-content h2.inline {border-bottom: none} a.page-toc-label , .jig-ncbismoothscroll a {text-decoration:none;border:0 !important} .temp-labeled-list .graphic {display:inline-block !important} .temp-labeled-list img{width:100%}</style><script type="text/javascript" src="/corehtml/pmc/js/jquery.hoverIntent.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/common.min.js?_=3.18"> </script><script type="text/javascript" src="/corehtml/pmc/js/large-obj-scrollbars.min.js"> </script><script type="text/javascript">window.name="mainwindow";</script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/book-toc.min.js"> </script><script type="text/javascript" src="/corehtml/pmc/js/bookshelf/2.26/books.min.js"> </script><meta name="book-collection" content="NONE" />
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<div class="pre-content"><div><div class="bk_prnt"><p class="small">NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.</p><p>LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. </p></div><div class="iconblock clearfix whole_rhythm no_top_margin bk_noprnt"><a class="img_link icnblk_img" title="All Drug Records" href="/books/n/livertox/"><img class="source-thumb" src="/corehtml/pmc/pmcgifs/bookshelf/thumbs/th-livertox-lrg.png" alt="Cover of LiverTox" height="100px" width="80px" /></a><div class="icnblk_cntnt eight_col"><h2>LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].</h2><a data-jig="ncbitoggler" href="#__NBK548090_dtls__">Show details</a><div style="display:none" class="ui-widget" id="__NBK548090_dtls__"><div>Bethesda (MD): <a href="https://www.niddk.nih.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Institute of Diabetes and Digestive and Kidney Diseases</a>; 2012-.</div></div><div class="half_rhythm"><ul class="inline_list"><li style="margin-right:1em"><a class="bk_cntns" href="/books/n/livertox/">Drug Records</a></li></ul></div><div class="bk_noprnt"><form method="get" action="/books/n/livertox/" id="bk_srch"><div class="bk_search"><label for="bk_term" class="offscreen_noflow">Search term</label><input type="text" title="Search this book" id="bk_term" name="term" value="" data-jig="ncbiclearbutton" /> <input type="submit" class="jig-ncbibutton" value="Search this book" submit="false" style="padding: 0.1em 0.4em;" /></div></form></div></div><div class="icnblk_cntnt two_col"><div class="pagination bk_noprnt"><a class="active page_link prev" href="/books/n/livertox/Copanlisib/" title="Previous page in this title">< Prev</a><a class="active page_link next" href="/books/n/livertox/Corticosteroids/" title="Next page in this title">Next ></a></div></div></div></div></div>
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<div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><h1 id="_NBK548090_"><span class="title" itemprop="name">Copper</span></h1><p class="small">Last Update: <span itemprop="dateModified">October 30, 2017</span>.</p></div><div class="body-content whole_rhythm" itemprop="text"><div id="Copper.OVERVIEW"><h2 id="_Copper_OVERVIEW_">OVERVIEW</h2><div id="Copper.Introduction"><h3>Introduction</h3><p>Copper is an essential trace element that is included in some over-the-counter multivitamin and mineral supplements, even though copper deficiency is quite rare and supplementation is rarely needed. The amounts of copper found in typical supplements has not been associated with serum enzyme elevations or with clinically apparent liver injury. However, accidental or intentional copper overdose can cause an acute liver injury and chronic ingestion of excessive amounts of copper can result in copper overload and chronic liver injury.</p></div><div id="Copper.Background"><h3>Background</h3><p>Copper is a heavy metal and essential trace element that is found in many human enzymes and transcription factors. The recommended dietary allowance is approximately 1.5 mg per day. Adequate amounts of copper are found in most Western diets, with highest levels found in shellfish, chocolate and nuts. Total body copper concentrations are 50 to 120 mg (0.79 to 1.9 mmol), which is far lower than those of zinc or iron. Copper deficiency is rare and usually due to malnutrition and reduced dietary intake, but can also occur with strict vegetarian diets. Chronic oral exposure to excessive amounts of copper can result in liver injury which is also typical of <a class="def" href="/books/n/livertox/glossary/def-item/glossary.wilson-disease/">Wilson disease</a>, an inherited disease caused by a mutation in the ATPase7B gene, which encodes a hepatic enzyme responsible for the transmembrane transport and excretion of copper. The metabolic defect in Wilson disease leads to accumulation of free copper in liver and blood and secondarily in other organs, particularly brain and kidney. The disease usually presents in childhood or adolescence with neurologic syndromes, signs of advanced liver disease and hemolytic anemia. Excessive dietary intake or environmental exposure to copper is rare in the developed world, but is found in developing countries and particularly India. Nutritional supplements with copper generally have replacement doses of copper and available in many forms. Elemental copper for oral intake is not available in United States.</p></div><div id="Copper.Hepatotoxicity"><h3>Hepatotoxicity</h3><p>Acute hepatotoxicity of copper is usually the result of ingestion of toxic amounts (1 to 10 g), often as a suicide attempt. In children, accidental poisoning can occur, particularly with ingestion of coins. Initial symptoms may be metallic taste and gastrointestinal distress due to gastric or small bowel erosions. Acute overdoses of copper can lead to early appearance of cardiovascular collapse, coma and death within hours. Liver injury tends to arise after 24 to 72 hours and is characterized by marked elevations in serum aminotransferase levels, minimal increases in alkaline phosphatase, early appearance of hepatic failure, and elevation in prothrombin time and ensuing jaundice. Shock and renal failure may also be present as well as rhabdomyolysis and severe hemolytic anemia. The overall clinical pattern of the liver injury is that of acute hepatic necrosis, and the hepatic manifestations resemble the acute toxicity of iron and zinc, and can be reproduced in animals. Shock and rhabdomyolysis may contribute to the serum enzyme elevations while hemolytic anemia may account for some of the increase in total bilirubin levels. Therapy of copper overdose includes gastric lavage, fluid replacement, dimercaprol (BAL) and penicillamine, with blood transfusions for hemolytic anemia and dialysis for acute renal failure.</p><p>Chronic liver injury from copper occurs with <a class="def" href="/books/n/livertox/glossary/def-item/glossary.wilson-disease/">Wilson disease</a>, but has also been described after chronic excessive ingestion of copper and perhaps as a result of chronic environmental exposure, such as from copper tubing used in hemodialysis.</p><p><a class="def" href="/books/n/livertox/glossary/def-item/glossary.likelihood-score/">Likelihood score</a>: A[HD] (well known cause of acute and chronic liver injury but only when taken in high doses).</p><p>Drug Class: <a href="/books/n/livertox/TraceElementsAndMeta/">Trace Elements and Metals</a></p></div></div><div id="Copper.PRODUCT_INFORMATION"><h2 id="_Copper_PRODUCT_INFORMATION_">PRODUCT INFORMATION</h2><div id="Copper.BPI" class="box"><p>
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<b>REPRESENTATIVE TRADE NAMES</b>
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</p><p>Copper Sulfate – Generic</p><p>
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<b>DRUG CLASS</b>
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</p><p>Trace Elements and Metals</p><p>
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<a href="https://dailymed.nlm.nih.gov/dailymed/search.cfm?labeltype=all&query=copper" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">COMPLETE LABELING</a>
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</p><p>Product labeling at DailyMed, National Library of Medicine, NIH</p></div></div><div id="Copper.CHEMICAL_FORMULA_AND_STRUCTURE"><h2 id="_Copper_CHEMICAL_FORMULA_AND_STRUCTURE_">CHEMICAL FORMULA AND STRUCTURE</h2><div id="Copper.T1" class="table"><p class="large-table-link" style="display:none"><span class="right"><a href="/books/NBK548090/table/Copper.T1/?report=objectonly" target="object">View in own window</a></span></p><div class="large_tbl" id="__Copper.T1_lrgtbl__"><table><thead><tr><th id="hd_h_Copper.T1_1_1_1_1" rowspan="1" colspan="1" style="vertical-align:top;">DRUG</th><th id="hd_h_Copper.T1_1_1_1_2" rowspan="1" colspan="1" style="vertical-align:top;">CAS REGISTRY NUMBER</th><th id="hd_h_Copper.T1_1_1_1_3" rowspan="1" colspan="1" style="vertical-align:top;">MOLECULAR FORMULA</th><th id="hd_h_Copper.T1_1_1_1_4" rowspan="1" colspan="1" style="vertical-align:top;">STRUCTURE</th></tr></thead><tbody><tr><td headers="hd_h_Copper.T1_1_1_1_1" rowspan="1" colspan="1" style="vertical-align:top;">Cupric Sulfate</td><td headers="hd_h_Copper.T1_1_1_1_2" rowspan="1" colspan="1" style="vertical-align:top;">
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<a href="https://pubchem.ncbi.nlm.nih.gov/substance/134989998" ref="pagearea=body&targetsite=entrez&targetcat=link&targettype=pubchem">7758-98-7</a>
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</td><td headers="hd_h_Copper.T1_1_1_1_3" rowspan="1" colspan="1" style="vertical-align:top;">Cu.H2-O4-S</td><td headers="hd_h_Copper.T1_1_1_1_4" rowspan="1" colspan="1" style="vertical-align:top;">
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<div class="graphic"><img src="/books/NBK548090/bin/copper_structure.jpg" alt="Chemical Structure for Copper" /></div>
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</td></tr></tbody></table></div></div></div><div id="Copper.ANNOTATED_BIBLIOGRAPHY"><h2 id="_Copper_ANNOTATED_BIBLIOGRAPHY_">ANNOTATED BIBLIOGRAPHY</h2><p>References updated: 30 October 2017</p><ul class="first-line-outdent"><li><div class="bk_ref" id="Copper.R1">Zimmerman HJ. Copper poisoning. In, Zimmerman HJ. Hepatotoxicity: the adverse effects of drugs and other chemicals on the liver. 2nd ed. Philadelphia: Lippincott, 1999, p 347.<div><i>(Review of hepatotoxicity published in 1999 mentions that copper hepatotoxicity may be acute or chronic, the acute poisoning resembling iron hepatotoxicity, the chronic injury leading to cirrhosis and possibly being the cause of Indian childhood cirrhosis).</i></div></div></li><li><div class="bk_ref" id="Copper.R2">Kaplowitz N, DeLeve LD, eds. Drug-induced liver disease. 3rd ed. Amsterdam: Elsevier, 2013.<div><i>(Textbook on hepatotoxicity; the acute hepatotoxicity of copper is not discussed).</i></div></div></li><li><div class="bk_ref" id="Copper.R3">Byrns MC, Penning TM. Treatment of metal exposure. Environmental toxicology: carcinogens and heavy metals. In, Brunton LL, Chabner BA, Knollman BC, eds. Goodman & Gilman's the pharmacological basis of therapeutics. 12th ed. New York: McGraw-Hill, 2011, pp. 1872 -6.<div><i>(Textbook of pharmacology and therapeutics).</i></div></div></li><li><div class="bk_ref" id="Copper.R4">Turnlund JR. Copper. In, Shils ME, Olson JA, Shihe M, Ross AC, eds. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins, 1999, pp. 241-252.<div><i>(Textbook of nutrition).</i></div></div></li><li><div class="bk_ref" id="Copper.R5">Semple AB, Parry WH, Phillips DE. Acute copper poisoning. An outbreak traced to contaminated water from a corroded geyser. Lancet 1960; 2 (7152): 700-1. [<a href="https://pubmed.ncbi.nlm.nih.gov/13750037" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 13750037</span></a>]<div><i>(18 workers in a factory developed gastroenteritis after drinking tea from a single teapot contaminated with copper caused by corrosion of copper pipes; no clinical details given).</i></div></div></li><li><div class="bk_ref" id="Copper.R6">Chowdhury AK, Ghosh S, Pal D. Acute copper sulphate poisoning. J Indian Med Assoc 1961; 36: 330-6. [<a href="https://pubmed.ncbi.nlm.nih.gov/13693318" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 13693318</span></a>]<div><i>(Review of 20 cases of acute copper poisoning, marked by metallic taste, epigastric pain and nausea followed by vomiting, tachycardia, hypotension and jaundice [50%] and/or hemolysis [50%]).</i></div></div></li><li><div class="bk_ref" id="Copper.R7">Gupta PS, Bhargava SP, Sharma ML. Acute copper sulphate poisoning with special reference to its management with corticosteroid therapy. J Assoc Physicians India 1962; 10: 287-92. [<a href="https://pubmed.ncbi.nlm.nih.gov/13903000" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 13903000</span></a>]<div><i>(Review of 150 cases of copper poisoning seen at a single hospital in New Delhi over a 5 year period treated with gastric lavage, dimercaprol [BAL], fluids, transfusions, sedatives and corticosteroids; patient ages 13 to 60 years, 102 cases were mild and 48 severe; jaundice arising in 19%, circulatory collapse in 7% and death in 24 [16%]).</i></div></div></li><li><div class="bk_ref" id="Copper.R8">Wahl PK, Lahiri B, Mathur KS, Kehar U, Wahi PN. Acute copper sulphate poisoning. J Assoc Physicians India 1963; 11: 93-103. [<a href="https://pubmed.ncbi.nlm.nih.gov/13998300" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 13998300</span></a>]<div><i>(Review of 50 cases of copper poisoning admitted over a 2 year period to a single hospital in India, treated with gastric lavage, dimercaprol [BAL] and fluids, 17 patients [34%] developing jaundice, arising between days 2 and 5, ALT ranging from 30 to 150 U/L and autopsy in 7 showing focal necrosis and fatty change in the liver).</i></div></div></li><li><div class="bk_ref" id="Copper.R9">Chuttani HK, Gupta PS, Gulati S, Gupta DN. Acute copper sulfate poisoning. Am J Med 1965; 39: 849-54. [<a href="https://pubmed.ncbi.nlm.nih.gov/5833579" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 5833579</span></a>]<div><i>(Description of 53 patients with acute copper poisoning, ages 14 to 60 years, 32 men and 21 women, usually with suicidal intent, presenting with metallic taste, nausea, vomiting and epigastric burning, jaundice arising in 23%, usually on days 2 or 3, leading to death in some or resolving in 2-5 days, liver showing centrilobular necrosis and cholestasis).</i></div></div></li><li><div class="bk_ref" id="Copper.R10">Fairbanks VF. Copper sulfate-induced hemolytic anemia. Inhibition of glucose-6-phosphate dehydrogenase and other possible etiologic mechanisms. Arch Intern Med 1967; 120: 428-32. [<a href="https://pubmed.ncbi.nlm.nih.gov/4293707" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 4293707</span></a>]<div><i>(22 year old woman had accidental ingestion of copper sulfate and developed nausea, vomiting and diarrhea for 2 days followed by dark urine and hemolysis [hematocrit falling to 20%], with slow recovery; all liver tests were normal).</i></div></div></li><li><div class="bk_ref" id="Copper.R11">Singh MM, Singh G. Biochemical changes in blood in cases of acute copper sulphate poisoning. J Indian Med Assoc 1968; 50: 549-54. [<a href="https://pubmed.ncbi.nlm.nih.gov/5708633" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 5708633</span></a>]<div><i>(Among 40 patients with acute copper poisoning, 27 were men, 13 women, ages 13 to 85 years, AST levels ranged from 36-3400 U/L, ALT 66-440 U/L, bilirubin 0.4-30 mg/dL [most less than 2.0 mg/dL] and 4 patients died, one of hepatic failure and three from hemolysis).</i></div></div></li><li><div class="bk_ref" id="Copper.R12">Deodhar LP, Deshpande CK. Acute copper sulphate poisoning. J Postgrad Med 1968; 14: 38-41. [<a href="https://pubmed.ncbi.nlm.nih.gov/5648509" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 5648509</span></a>]<div><i>(Seven autopsied cases of acute copper intoxication, included 5 who died within hours of presentation and 2 on day 5 with jaundice [bilirubin 7.0 and 7.7 mg/dL] and "cloudy and fatty degeneration of liver cells", with focal and centrilobular necrosis).</i></div></div></li><li><div class="bk_ref" id="Copper.R13">Papadoyanakis N, Katsilambros N, Patsourakos B. Acute copper sulfate poisoning with jaundice. J Ir Med Assoc 1969; 62: 99-100. [<a href="https://pubmed.ncbi.nlm.nih.gov/5776964" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 5776964</span></a>]<div><i>(36 year old man took and overdose of copper sulfate and was admitted in coma three hours later and developed hemolytic anemia and jaundice the following day [bilirubin rising to 6.6 mg/dL, AST 190 U/L], dying 11 days after ingestion and autopsy showing cholestasis and inflammation, but "necrosis was not seen").</i></div></div></li><li><div class="bk_ref" id="Copper.R14">Manzler AD, Schreiner AW. Copper-induced acute hemolytic anemia. A new complication of hemodialysis. Ann Intern Med 1970; 73: 409-12. [<a href="https://pubmed.ncbi.nlm.nih.gov/5455992" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 5455992</span></a>]<div><i>(3 men developed copper intoxication during hemodialysis with acute onset of nausea, diarrhea and lethargy and acute hemolysis; no mention of liver test abnormalities).</i></div></div></li><li><div class="bk_ref" id="Copper.R15">Chugh KS, Singhal PC, Sharma BK. Letter: Methemoglobinemia in acute copper sulfate poisoning. Ann Intern Med 1975; 82: 226-7. [<a href="https://pubmed.ncbi.nlm.nih.gov/1115446" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 1115446</span></a>]<div><i>(27 year old man took an overdose of copper sulfate which led to vomiting and lethargy followed by cyanosis, oliguria, methemoglobinemia, intravascular hemolysis, shock and death 16 hours after the ingestion).</i></div></div></li><li><div class="bk_ref" id="Copper.R16">Klein WJ Jr, Metz EN, Price AR. Acute copper intoxication. A hazard of hemodialysis. Arch Intern Med 1972; 129: 578-82. [<a href="https://pubmed.ncbi.nlm.nih.gov/5019446" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 5019446</span></a>]<div><i>(Hemodialysis using copper tubing can result in significant copper exposure; 3 adults, ages 35 to 53 years, developed headache, myalgias, fatigue, diarrhea and nausea during hemodialysis with severe hemolytic anemia, metabolic acidosis, high serum copper levels, progressive coma and death, sometimes with minor AST and bilirubin elevations).</i></div></div></li><li><div class="bk_ref" id="Copper.R17">Agarwal BN, Bray SH, Bercz P, Plotzker R, Labovitz E. Ineffectiveness of hemodialysis in copper sulphate poisoning. Nephron 1975; 15: 74-7. [<a href="https://pubmed.ncbi.nlm.nih.gov/1128758" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 1128758</span></a>]<div><i>(41 year old woman took an overdose of copper sulfate developing vomiting and diarrhea, and was treated with fluids, EDTA, gastric lavage and hemodialysis, but had progressive hemolysis and liver and renal failure [bilirubin 0.6 mg initially rising to 20.6 mg/dL, AST to >6000 U/L, Alk P 139 U/L, LDH 8,500 U/L, CPK 4,100 U/L], dying after 5 days).</i></div></div></li><li><div class="bk_ref" id="Copper.R18">Stein RS, Jenkins D, Korns ME. Letter: Death after use of cupric sulfate as emetic. JAMA 1976; 235: 801. [<a href="https://pubmed.ncbi.nlm.nih.gov/946302" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 946302</span></a>]<div><i>(44 year old woman with a three-quarter gastrectomy was given cupric sulfate as an emetic after an overdose of diazepam and developed lethargy and hypotension one hour later, followed by severe hemolytic anemia, respiratory, hepatic and renal failure, dying 6 days later).</i></div></div></li><li><div class="bk_ref" id="Copper.R19">Walsh FM, Crosson FJ, Bayley M, McReynolds J, Pearson BJ. Acute copper intoxication. Pathophysiology and therapy with a case report. Am J Dis Child 1977; 131: 149-51. [<a href="https://pubmed.ncbi.nlm.nih.gov/835530" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 835530</span></a>]<div><i>(18 month old boy drank a copper sulfate solution and developed nausea, vomiting and lethargy, high serum copper [1,650 μg/dL] and hemolysis, responding to dimercaprol [BAL] treatment with resolution within one week, liver tests remaining normal).</i></div></div></li><li><div class="bk_ref" id="Copper.R20">Chugh KS, Sharma BK, Singhal PC, Das KC, Datta BN. Acute renal failure following copper sulphate intoxication. Postgrad Med J 1977; 53: 18-23. [<a href="/pmc/articles/PMC2496546/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC2496546</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/876909" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 876909</span></a>]<div><i>(Among 29 patients with acute copper poisoning admitted to a referral hospital in India over a 10 year period, 11 [38%] presented with acute renal failure, usually after 3-8 days [creatinine 2.5-14.5 mg/dL] and liver injury [27%] [bilirubin 1.5-14.5 mg/dL, serum copper 115-8269 µg/dL, hemoglobin 2-9 g/dL]).</i></div></div></li><li><div class="bk_ref" id="Copper.R21">Chugh KS, Sakhuja V. Acute copper intoxication. Int J Artif Organs 1979; 2: 181-2. [<a href="https://pubmed.ncbi.nlm.nih.gov/457302" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 457302</span></a>]<div><i>(Brief review of the clinical manifestations and management of acute copper intoxication).</i></div></div></li><li><div class="bk_ref" id="Copper.R22">Sternlieb I. Copper and the liver. Gastroenterology 1980; 78: 1615-28. [<a href="https://pubmed.ncbi.nlm.nih.gov/6245986" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 6245986</span></a>]<div><i>(Review of the metabolism of copper and its role in Wilson disease).</i></div></div></li><li><div class="bk_ref" id="Copper.R23">Schwartz E, Schmidt E. Refractory shock secondary to copper sulfate ingestion. Ann Emerg Med 1986; 15: 952-4. [<a href="https://pubmed.ncbi.nlm.nih.gov/3740585" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 3740585</span></a>]<div><i>(62 year old man took an overdose of copper sulfate and developed nausea, vomiting and stupor with persistent hypotension followed by severe hemolytic anemia and elevated liver enzymes and death, no details of liver tests provided).</i></div></div></li><li><div class="bk_ref" id="Copper.R24">Yelin G, Taff ML, Sadowski GE. Copper toxicity following massive ingestion of coins. Am J Forensic Med Pathol 1987; 8: 78-85. [<a href="https://pubmed.ncbi.nlm.nih.gov/3578211" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 3578211</span></a>]<div><i>(58 year old woman with severe neuropsychiatric disability, developed nausea, weight loss, jaundice and stupor [bilirubin 11.7 mg/dL, direct bilirubin 7.0 mg/dL, ALT 53 U/L, Alk P 2.2 U/L, pH 6.86, lactate 30.9 mg/dL, hemoglobin 4.6 g/dL, reticulocyte count >20%] and died in coma 38 hours later, autopsy showing 275 coins in stomach and liver with fat, Mallory bodies, fibrosis and excess copper).</i></div></div></li><li><div class="bk_ref" id="Copper.R25">Mueller PD, Benowitz NL. Toxicologic causes of acute abdominal disorders. Emerg Med Clin North Am 1989; 7: 667-82. [<a href="https://pubmed.ncbi.nlm.nih.gov/2663462" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 2663462</span></a>]<div><i>(Review of gastrointestinal toxicity of agents including iron, mercury and copper).</i></div></div></li><li><div class="bk_ref" id="Copper.R26">Hantson P, Lievens M, Mahieu P. Accidental ingestion of a zinc and copper sulfate preparation. J Toxicol Clin Toxicol 1996; 34: 725-30. [<a href="https://pubmed.ncbi.nlm.nih.gov/8941204" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 8941204</span></a>]<div><i>(86 year old woman inadvertently drank a zinc and copper sulfate solution, rapidly developed vomiting and watery diarrhea [copper 209 µg/dL, normal <140: zinc 1979 µg/dL, normal <123], was treated with gastric lavage, hydration, penicillamine and dimercaprol [BAL], but developed hypotension, respiratory and renal failure, while liver tests remained normal; she ultimately recovered).</i></div></div></li><li><div class="bk_ref" id="Copper.R27">Strubelt O, Kremer J, Tilse A, Keogh J, Pentz R, Younes M. Comparative studies on the toxicity of mercury, cadmium, and copper toward the isolated perfused rat liver. J Toxicol Environ Health 1996; 47: 267-83. [<a href="https://pubmed.ncbi.nlm.nih.gov/8604150" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 8604150</span></a>]<div><i>(Comparison of toxicity of equimolar amounts of mercury, cadmium and copper in an isolated, perfused rat liver system found similar patterns of toxicity which appeared to be mitochondrial with reductions in ATP levels).</i></div></div></li><li><div class="bk_ref" id="Copper.R28">Bennett DR, Baird CJ, Chan KM, Crookes PF, Bremner CG, Gottlieb MM, Naritoku WY. Zinc toxicity following massive coin ingestion. Am J Forensic Med Pathol 1997; 18: 148-53. [<a href="https://pubmed.ncbi.nlm.nih.gov/9185931" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 9185931</span></a>]<div><i>(55 year old man with schizophrenia developed nausea, anorexia, epigastric pain and gastrointestinal bleeding, and ultimately was found to have 461 coins in the stomach which were removed surgically, but he developed renal and hepatic failure [peak bilirubin 12.2 mg/dL, ALT 341 U/L, AST 1141 U/L], autopsy showing massive hepatic and acute tubular necrosis).</i></div></div></li><li><div class="bk_ref" id="Copper.R29">Rodeck B, Kardoff R, Melter M. Treatment of copper associated liver disease in childhood. Eur J Med Res 1999; 4: 253-6. [<a href="https://pubmed.ncbi.nlm.nih.gov/10383883" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 10383883</span></a>]<div><i>(Two German children, ages 6 and 10 months, developed abdominal swelling and ascites [bilirubin 3.0 and 8.8 mg/dL, ALT 325 and 170 U/L, GGT 140 U/L], high copper levels found in liver and in well water, one improved with penicillamine therapy, but the second required liver transplantation).</i></div></div></li><li><div class="bk_ref" id="Copper.R30">Takeda T, Yukioka T, Shimazaki S. Cupric sulfate intoxication with rhabdomyolysis, treated with chelating agents and blood purification. Intern Med 2000; 39: 253-5. [<a href="https://pubmed.ncbi.nlm.nih.gov/10772131" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 10772131</span></a>]<div><i>(18 year old man took an overdose of cupric sulfate and developed vomiting and lethargy [serum copper 142 µg/dL, normal <131], was treated with gastric lavage, penicillamine and dimercaprol [BAL], but developed myoglobinemia, hemolysis and rhabdomyolysis [peak CK 3,804 U/L on day 6] with mild renal and liver injury, ultimately resolving after 18 days).</i></div></div></li><li><div class="bk_ref" id="Copper.R31">Dietrich AM, Glindemann D, Pizarro F, Gidi V, Olivares M, Araya M, Camper A, et al. Health and aesthetic impacts of copper corrosion on drinking water. Water Sci Technol 2004; 49(2): 55-62. [<a href="https://pubmed.ncbi.nlm.nih.gov/14982164" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 14982164</span></a>]<div><i>(Corrosion of copper pipes can cause excess copper in the water supply that is associated with metallic taste and increase in gastrointestinal illness).</i></div></div></li><li><div class="bk_ref" id="Copper.R32">Srivastava A, Peshin SS, Kaleekal T, Gupta SK. An epidemiological study of poisoning cases reported to the National Poisons Information Centre, All India Institute of Medical Sciences, New Delhi. Hum Exp Toxicol 2005; 24: 279-85. [<a href="https://pubmed.ncbi.nlm.nih.gov/16004194" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 16004194</span></a>]<div><i>(Among 2719 calls to an Indian poisoning center over a 3 year period, 48 [2%] were concerning copper sulfate).</i></div></div></li><li><div class="bk_ref" id="Copper.R33">Donoso A, Cruces P, Camacho J, Rí JC, Paris E, Mieres JJ. Acute respiratory distress syndrome resulting from inhalation of powdered copper. Clin Toxicol (Phila) 2007; 45: 714-6. [<a href="https://pubmed.ncbi.nlm.nih.gov/17849249" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 17849249</span></a>]<div><i>(2 year old girl spilled copper powder on her face and inhaled some of the contents, developing cough, dyspnea and cyanosis and, on admission, had hypoxia and acidosis, developing respiratory and renal failure and evidence of liver injury over the next several days [AST 105 U/L, ammonia 120 µmol/L, prothrombin index 20%], but ultimately recovered).</i></div></div></li><li><div class="bk_ref" id="Copper.R34">Franchitto N, Gandia-Mailly P, Georges B, Galinier A, Telmon N, DucasséL, Rougé. Acute copper sulphate poisoning: a case report and literature review. Resuscitation 2008; 78: 92-6. [<a href="https://pubmed.ncbi.nlm.nih.gov/18482790" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18482790</span></a>]<div><i>(29 year old man developed vomiting and diarrhea shortly after taking overdose of copper sulfate [homemade rat poison], with fever and acute psychosis, initially with normal liver and renal tests, developing mild hemolytic anemia and renal dysfunction, treated with EDTA and dimercaprol [BAL], and resolving within 1 week).</i></div></div></li><li><div class="bk_ref" id="Copper.R35">Hassan S, Shaikh MU, Ali N, Riaz M. Copper sulphate toxicity in a young male complicated by methemoglobinemia, rhabdomyolysis and renal failure. J Coll Physicians Surg Pak 2010; 20 (7): 490-1. [<a href="https://pubmed.ncbi.nlm.nih.gov/20642956" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 20642956</span></a>]<div><i>(22 year old man accidentally drank a cup of copper sulfate and developed severe vomiting, abdominal pain and dehydration, treated with gastric lavage, penicillamine and dimercaprol [BAL], with increase in methemoglobinemia, acute renal failure, liver dysfunction [bilirubin 2.9 mg/dL, ALT 85 U/L, Alk P 30 U/L] and adult respiratory distress syndrome, eventually improving and resolving within 2 weeks).</i></div></div></li><li><div class="bk_ref" id="Copper.R36">Reuben A, Koch DG, Lee WM; Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatology 2010; 52: 2065-76. [<a href="/pmc/articles/PMC3992250/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC3992250</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/20949552" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 20949552</span></a>]<div><i>(Among 1198 patients with acute liver failure enrolled in a US prospective study between 1998 and 2007, 133 were attributed to drug induced liver injury, but none were attributed to ingestion of copper).</i></div></div></li><li><div class="bk_ref" id="Copper.R37">Devarbhavi H, Dierkhising R, Kremers WK, Sandeep MS, Karanth D, Adarsh CK. Single-center experience with drug-induced liver injury from India: causes, outcome, prognosis, and predictors of mortality. Am J Gastroenterol 2010; 105: 2396-404. [<a href="https://pubmed.ncbi.nlm.nih.gov/20648003" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 20648003</span></a>]<div><i>(Among 313 cases of drug induced liver injury seen between 1997 and 2008 at a large hospital in Bangalore, India, none were attributed to copper ingestion or copper overdoses).</i></div></div></li><li><div class="bk_ref" id="Copper.R38">Valsami S, Stamoulis K, Lydataki E, Fountoulaki-Paparizos L. Acute copper sulphate poisoning: a forgotten cause of severe intravascular haemolysis. Br J Haematol 2012; 156: 294. [<a href="https://pubmed.ncbi.nlm.nih.gov/21981599" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 21981599</span></a>]<div><i>(25 year old man presented 18 hours after overdose with copper sulfate with hemolytic anemia [hematocrit initially 44% falling to 25% in 3 days], with rhabdomyolysis and mild renal and liver impairment).</i></div></div></li><li><div class="bk_ref" id="Copper.R39">Naha K, Saravu K, Shastry BA. Blue vitriol poisoning: a 10-year experience in a tertiary care hospital. Clin Toxicol (Phila) 2012; 50: 197-201. [<a href="https://pubmed.ncbi.nlm.nih.gov/22372787" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 22372787</span></a>]<div><i>(Among 35 cases of acute copper poisoning presenting at a single referral center in Southern India over a 10 year period, the average age was 29 years, symptoms included vomiting [85%], diarrhea [46%], epigastric pain [43%], blood in stool [31%), hematuria [26%], burning chest pain [17%] and jaundice [37%] and 8 patients died).</i></div></div></li><li><div class="bk_ref" id="Copper.R40">Weiss KH, Stremmel W. Evolving perspectives in Wilson disease diagnosis: treatment and monitoring. Curr Gastroenterol Rep 2012; 14: 1-7. [<a href="https://pubmed.ncbi.nlm.nih.gov/22083169" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 22083169</span></a>]<div><i>(Review of the diagnosis and management of Wilson disease, including the role of genetic testing and the choice of medical therapies).</i></div></div></li><li><div class="bk_ref" id="Copper.R41">Rifkin J, Miller MD. Copper-associated hepatitis in a Pembroke Welsh corgi. Can Vet J 2014; 55: 573-6. [<a href="/pmc/articles/PMC4022027/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC4022027</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/24891642" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 24891642</span></a>]<div><i>(6 year old Welsh corgi developed poor appetite and weight loss and was found to have liver injury [bilirubin not given, ALT 1366 U/L, Alk P 201 U/L], laparotomy showing an abnormal looking liver with fatty change, fibrosis and excessive copper, later responding to penicillamine, ursodiol andS-adenosylvmethionine with normalization of ALT levels).</i></div></div></li><li><div class="bk_ref" id="Copper.R42">Breuer C, Oh J, Nolkemper D, Achilles EG, Fischer L, Eglite I, Guesmer C, et al. Successful detoxification and liver transplantation in a severe poisoning with a chemical wood preservative containing chromium, copper, and arsenic. Transplantation 2015; 99: e29-30. [<a href="https://pubmed.ncbi.nlm.nih.gov/25827325" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 25827325</span></a>]<div><i>(4 year old boy ingested wood preservative with chromated copper arsenate and rapidly developed abdominal pain and vomiting followed by acute liver and kidney failure treated with dialysis, BAL and liver transplantation 5 days later; liver showing "toxic liver damage").</i></div></div></li><li><div class="bk_ref" id="Copper.R43">Chalasani N, Bonkovsky HL, Fontana R, Lee W, Stolz A, Talwalkar J, Reddy KR, et al.; United States Drug Induced Liver Injury Network. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN Prospective Study. Gastroenterology 2015; 148: 1340-52.e7. [<a href="/pmc/articles/PMC4446235/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC4446235</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/25754159" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 25754159</span></a>]<div><i>(Among 899 cases of drug induced liver injury enrolled in a US prospective study between 2004 and 2013, none of the cases were attributed to copper ingestion).</i></div></div></li></ul></div><div id="bk_toc_contnr"></div></div></div>
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<div xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"></div><div class="portlet"><div class="portlet_head"><div class="portlet_title"><h3><span>Views</span></h3></div><a name="Shutter" sid="1" href="#" class="portlet_shutter" title="Show/hide content" remembercollapsed="true" pgsec_name="PDF_download" id="Shutter"></a></div><div class="portlet_content"><ul xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="simple-list"><li><a href="/books/NBK548090/?report=reader">PubReader</a></li><li><a href="/books/NBK548090/?report=printable">Print View</a></li><li><a data-jig="ncbidialog" href="#_ncbi_dlg_citbx_NBK548090" data-jigconfig="width:400,modal:true">Cite this Page</a><div id="_ncbi_dlg_citbx_NBK548090" style="display:none" title="Cite this Page"><div class="bk_tt">LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. 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<a href="https://www.ncbi.nlm.nih.gov/sites/entrez?cmd=search&db=pubmed&pubmedfilters=true&term=(Copper/AE)+AND+Human%5BMH%5D+AND+(drug+induced+liver+injury+OR+jaundice/CI+OR+bile+duct+diseases/CI+OR+liver/DE+OR+liver+diseases/CI)+AND+(%221900/1/1%22%5BEDat%5D%3A%222999/12/31%22%5BEDat%5D)" ref="pagearea=document-links&targetsite=external&targetcat=link&targettype=uri">Recent References on Copper: from PubMed.gov</a>
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Epub 2014 Sep 16.</em></div></div></li><li class="brieflinkpopper two_line"><a class="brieflinkpopperctrl" href="/pubmed/20180042" ref="ordinalpos=1&linkpos=3&log$=relatedarticles&logdbfrom=pubmed">Effects of multivitamin/mineral supplementation on trace element levels in serum and follicular fluid of women undergoing in vitro fertilization (IVF).</a><span class="source">[Biol Trace Elem Res. 2011]</span><div class="brieflinkpop offscreen_noflow">Effects of multivitamin/mineral supplementation on trace element levels in serum and follicular fluid of women undergoing in vitro fertilization (IVF).<div class="brieflinkpopdesc"><em xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="author">Özkaya MO, Nazıroğlu M, Barak C, Berkkanoglu M. </em><em xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="cit">Biol Trace Elem Res. 2011 Jan; 139(1):1-9. Epub 2010 Feb 24.</em></div></div></li><li class="brieflinkpopper two_line"><a class="brieflinkpopperctrl" href="/pubmed/10813454" ref="ordinalpos=1&linkpos=4&log$=relatedarticles&logdbfrom=pubmed">Experimental copper and chromium deficiency and additional molybdenum supplementation in goats. II. Concentrations of trace and minor elements in liver, kidneys and ribs: haematology and clinical chemistry.</a><span class="source">[Sci Total Environ. 2000]</span><div class="brieflinkpop offscreen_noflow">Experimental copper and chromium deficiency and additional molybdenum supplementation in goats. II. Concentrations of trace and minor elements in liver, kidneys and ribs: haematology and clinical chemistry.<div class="brieflinkpopdesc"><em xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="author">Frank A, Danielsson R, Jones B. </em><em xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="cit">Sci Total Environ. 2000 Apr 17; 249(1-3):143-70. </em></div></div></li><li class="brieflinkpopper two_line"><a class="brieflinkpopperctrl" href="/pubmed/9891606" ref="ordinalpos=1&linkpos=5&log$=relatedreviews&logdbfrom=pubmed"><span xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="invert">Review</span> The role of copper, molybdenum, selenium, and zinc in nutrition and health.</a><span class="source">[Clin Lab Med. 1998]</span><div class="brieflinkpop offscreen_noflow"><span xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="invert">Review</span> The role of copper, molybdenum, selenium, and zinc in nutrition and health.<div class="brieflinkpopdesc"><em xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="author">Chan S, Gerson B, Subramaniam S. </em><em xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="cit">Clin Lab Med. 1998 Dec; 18(4):673-85. </em></div></div></li></ul><a class="seemore" href="/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed_reviews&uid=31643420" ref="ordinalpos=1&log$=relatedreviews_seeall&logdbfrom=pubmed">See reviews...</a><a class="seemore" href="/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed&uid=31643420" ref="ordinalpos=1&log$=relatedarticles_seeall&logdbfrom=pubmed">See all...</a></div></div><div class="portlet"><div class="portlet_head"><div class="portlet_title"><h3><span>Recent Activity</span></h3></div><a name="Shutter" sid="1" href="#" class="portlet_shutter" title="Show/hide content" remembercollapsed="true" pgsec_name="recent_activity" id="Shutter"></a></div><div class="portlet_content"><div xmlns:np="http://ncbi.gov/portal/XSLT/namespace" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" id="HTDisplay" class=""><div class="action"><a href="javascript:historyDisplayState('ClearHT')">Clear</a><a href="javascript:historyDisplayState('HTOff')" class="HTOn">Turn Off</a><a href="javascript:historyDisplayState('HTOn')" class="HTOff">Turn On</a></div><ul id="activity"><li class="ra_rcd ralinkpopper two_line"><a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=1" href="/portal/utils/pageresolver.fcgi?recordid=67c8debcab82281a8032f51a">Copper - LiverTox</a><div class="ralinkpop offscreen_noflow">Copper - LiverTox<div class="brieflinkpopdesc"></div></div><div class="tertiary"></div></li><li class="ra_rcd ralinkpopper two_line"><a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=2" href="/portal/utils/pageresolver.fcgi?recordid=67c8debbab82281a8032ed50">Copanlisib - LiverTox</a><div class="ralinkpop offscreen_noflow">Copanlisib - LiverTox<div class="brieflinkpopdesc"></div></div><div class="tertiary"></div></li><li class="ra_rcd ralinkpopper two_line"><a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=3" href="/portal/utils/pageresolver.fcgi?recordid=67c8debaab82281a8032ea0c">Comfrey - LiverTox</a><div class="ralinkpop offscreen_noflow">Comfrey - LiverTox<div class="brieflinkpopdesc"></div></div><div class="tertiary"></div></li><li class="ra_rcd ralinkpopper two_line"><a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=4" href="/portal/utils/pageresolver.fcgi?recordid=67c8deb9b15b832ebc062d45">Colony Stimulating Factors - LiverTox</a><div class="ralinkpop offscreen_noflow">Colony Stimulating Factors - LiverTox<div class="brieflinkpopdesc"></div></div><div class="tertiary"></div></li><li class="ra_rcd ralinkpopper two_line"><a class="htb ralinkpopperctrl" ref="log$=activity&linkpos=5" href="/portal/utils/pageresolver.fcgi?recordid=67c8deb8ab82281a8032e470">Colestipol - LiverTox</a><div class="ralinkpop offscreen_noflow">Colestipol - LiverTox<div class="brieflinkpopdesc"></div></div><div class="tertiary"></div></li></ul><p class="HTOn">Your browsing activity is empty.</p><p class="HTOff">Activity recording is turned off.</p><p id="turnOn" class="HTOff"><a href="javascript:historyDisplayState('HTOn')">Turn recording back on</a></p><a class="seemore" href="/sites/myncbi/recentactivity">See more...</a></div></div></div>
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<a href="https://www.nih.gov/institutes-nih/nih-office-director/office-communications-public-liaison/freedom-information-act-office" class="text-white">FOIA</a><br />
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<a href="https://www.hhs.gov/vulnerability-disclosure-policy/index.html" class="text-white" id="vdp">HHS Vulnerability Disclosure</a></p>
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</div>
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<div class="col-lg-3 col-12 centered-lg">
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<p><a class="supportLink text-white" href="https://support.nlm.nih.gov/">Help</a><br />
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<a href="https://www.nlm.nih.gov/accessibility.html" class="text-white">Accessibility</a><br />
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<a href="https://www.nlm.nih.gov/careers/careers.html" class="text-white">Careers</a></p>
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<li>
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<a class="text-white" href="https://www.nih.gov/">NIH</a>
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<a class="text-white" href="https://www.hhs.gov/">HHS</a>
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