The syndrome of congenital goiter with butanol-insoluble serum iodine
Identifieur interne : 002294 ( Istex/Corpus ); précédent : 002293; suivant : 002295The syndrome of congenital goiter with butanol-insoluble serum iodine
Auteurs : Leslie J. Degroot ; John B. StanburySource :
- The American Journal of Medicine [ 0002-9343 ] ; 1959.
Abstract
Clinical and laboratory data on five patients suffering from one variety of congenital hypothyroidism with goiter are reported, and similar cases from the literature are reviewed. In these patients hypothyroidism and goiter develop early in life. They may suffer permanent physical and mental retardation unless the disorder is detected and adequate replacement therapy is given. There is increased RaI131 uptake by the thyroid and no release of I131 upon administration of potassium thiocyanate. The deiodinase activity is normal.An abnormal iodinated polypeptide or protein is secreted by the thyroid. It is detected by its failure to extract into n-butanol from acidified serum. A similar complex is present in the urine. Abnormalities in the distribution of I131 in the thyroid subcellular particulate fractions and in the thyroidal proteins have been detected in the two glands which have been available for analysis.This syndrome may be the expression of a congenital defect in thyroglobulin synthesis. Similar observations in certain patients with adenomatous colloid goiter suggest that this type of congenital goiter and a type of adenomatous colloid goiter may represent different levels of expression of a common genetic defect.
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DOI: 10.1016/0002-9343(59)90044-0
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Stanbury</name><affiliation><mods:affiliation>Boston, Massachusetts USA</mods:affiliation></affiliation><affiliation><mods:affiliation>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:05E91BB902ABEAED2AFEFE14249446DCD6CE78C7</idno><date when="1959" year="1959">1959</date><idno type="doi">10.1016/0002-9343(59)90044-0</idno><idno type="url">https://api.istex.fr/document/05E91BB902ABEAED2AFEFE14249446DCD6CE78C7/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002294</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The syndrome of congenital goiter with butanol-insoluble serum iodine</title><author><name sortKey="Degroot, Leslie J" sort="Degroot, Leslie J" uniqKey="Degroot L" first="Leslie J." last="Degroot">Leslie J. Degroot</name><affiliation><mods:affiliation>Fellow of the National Foundation for Infantile Paralysis Boston, Massachusetts USA</mods:affiliation></affiliation><affiliation><mods:affiliation>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</mods:affiliation></affiliation></author><author><name sortKey="Stanbury, John B" sort="Stanbury, John B" uniqKey="Stanbury J" first="John B." last="Stanbury">John B. Stanbury</name><affiliation><mods:affiliation>Boston, Massachusetts USA</mods:affiliation></affiliation><affiliation><mods:affiliation>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="ISSN">0002-9343</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1959">1959</date><biblScope unit="volume">27</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="586">586</biblScope><biblScope unit="page" to="595">595</biblScope></imprint><idno type="ISSN">0002-9343</idno></series><idno type="istex">05E91BB902ABEAED2AFEFE14249446DCD6CE78C7</idno><idno type="DOI">10.1016/0002-9343(59)90044-0</idno><idno type="PII">0002-9343(59)90044-0</idno><idno type="ArticleID">59900440</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-9343</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Clinical and laboratory data on five patients suffering from one variety of congenital hypothyroidism with goiter are reported, and similar cases from the literature are reviewed. In these patients hypothyroidism and goiter develop early in life. They may suffer permanent physical and mental retardation unless the disorder is detected and adequate replacement therapy is given. There is increased RaI131 uptake by the thyroid and no release of I131 upon administration of potassium thiocyanate. The deiodinase activity is normal.An abnormal iodinated polypeptide or protein is secreted by the thyroid. It is detected by its failure to extract into n-butanol from acidified serum. A similar complex is present in the urine. Abnormalities in the distribution of I131 in the thyroid subcellular particulate fractions and in the thyroidal proteins have been detected in the two glands which have been available for analysis.This syndrome may be the expression of a congenital defect in thyroglobulin synthesis. Similar observations in certain patients with adenomatous colloid goiter suggest that this type of congenital goiter and a type of adenomatous colloid goiter may represent different levels of expression of a common genetic defect.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Leslie J. DeGroot M.D.</name><affiliations><json:string>Fellow of the National Foundation for Infantile Paralysis Boston, Massachusetts USA</json:string><json:string>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</json:string></affiliations></json:item><json:item><name>John B. Stanbury M.D.</name><affiliations><json:string>Boston, Massachusetts USA</json:string><json:string>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</json:string></affiliations></json:item></author><articleId><json:string>59900440</json:string></articleId><language><json:string>eng</json:string></language><abstract>Clinical and laboratory data on five patients suffering from one variety of congenital hypothyroidism with goiter are reported, and similar cases from the literature are reviewed. In these patients hypothyroidism and goiter develop early in life. They may suffer permanent physical and mental retardation unless the disorder is detected and adequate replacement therapy is given. There is increased RaI131 uptake by the thyroid and no release of I131 upon administration of potassium thiocyanate. The deiodinase activity is normal.An abnormal iodinated polypeptide or protein is secreted by the thyroid. It is detected by its failure to extract into n-butanol from acidified serum. A similar complex is present in the urine. Abnormalities in the distribution of I131 in the thyroid subcellular particulate fractions and in the thyroidal proteins have been detected in the two glands which have been available for analysis.This syndrome may be the expression of a congenital defect in thyroglobulin synthesis. Similar observations in certain patients with adenomatous colloid goiter suggest that this type of congenital goiter and a type of adenomatous colloid goiter may represent different levels of expression of a common genetic defect.</abstract><qualityIndicators><score>7.72</score><pdfVersion>1.4</pdfVersion><pdfPageSize>540 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1239</abstractCharCount><pdfWordCount>5018</pdfWordCount><pdfCharCount>34182</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>185</abstractWordCount></qualityIndicators><title>The syndrome of congenital goiter with butanol-insoluble serum iodine</title><pii><json:string>0002-9343(59)90044-0</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>16</volume><pages><first>272</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Fed. 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In these patients hypothyroidism and goiter develop early in life. They may suffer permanent physical and mental retardation unless the disorder is detected and adequate replacement therapy is given. There is increased RaI131 uptake by the thyroid and no release of I131 upon administration of potassium thiocyanate. The deiodinase activity is normal.An abnormal iodinated polypeptide or protein is secreted by the thyroid. It is detected by its failure to extract into n-butanol from acidified serum. A similar complex is present in the urine. Abnormalities in the distribution of I131 in the thyroid subcellular particulate fractions and in the thyroidal proteins have been detected in the two glands which have been available for analysis.This syndrome may be the expression of a congenital defect in thyroglobulin synthesis. Similar observations in certain patients with adenomatous colloid goiter suggest that this type of congenital goiter and a type of adenomatous colloid goiter may represent different levels of expression of a common genetic defect.</p></abstract></profileDesc><revisionDesc><change when="1959">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AJM</jid><aid>59900440</aid><ce:pii>0002-9343(59)90044-0</ce:pii><ce:doi>10.1016/0002-9343(59)90044-0</ce:doi><ce:copyright type="unknown" year="1959"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>Supported in part by Grants A-1880 and A-446 (C4) from the U.S. Public Health Service.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Clinical study</ce:textfn></ce:dochead><ce:title>The syndrome of congenital goiter with butanol-insoluble serum iodine</ce:title><ce:author-group><ce:author><ce:given-name>Leslie J.</ce:given-name><ce:surname>DeGroot</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="AFF2"><ce:sup loc="post">†</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>John B.</ce:given-name><ce:surname>Stanbury</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Boston, Massachusetts USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>†</ce:label><ce:textfn>Fellow of the National Foundation for Infantile Paralysis Boston, Massachusetts USA</ce:textfn></ce:affiliation><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</ce:note-para></ce:footnote></ce:author-group><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Clinical and laboratory data on five patients suffering from one variety of congenital hypothyroidism with goiter are reported, and similar cases from the literature are reviewed. In these patients hypothyroidism and goiter develop early in life. They may suffer permanent physical and mental retardation unless the disorder is detected and adequate replacement therapy is given. There is increased RaI<ce:sup loc="post">131</ce:sup> uptake by the thyroid and no release of I<ce:sup loc="post">131</ce:sup> upon administration of potassium thiocyanate. The deiodinase activity is normal.</ce:simple-para><ce:simple-para view="all" id="simple-para.0015">An abnormal iodinated polypeptide or protein is secreted by the thyroid. It is detected by its failure to extract into n-butanol from acidified serum. A similar complex is present in the urine. Abnormalities in the distribution of I<ce:sup loc="post">131</ce:sup> in the thyroid subcellular particulate fractions and in the thyroidal proteins have been detected in the two glands which have been available for analysis.</ce:simple-para><ce:simple-para view="all" id="simple-para.0020">This syndrome may be the expression of a congenital defect in thyroglobulin synthesis. Similar observations in certain patients with adenomatous colloid goiter suggest that this type of congenital goiter and a type of adenomatous colloid goiter may represent different levels of expression of a common genetic defect.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The syndrome of congenital goiter with butanol-insoluble serum iodine</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>The syndrome of congenital goiter with butanol-insoluble serum iodine</title></titleInfo><name type="personal"><namePart type="given">Leslie J.</namePart><namePart type="family">DeGroot</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Fellow of the National Foundation for Infantile Paralysis Boston, Massachusetts USA</affiliation><affiliation>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John B.</namePart><namePart type="family">Stanbury</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Boston, Massachusetts USA</affiliation><affiliation>1From the Department of Medicine, Harvard Medical School and the Medical Services of the Massachusetts General Hospital, Boston, Massachusetts.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1959</dateIssued><copyrightDate encoding="w3cdtf">1959</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Clinical and laboratory data on five patients suffering from one variety of congenital hypothyroidism with goiter are reported, and similar cases from the literature are reviewed. In these patients hypothyroidism and goiter develop early in life. They may suffer permanent physical and mental retardation unless the disorder is detected and adequate replacement therapy is given. There is increased RaI131 uptake by the thyroid and no release of I131 upon administration of potassium thiocyanate. The deiodinase activity is normal.An abnormal iodinated polypeptide or protein is secreted by the thyroid. It is detected by its failure to extract into n-butanol from acidified serum. A similar complex is present in the urine. Abnormalities in the distribution of I131 in the thyroid subcellular particulate fractions and in the thyroidal proteins have been detected in the two glands which have been available for analysis.This syndrome may be the expression of a congenital defect in thyroglobulin synthesis. Similar observations in certain patients with adenomatous colloid goiter suggest that this type of congenital goiter and a type of adenomatous colloid goiter may represent different levels of expression of a common genetic defect.</abstract><note>Supported in part by Grants A-1880 and A-446 (C4) from the U.S. Public Health Service.</note><note type="content">Section title: Clinical study</note><relatedItem type="host"><titleInfo><title>The American Journal of Medicine</title></titleInfo><titleInfo type="abbreviated"><title>AJM</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">195910</dateIssued></originInfo><identifier type="ISSN">0002-9343</identifier><identifier type="PII">S0002-9343(00)X0204-5</identifier><part><date>195910</date><detail type="volume"><number>27</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue pages"><start>A1</start><end>A80</end></extent><extent unit="issue pages"><start>A81</start><end>A161</end></extent><extent unit="issue pages"><start>525</start><end>688</end></extent><extent unit="pages"><start>586</start><end>595</end></extent></part></relatedItem><identifier type="istex">05E91BB902ABEAED2AFEFE14249446DCD6CE78C7</identifier><identifier type="DOI">10.1016/0002-9343(59)90044-0</identifier><identifier type="PII">0002-9343(59)90044-0</identifier><identifier type="ArticleID">59900440</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/05E91BB902ABEAED2AFEFE14249446DCD6CE78C7/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><analytic><title level="a" type="main">Sporadic hypothyroidism associated with goiter</title><author><persName><forename type="first">A</forename><forename type="middle">M</forename><surname>Digeorge</surname></persName></author><author><persName><forename type="first">K</forename><forename type="middle">E</forename><surname>Pashkis</surname></persName></author></analytic><monogr><title level="j">J. 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