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Lead poisoning: case studies

Identifieur interne : 001A30 ( Pmc/Corpus ); précédent : 001A29; suivant : 001A31

Lead poisoning: case studies

Auteurs : J N Gordon ; A. Taylor ; P N Bennett

Source :

British Journal of Clinical Pharmacology [ 0306-5251 ] ; 2002.

RBID : PMC:1874356

Abstract

Early clinical features of lead toxicity are non-specific and an occupational history is particularly valuable.

Lead in the body comprises 2% in the blood (t_1/2 35 days) and 95% in bone and dentine (t_1/2 20–30 years). Blood lead may remain elevated for years after cessation from long exposure, due to redistribution from bone.

Blood lead concentration is the most widely used marker for inorganic lead exposure. Zinc protoporphyrin (ZPP) concentration in blood usefully reflects lead exposure over the prior 3 months.

Symptomatic patients with blood lead concentration >2.4 µmol l⁻¹ (50 µg dl⁻¹) or in any event >3.8 µmol l⁻¹ (80 µg dl⁻¹) should receive sodium calciumedetate i.v., followed by succimer by mouth for 19 days.

Asymptomatic patients with blood lead concentration >2.4 µmol l⁻¹ (50 µg dl⁻¹) may be treated with succimer alone.

Sodium calciumedetate should be given with dimercaprol to treat lead encephalopathy.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874356

DOI: 10.1046/j.1365-2125.2002.01580.x
PubMed: 11994050
PubMed Central: 1874356

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PMC:1874356

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Lead poisoning: case studies</title>
<author><name sortKey="Gordon, J N" sort="Gordon, J N" uniqKey="Gordon J" first="J N" last="Gordon">J N Gordon</name>
</author>
<author><name sortKey="Taylor, A" sort="Taylor, A" uniqKey="Taylor A" first="A" last="Taylor">A. Taylor</name>
</author>
<author><name sortKey="Bennett, P N" sort="Bennett, P N" uniqKey="Bennett P" first="P N" last="Bennett">P N Bennett</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">11994050</idno>
<idno type="pmc">1874356</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874356</idno>
<idno type="RBID">PMC:1874356</idno>
<idno type="doi">10.1046/j.1365-2125.2002.01580.x</idno>
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<idno type="wicri:Area/Pmc/Corpus">001A30</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Lead poisoning: case studies</title>
<author><name sortKey="Gordon, J N" sort="Gordon, J N" uniqKey="Gordon J" first="J N" last="Gordon">J N Gordon</name>
</author>
<author><name sortKey="Taylor, A" sort="Taylor, A" uniqKey="Taylor A" first="A" last="Taylor">A. Taylor</name>
</author>
<author><name sortKey="Bennett, P N" sort="Bennett, P N" uniqKey="Bennett P" first="P N" last="Bennett">P N Bennett</name>
</author>
</analytic>
<series><title level="j">British Journal of Clinical Pharmacology</title>
<idno type="ISSN">0306-5251</idno>
<idno type="eISSN">1365-2125</idno>
<imprint><date when="2002">2002</date>
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<profileDesc><textClass></textClass>
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<front><div type="abstract" xml:lang="en"><p>Early clinical features of lead toxicity are non-specific and an occupational history is particularly valuable.</p>
<p>Lead in the body comprises 2% in the blood (<italic>t</italic>
<sub>1/2</sub>
 35 days) and 95% in bone and dentine (<italic>t</italic>
<sub>1/2</sub>
 20–30 years). Blood lead may remain elevated for years after cessation from long exposure, due to redistribution from bone.</p>
<p>Blood lead concentration is the most widely used marker for inorganic lead exposure. Zinc protoporphyrin (ZPP) concentration in blood usefully reflects lead exposure over the prior 3 months.</p>
<p>Symptomatic patients with blood lead concentration >2.4 µmol l<sup>−1</sup>
 (50 µg dl<sup>−1</sup>
) or in any event >3.8 µmol l<sup>−1</sup>
 (80 µg dl<sup>−1</sup>
) should receive sodium calciumedetate i.v., followed by succimer by mouth for 19 days.</p>
<p>Asymptomatic patients with blood lead concentration >2.4 µmol l<sup>−1</sup>
 (50 µg dl<sup>−1</sup>
) may be treated with succimer alone.</p>
<p>Sodium calciumedetate should be given with dimercaprol to treat lead encephalopathy.</p>
</div>
</front>
</TEI>
<pmc article-type="case-report"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <front><journal-meta><journal-id journal-id-type="nlm-ta">Br J Clin Pharmacol</journal-id>
<journal-id journal-id-type="publisher-id">bcp</journal-id>
<journal-title>British Journal of Clinical Pharmacology</journal-title>
<issn pub-type="ppub">0306-5251</issn>
<issn pub-type="epub">1365-2125</issn>
<publisher><publisher-name>Blackwell Science Inc</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">11994050</article-id>
<article-id pub-id-type="pmc">1874356</article-id>
<article-id pub-id-type="doi">10.1046/j.1365-2125.2002.01580.x</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Case Report</subject>
</subj-group>
</article-categories>
<title-group><article-title>Lead poisoning: case studies</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Gordon</surname>
<given-names>J N</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Taylor</surname>
<given-names>A</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Bennett</surname>
<given-names>P N</given-names>
</name>
</contrib>
<aff><institution>Directorates of Medicine and Laboratory Services, Royal United Hospital</institution>
<addr-line>Combe Park, Bath BA1 3NG</addr-line>
<institution>Department of Medical Sciences, 3E 2.10, University of Bath Claverton Down</institution>
<addr-line>Bath BA2 7AY</addr-line>
</aff>
</contrib-group>
<author-notes><corresp id="cor1"><italic>Correspondence</italic>
: Dr P. N. Bennett, Department of Medical Sciences, 3E 2.10, University of Bath Claverton Down, Bath BA2 7AY, UK.</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>5</month>
<year>2002</year>
</pub-date>
<volume>53</volume>
<issue>5</issue>
<fpage>451</fpage>
<lpage>458</lpage>
<history><date date-type="received"><day>07</day>
<month>11</month>
<year>2001</year>
</date>
<date date-type="accepted"><day>07</day>
<month>11</month>
<year>2001</year>
</date>
</history>
<copyright-statement>© 2002 Blackwell Science Ltd</copyright-statement>
<copyright-year>2002</copyright-year>
<abstract><p>Early clinical features of lead toxicity are non-specific and an occupational history is particularly valuable.</p>
<p>Lead in the body comprises 2% in the blood (<italic>t</italic>
<sub>1/2</sub>
 35 days) and 95% in bone and dentine (<italic>t</italic>
<sub>1/2</sub>
 20–30 years). Blood lead may remain elevated for years after cessation from long exposure, due to redistribution from bone.</p>
<p>Blood lead concentration is the most widely used marker for inorganic lead exposure. Zinc protoporphyrin (ZPP) concentration in blood usefully reflects lead exposure over the prior 3 months.</p>
<p>Symptomatic patients with blood lead concentration >2.4 µmol l<sup>−1</sup>
 (50 µg dl<sup>−1</sup>
) or in any event >3.8 µmol l<sup>−1</sup>
 (80 µg dl<sup>−1</sup>
) should receive sodium calciumedetate i.v., followed by succimer by mouth for 19 days.</p>
<p>Asymptomatic patients with blood lead concentration >2.4 µmol l<sup>−1</sup>
 (50 µg dl<sup>−1</sup>
) may be treated with succimer alone.</p>
<p>Sodium calciumedetate should be given with dimercaprol to treat lead encephalopathy.</p>
</abstract>
<kwd-group><kwd>chelating agents</kwd>
<kwd>lead paint</kwd>
<kwd>lead</kwd>
<kwd>occupational exposure</kwd>
<kwd>review</kwd>
<kwd>sodium calcium edetate</kwd>
<kwd>succimer</kwd>
<kwd>toxicity</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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Lead poisoning: case studies

Lead poisoning: case studies

Source :

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki