Increased Prevalence of TG and TPO Mutations in Sudanese Children With Congenital Hypothyroidism
Abstract Context Congenital hypothyroidism (CH) is due to dyshormonogenesis in 10% to 15% of subjects worldwide but accounts for 60% of CH cases in the Sudan. Objective To investigate the molecular basis of CH in Sudanese families. Design Clinical phenotype reporting and serum thyroid hormone measur...
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creator | Bruellman, Ryan J Watanabe, Yui Ebrhim, Reham S Creech, Matthew K Abdullah, Mohamed A Dumitrescu, Alexandra M Refetoff, Samuel Weiss, Roy E |
description | Abstract
Context
Congenital hypothyroidism (CH) is due to dyshormonogenesis in 10% to 15% of subjects worldwide but accounts for 60% of CH cases in the Sudan.
Objective
To investigate the molecular basis of CH in Sudanese families.
Design
Clinical phenotype reporting and serum thyroid hormone measurements. Deoxyribonucelic acid extraction for whole-exome sequencing and Sanger sequencing.
Setting
University research center.
Patients
Twenty-six Sudanese families with CH.
Intervention
Clinical evaluation, thyroid function tests, genetic sequencing, and analysis. Our samples and information regarding samples from the literature were used to compare TG (thyroglobulin) and TPO (thyroid peroxidase) mutation rates in the Sudanese population with all populations.
Results
Mutations were found in dual-oxidase 1 (DUOX1), dual-oxidase 2 (DUOX2), iodotyrosine deiodinase (IYD), solute-carrier (SLC) 26A4, SLC26A7, SLC5A5, TG, and TPO genes. The molecular basis of the CH in 7 families remains unknown. TG mutations were significantly higher on average in the Sudanese population compared with the average number of TG mutations in other populations (P < 0.05).
Conclusions
All described mutations occur in domains important for protein structure and function, predicting the CH phenotype. Genotype prediction based on phenotype includes low or undetectable thyroglobulin levels for TG gene mutations and markedly higher thyroglobulin levels for TPO mutations. The reasons for higher incidence of TG gene mutations include gene length and possible positive genetic selection due to endemic iodine deficiency. |
doi_str_mv | 10.1210/clinem/dgz297 |
format | Article |
fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7093074</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A639969191</galeid><oup_id>10.1210/clinem/dgz297</oup_id><sourcerecordid>A639969191</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5577-b6cd775c03546920f68624355e08e0d24ad8318435597a5071e8ab63a98d66913</originalsourceid><addsrcrecordid>eNqFksFrFDEUxgdR7Fo9epWAFy_TJpPJZHIRyqJtodKCK3qL2eTNTmomWZOZlvWvN-uu1YoiOQSS3_ve9x5fUTwn-IhUBB9rZz0Mx2b1rRL8QTEjomYlJ4I_LGYYV6QUvPp0UDxJ6RpjUteMPi4OKGkbzkQ7Kz6fex1BJTDoKsKNcuA1oNChxSlS3qDF1SV6N41qtMEnZD16PxnlIQGa99aZCB59tGOP5sGvwNtROXS2WYex38RgjU3D0-JRp1yCZ_v7sPjw9s1iflZeXJ6ez08uSs0Y5-Wy0YZzpjFldSMq3DVtU9WUMcAtYFPVyrTZ9fZFcMUwJ9CqZUOVaE3TCEIPi9c73fW0HMBo8GNUTq6jHVTcyKCsvP_jbS9X4UZyLCjmdRZ4tReI4esEaZSDTRqcy-OGKcmKUoybqmU0oy__QK_DFH0eT2bPBFNak_oXtcpbldZ3IffVW1F50lAhsusfvo_-QuVjYLA6eOhsfr9XUO4KdAwpRejuZiRYbiMhd5GQu0hk_sXvi7mjf2YgA2QH3AY3Qkxf3HQLUfag3Nj_U3S_rDCt_9P_Ozgz0QM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2431033414</pqid></control><display><type>article</type><title>Increased Prevalence of TG and TPO Mutations in Sudanese Children With Congenital Hypothyroidism</title><source>ProQuest One Community College</source><source>MEDLINE</source><source>ProQuest Central (Alumni Edition)</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>ProQuest Central UK/Ireland</source><source>Alma/SFX Local Collection</source><source>ProQuest Central</source><creator>Bruellman, Ryan J ; Watanabe, Yui ; Ebrhim, Reham S ; Creech, Matthew K ; Abdullah, Mohamed A ; Dumitrescu, Alexandra M ; Refetoff, Samuel ; Weiss, Roy E</creator><creatorcontrib>Bruellman, Ryan J ; Watanabe, Yui ; Ebrhim, Reham S ; Creech, Matthew K ; Abdullah, Mohamed A ; Dumitrescu, Alexandra M ; Refetoff, Samuel ; Weiss, Roy E</creatorcontrib><description>Abstract
Context
Congenital hypothyroidism (CH) is due to dyshormonogenesis in 10% to 15% of subjects worldwide but accounts for 60% of CH cases in the Sudan.
Objective
To investigate the molecular basis of CH in Sudanese families.
Design
Clinical phenotype reporting and serum thyroid hormone measurements. Deoxyribonucelic acid extraction for whole-exome sequencing and Sanger sequencing.
Setting
University research center.
Patients
Twenty-six Sudanese families with CH.
Intervention
Clinical evaluation, thyroid function tests, genetic sequencing, and analysis. Our samples and information regarding samples from the literature were used to compare TG (thyroglobulin) and TPO (thyroid peroxidase) mutation rates in the Sudanese population with all populations.
Results
Mutations were found in dual-oxidase 1 (DUOX1), dual-oxidase 2 (DUOX2), iodotyrosine deiodinase (IYD), solute-carrier (SLC) 26A4, SLC26A7, SLC5A5, TG, and TPO genes. The molecular basis of the CH in 7 families remains unknown. TG mutations were significantly higher on average in the Sudanese population compared with the average number of TG mutations in other populations (P < 0.05).
Conclusions
All described mutations occur in domains important for protein structure and function, predicting the CH phenotype. Genotype prediction based on phenotype includes low or undetectable thyroglobulin levels for TG gene mutations and markedly higher thyroglobulin levels for TPO mutations. The reasons for higher incidence of TG gene mutations include gene length and possible positive genetic selection due to endemic iodine deficiency.</description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/clinem/dgz297</identifier><identifier>PMID: 31867598</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>Adolescent ; Autoantigens - genetics ; Child ; Child, Preschool ; Clinical ; Congenital diseases ; Congenital Hypothyroidism - epidemiology ; Congenital Hypothyroidism - genetics ; Diagnosis ; Dual Oxidases - genetics ; Family ; Female ; Gene Frequency ; Gene mutations ; Genetic analysis ; Genetic aspects ; Genetic Association Studies ; Genetic disorders ; Genetic Predisposition to Disease ; Genotype & phenotype ; Genotypes ; Health aspects ; Humans ; Hypothyroidism ; Infant ; Infant, Newborn ; Iodide peroxidase ; Iodide Peroxidase - genetics ; Iodine ; Iron-Binding Proteins - genetics ; Male ; Mutation ; Mutation rates ; Pediatric research ; Pedigree ; Phenotypes ; Polymorphism, Single Nucleotide ; Prevalence ; Protein structure ; Structure-function relationships ; Sudan - epidemiology ; Thyroglobulin ; Thyroglobulin - genetics ; Thyroid ; Thyroid gland ; Thyroid hormones</subject><ispartof>The journal of clinical endocrinology and metabolism, 2020-05, Vol.105 (5), p.1564-1572</ispartof><rights>Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2019</rights><rights>Copyright © Oxford University Press 2015</rights><rights>Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><rights>COPYRIGHT 2020 Oxford University Press</rights><rights>Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5577-b6cd775c03546920f68624355e08e0d24ad8318435597a5071e8ab63a98d66913</citedby><cites>FETCH-LOGICAL-c5577-b6cd775c03546920f68624355e08e0d24ad8318435597a5071e8ab63a98d66913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2431033414?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,780,784,885,21388,21389,27924,27925,33530,33531,33744,33745,43659,43805,64385,64387,64389,72469,73123,73128,73129,73131</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31867598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bruellman, Ryan J</creatorcontrib><creatorcontrib>Watanabe, Yui</creatorcontrib><creatorcontrib>Ebrhim, Reham S</creatorcontrib><creatorcontrib>Creech, Matthew K</creatorcontrib><creatorcontrib>Abdullah, Mohamed A</creatorcontrib><creatorcontrib>Dumitrescu, Alexandra M</creatorcontrib><creatorcontrib>Refetoff, Samuel</creatorcontrib><creatorcontrib>Weiss, Roy E</creatorcontrib><title>Increased Prevalence of TG and TPO Mutations in Sudanese Children With Congenital Hypothyroidism</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description>Abstract
Context
Congenital hypothyroidism (CH) is due to dyshormonogenesis in 10% to 15% of subjects worldwide but accounts for 60% of CH cases in the Sudan.
Objective
To investigate the molecular basis of CH in Sudanese families.
Design
Clinical phenotype reporting and serum thyroid hormone measurements. Deoxyribonucelic acid extraction for whole-exome sequencing and Sanger sequencing.
Setting
University research center.
Patients
Twenty-six Sudanese families with CH.
Intervention
Clinical evaluation, thyroid function tests, genetic sequencing, and analysis. Our samples and information regarding samples from the literature were used to compare TG (thyroglobulin) and TPO (thyroid peroxidase) mutation rates in the Sudanese population with all populations.
Results
Mutations were found in dual-oxidase 1 (DUOX1), dual-oxidase 2 (DUOX2), iodotyrosine deiodinase (IYD), solute-carrier (SLC) 26A4, SLC26A7, SLC5A5, TG, and TPO genes. The molecular basis of the CH in 7 families remains unknown. TG mutations were significantly higher on average in the Sudanese population compared with the average number of TG mutations in other populations (P < 0.05).
Conclusions
All described mutations occur in domains important for protein structure and function, predicting the CH phenotype. Genotype prediction based on phenotype includes low or undetectable thyroglobulin levels for TG gene mutations and markedly higher thyroglobulin levels for TPO mutations. The reasons for higher incidence of TG gene mutations include gene length and possible positive genetic selection due to endemic iodine deficiency.</description><subject>Adolescent</subject><subject>Autoantigens - genetics</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Clinical</subject><subject>Congenital diseases</subject><subject>Congenital Hypothyroidism - epidemiology</subject><subject>Congenital Hypothyroidism - genetics</subject><subject>Diagnosis</subject><subject>Dual Oxidases - genetics</subject><subject>Family</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Gene mutations</subject><subject>Genetic analysis</subject><subject>Genetic aspects</subject><subject>Genetic Association Studies</subject><subject>Genetic disorders</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hypothyroidism</subject><subject>Infant</subject><subject>Infant, Newborn</subject><subject>Iodide peroxidase</subject><subject>Iodide Peroxidase - genetics</subject><subject>Iodine</subject><subject>Iron-Binding Proteins - genetics</subject><subject>Male</subject><subject>Mutation</subject><subject>Mutation rates</subject><subject>Pediatric research</subject><subject>Pedigree</subject><subject>Phenotypes</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prevalence</subject><subject>Protein structure</subject><subject>Structure-function relationships</subject><subject>Sudan - epidemiology</subject><subject>Thyroglobulin</subject><subject>Thyroglobulin - genetics</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid hormones</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFksFrFDEUxgdR7Fo9epWAFy_TJpPJZHIRyqJtodKCK3qL2eTNTmomWZOZlvWvN-uu1YoiOQSS3_ve9x5fUTwn-IhUBB9rZz0Mx2b1rRL8QTEjomYlJ4I_LGYYV6QUvPp0UDxJ6RpjUteMPi4OKGkbzkQ7Kz6fex1BJTDoKsKNcuA1oNChxSlS3qDF1SV6N41qtMEnZD16PxnlIQGa99aZCB59tGOP5sGvwNtROXS2WYex38RgjU3D0-JRp1yCZ_v7sPjw9s1iflZeXJ6ez08uSs0Y5-Wy0YZzpjFldSMq3DVtU9WUMcAtYFPVyrTZ9fZFcMUwJ9CqZUOVaE3TCEIPi9c73fW0HMBo8GNUTq6jHVTcyKCsvP_jbS9X4UZyLCjmdRZ4tReI4esEaZSDTRqcy-OGKcmKUoybqmU0oy__QK_DFH0eT2bPBFNak_oXtcpbldZ3IffVW1F50lAhsusfvo_-QuVjYLA6eOhsfr9XUO4KdAwpRejuZiRYbiMhd5GQu0hk_sXvi7mjf2YgA2QH3AY3Qkxf3HQLUfag3Nj_U3S_rDCt_9P_Ozgz0QM</recordid><startdate>20200501</startdate><enddate>20200501</enddate><creator>Bruellman, Ryan J</creator><creator>Watanabe, Yui</creator><creator>Ebrhim, Reham S</creator><creator>Creech, Matthew K</creator><creator>Abdullah, Mohamed A</creator><creator>Dumitrescu, Alexandra M</creator><creator>Refetoff, Samuel</creator><creator>Weiss, Roy E</creator><general>Oxford University Press</general><general>Copyright Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200501</creationdate><title>Increased Prevalence of TG and TPO Mutations in Sudanese Children With Congenital Hypothyroidism</title><author>Bruellman, Ryan J ; Watanabe, Yui ; Ebrhim, Reham S ; Creech, Matthew K ; Abdullah, Mohamed A ; Dumitrescu, Alexandra M ; Refetoff, Samuel ; Weiss, Roy E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5577-b6cd775c03546920f68624355e08e0d24ad8318435597a5071e8ab63a98d66913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adolescent</topic><topic>Autoantigens - genetics</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Clinical</topic><topic>Congenital diseases</topic><topic>Congenital Hypothyroidism - epidemiology</topic><topic>Congenital Hypothyroidism - genetics</topic><topic>Diagnosis</topic><topic>Dual Oxidases - genetics</topic><topic>Family</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Gene mutations</topic><topic>Genetic analysis</topic><topic>Genetic aspects</topic><topic>Genetic Association Studies</topic><topic>Genetic disorders</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Hypothyroidism</topic><topic>Infant</topic><topic>Infant, Newborn</topic><topic>Iodide peroxidase</topic><topic>Iodide Peroxidase - genetics</topic><topic>Iodine</topic><topic>Iron-Binding Proteins - genetics</topic><topic>Male</topic><topic>Mutation</topic><topic>Mutation rates</topic><topic>Pediatric research</topic><topic>Pedigree</topic><topic>Phenotypes</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prevalence</topic><topic>Protein structure</topic><topic>Structure-function relationships</topic><topic>Sudan - epidemiology</topic><topic>Thyroglobulin</topic><topic>Thyroglobulin - genetics</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid hormones</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bruellman, Ryan J</creatorcontrib><creatorcontrib>Watanabe, Yui</creatorcontrib><creatorcontrib>Ebrhim, Reham S</creatorcontrib><creatorcontrib>Creech, Matthew K</creatorcontrib><creatorcontrib>Abdullah, Mohamed A</creatorcontrib><creatorcontrib>Dumitrescu, Alexandra M</creatorcontrib><creatorcontrib>Refetoff, Samuel</creatorcontrib><creatorcontrib>Weiss, Roy E</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bruellman, Ryan J</au><au>Watanabe, Yui</au><au>Ebrhim, Reham S</au><au>Creech, Matthew K</au><au>Abdullah, Mohamed A</au><au>Dumitrescu, Alexandra M</au><au>Refetoff, Samuel</au><au>Weiss, Roy E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Prevalence of TG and TPO Mutations in Sudanese Children With Congenital Hypothyroidism</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2020-05-01</date><risdate>2020</risdate><volume>105</volume><issue>5</issue><spage>1564</spage><epage>1572</epage><pages>1564-1572</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><abstract>Abstract
Context
Congenital hypothyroidism (CH) is due to dyshormonogenesis in 10% to 15% of subjects worldwide but accounts for 60% of CH cases in the Sudan.
Objective
To investigate the molecular basis of CH in Sudanese families.
Design
Clinical phenotype reporting and serum thyroid hormone measurements. Deoxyribonucelic acid extraction for whole-exome sequencing and Sanger sequencing.
Setting
University research center.
Patients
Twenty-six Sudanese families with CH.
Intervention
Clinical evaluation, thyroid function tests, genetic sequencing, and analysis. Our samples and information regarding samples from the literature were used to compare TG (thyroglobulin) and TPO (thyroid peroxidase) mutation rates in the Sudanese population with all populations.
Results
Mutations were found in dual-oxidase 1 (DUOX1), dual-oxidase 2 (DUOX2), iodotyrosine deiodinase (IYD), solute-carrier (SLC) 26A4, SLC26A7, SLC5A5, TG, and TPO genes. The molecular basis of the CH in 7 families remains unknown. TG mutations were significantly higher on average in the Sudanese population compared with the average number of TG mutations in other populations (P < 0.05).
Conclusions
All described mutations occur in domains important for protein structure and function, predicting the CH phenotype. Genotype prediction based on phenotype includes low or undetectable thyroglobulin levels for TG gene mutations and markedly higher thyroglobulin levels for TPO mutations. The reasons for higher incidence of TG gene mutations include gene length and possible positive genetic selection due to endemic iodine deficiency.</abstract><cop>US</cop><pub>Oxford University Press</pub><pmid>31867598</pmid><doi>10.1210/clinem/dgz297</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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source | ProQuest One Community College; MEDLINE; ProQuest Central (Alumni Edition); Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection; ProQuest Central |
subjects | Adolescent Autoantigens - genetics Child Child, Preschool Clinical Congenital diseases Congenital Hypothyroidism - epidemiology Congenital Hypothyroidism - genetics Diagnosis Dual Oxidases - genetics Family Female Gene Frequency Gene mutations Genetic analysis Genetic aspects Genetic Association Studies Genetic disorders Genetic Predisposition to Disease Genotype & phenotype Genotypes Health aspects Humans Hypothyroidism Infant Infant, Newborn Iodide peroxidase Iodide Peroxidase - genetics Iodine Iron-Binding Proteins - genetics Male Mutation Mutation rates Pediatric research Pedigree Phenotypes Polymorphism, Single Nucleotide Prevalence Protein structure Structure-function relationships Sudan - epidemiology Thyroglobulin Thyroglobulin - genetics Thyroid Thyroid gland Thyroid hormones |
title | Increased Prevalence of TG and TPO Mutations in Sudanese Children With Congenital Hypothyroidism |
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