Clinical assessment and molecular analysis of GnRHR and KAL1 genes in males with idiopathic hypogonadotrophic hypogonadism
Summary Objective The pathogenesis of idiopathic hypogonadotrophic hypogonadism (IHH) is mostly unclear. We characterized the clinical findings and molecular analysis of GnRHR and KAL1 genes in 26 Brazilian males with IHH with and without hyposmia/anosmia. Design Clinical assessment was performed...
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| Veröffentlicht in: | Clinical endocrinology (Oxford) 2007-02, Vol.66 (2), p.173-179 |
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| creator | Versiani, Beatriz R. Trarbach, Ericka Koenigkam-Santos, Marcel Dos Santos, Antonio Carlos Elias, Lucila L. K. Moreira, Ayrton C. Latronico, Ana Claudia De Castro, Margaret |
| description | Summary
Objective The pathogenesis of idiopathic hypogonadotrophic hypogonadism (IHH) is mostly unclear. We characterized the clinical findings and molecular analysis of GnRHR and KAL1 genes in 26 Brazilian males with IHH with and without hyposmia/anosmia.
Design Clinical assessment was performed for endocrine status, olfactory structure and function, renal lesion, and mirror movement. The diagnosis of Kallmann syndrome (KS) included HH and the clinical complaint of hyposmia/anosmia or decreased olfactory acuity obtained by the Smell Identification Test™ (SIT). We analysed GnRHR and KAL1 genes using the polymerase chain reaction (PCR) direct sequencing method.
Results A variable degree of HH was observed, including various clinical abnormalities, such as cryptorchidism, hearing loss, strabismus, cleft lip/palate, high‐arched palate, dental agenesis, psychiatric disorders, learning dysfunction, and bimanual synkinesia. Twenty‐two out of 26 patients with IHH (85%) were classified as KS. Abnormalities of olfactory bulbs/sulci were observed in 79% of KS patients. One‐third of KS patients had renal defects and 45·5% had a positive family history. GnRHR gene sequence analysis showed no mutations. KAL1 sequence analysis identified two novel missense mutations: c.1061A to G in exon 7 (N304S) and c.1583C to A in exon 10 (S478X). We also observed a 14‐bp deletion within exon 11 that caused a premature termination. According to the National Center for Biotechnology Information (NCBI)‐Single Nucleotide Polymorphism (SNP) database, two previously described polymorphisms (rs808119 and rs809446) were detected.
Conclusion KAL1 mutations accounted for 12% of KS patients. This low prevalence of KAL1 mutations indicates that other genes, such as the fibroblast growth factor receptor 1 (FGFR1) gene or other as yet undiscovered genes, epigenetic events and/or environmental factors might be involved in the aetiology and phenotypic variability of KS. |
| doi_str_mv | 10.1111/j.1365-2265.2006.02702.x |
| format | Article |
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Objective The pathogenesis of idiopathic hypogonadotrophic hypogonadism (IHH) is mostly unclear. We characterized the clinical findings and molecular analysis of GnRHR and KAL1 genes in 26 Brazilian males with IHH with and without hyposmia/anosmia.
Design Clinical assessment was performed for endocrine status, olfactory structure and function, renal lesion, and mirror movement. The diagnosis of Kallmann syndrome (KS) included HH and the clinical complaint of hyposmia/anosmia or decreased olfactory acuity obtained by the Smell Identification Test™ (SIT). We analysed GnRHR and KAL1 genes using the polymerase chain reaction (PCR) direct sequencing method.
Results A variable degree of HH was observed, including various clinical abnormalities, such as cryptorchidism, hearing loss, strabismus, cleft lip/palate, high‐arched palate, dental agenesis, psychiatric disorders, learning dysfunction, and bimanual synkinesia. Twenty‐two out of 26 patients with IHH (85%) were classified as KS. Abnormalities of olfactory bulbs/sulci were observed in 79% of KS patients. One‐third of KS patients had renal defects and 45·5% had a positive family history. GnRHR gene sequence analysis showed no mutations. KAL1 sequence analysis identified two novel missense mutations: c.1061A to G in exon 7 (N304S) and c.1583C to A in exon 10 (S478X). We also observed a 14‐bp deletion within exon 11 that caused a premature termination. According to the National Center for Biotechnology Information (NCBI)‐Single Nucleotide Polymorphism (SNP) database, two previously described polymorphisms (rs808119 and rs809446) were detected.
Conclusion KAL1 mutations accounted for 12% of KS patients. This low prevalence of KAL1 mutations indicates that other genes, such as the fibroblast growth factor receptor 1 (FGFR1) gene or other as yet undiscovered genes, epigenetic events and/or environmental factors might be involved in the aetiology and phenotypic variability of KS.</description><identifier>ISSN: 0300-0664</identifier><identifier>EISSN: 1365-2265</identifier><identifier>DOI: 10.1111/j.1365-2265.2006.02702.x</identifier><identifier>PMID: 17223984</identifier><identifier>CODEN: CLECAP</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; Biological and medical sciences ; Case-Control Studies ; Child ; Child, Preschool ; Endocrinopathies ; Extracellular Matrix Proteins - genetics ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; Gene Frequency ; Humans ; Hypogonadism - diagnosis ; Hypogonadism - genetics ; Hypothalamus. Hypophysis. Epiphysis (diseases) ; Kallmann Syndrome - diagnosis ; Kallmann Syndrome - genetics ; Male ; Medical sciences ; Mutation, Missense ; Nerve Tissue Proteins - genetics ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Olfaction Disorders - diagnosis ; Olfaction Disorders - genetics ; Receptors, LHRH - genetics ; Sequence Analysis, DNA ; Vertebrates: endocrinology</subject><ispartof>Clinical endocrinology (Oxford), 2007-02, Vol.66 (2), p.173-179</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4352-527c173eb15d2f62ccd7bcfe6c74a8a8305743aa82c9206e0decd83c50e8c6b43</citedby><cites>FETCH-LOGICAL-c4352-527c173eb15d2f62ccd7bcfe6c74a8a8305743aa82c9206e0decd83c50e8c6b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2265.2006.02702.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2265.2006.02702.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18487463$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17223984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Versiani, Beatriz R.</creatorcontrib><creatorcontrib>Trarbach, Ericka</creatorcontrib><creatorcontrib>Koenigkam-Santos, Marcel</creatorcontrib><creatorcontrib>Dos Santos, Antonio Carlos</creatorcontrib><creatorcontrib>Elias, Lucila L. K.</creatorcontrib><creatorcontrib>Moreira, Ayrton C.</creatorcontrib><creatorcontrib>Latronico, Ana Claudia</creatorcontrib><creatorcontrib>De Castro, Margaret</creatorcontrib><title>Clinical assessment and molecular analysis of GnRHR and KAL1 genes in males with idiopathic hypogonadotrophic hypogonadism</title><title>Clinical endocrinology (Oxford)</title><addtitle>Clin Endocrinol (Oxf)</addtitle><description>Summary
Objective The pathogenesis of idiopathic hypogonadotrophic hypogonadism (IHH) is mostly unclear. We characterized the clinical findings and molecular analysis of GnRHR and KAL1 genes in 26 Brazilian males with IHH with and without hyposmia/anosmia.
Design Clinical assessment was performed for endocrine status, olfactory structure and function, renal lesion, and mirror movement. The diagnosis of Kallmann syndrome (KS) included HH and the clinical complaint of hyposmia/anosmia or decreased olfactory acuity obtained by the Smell Identification Test™ (SIT). We analysed GnRHR and KAL1 genes using the polymerase chain reaction (PCR) direct sequencing method.
Results A variable degree of HH was observed, including various clinical abnormalities, such as cryptorchidism, hearing loss, strabismus, cleft lip/palate, high‐arched palate, dental agenesis, psychiatric disorders, learning dysfunction, and bimanual synkinesia. Twenty‐two out of 26 patients with IHH (85%) were classified as KS. Abnormalities of olfactory bulbs/sulci were observed in 79% of KS patients. One‐third of KS patients had renal defects and 45·5% had a positive family history. GnRHR gene sequence analysis showed no mutations. KAL1 sequence analysis identified two novel missense mutations: c.1061A to G in exon 7 (N304S) and c.1583C to A in exon 10 (S478X). We also observed a 14‐bp deletion within exon 11 that caused a premature termination. According to the National Center for Biotechnology Information (NCBI)‐Single Nucleotide Polymorphism (SNP) database, two previously described polymorphisms (rs808119 and rs809446) were detected.
Conclusion KAL1 mutations accounted for 12% of KS patients. This low prevalence of KAL1 mutations indicates that other genes, such as the fibroblast growth factor receptor 1 (FGFR1) gene or other as yet undiscovered genes, epigenetic events and/or environmental factors might be involved in the aetiology and phenotypic variability of KS.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Endocrinopathies</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Deletion</subject><subject>Gene Frequency</subject><subject>Humans</subject><subject>Hypogonadism - diagnosis</subject><subject>Hypogonadism - genetics</subject><subject>Hypothalamus. Hypophysis. Epiphysis (diseases)</subject><subject>Kallmann Syndrome - diagnosis</subject><subject>Kallmann Syndrome - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mutation, Missense</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Olfaction Disorders - diagnosis</subject><subject>Olfaction Disorders - genetics</subject><subject>Receptors, LHRH - genetics</subject><subject>Sequence Analysis, DNA</subject><subject>Vertebrates: endocrinology</subject><issn>0300-0664</issn><issn>1365-2265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE9v0zAYhy0EYl3hKyBf4Jbg2PGfHThMZeuArohpiKPlOs7q4sQhb6q1fHqctdrEbb74td_nZ796EMIFyYu0Pm7yggmeUSp4TgkROaGS0Hz3Ak0eGy_RhDBCMiJEeYJOATaEEK6IfI1OCkkpO1PlBP2dBd96awI2AA6gce2ATVvhJgZnt8H06WTCHjzgWON5e3N189D_dr4o8J1rHWDf4saEVNz7YY195WNnhrW3eL3v4l1sTRWHPnb_3Xho3qBXtQng3h73Kfp5eXE7u8oW3-dfZueLzJaM04xTaQvJ3KrgFa0FtbaSK1s7YWVplFGMcFkyYxS1Z5QIRypnK8UsJ05ZsSrZFH04vNv18c_WwaAbD9aFYFoXt6CFKqlgTCZQHUDbR4De1brrfWP6vS6IHr3rjR716lGvHr3rB-96l6Lvjn9sV42rnoJH0Ql4fwQMJNt1b1rr4YlTpZJlmmKKPh24ex_c_tkD6NnFcqxSPjvkPQxu95g3_W8tJJNc_1rONf36Wd5eL39oxv4Benuu-g</recordid><startdate>200702</startdate><enddate>200702</enddate><creator>Versiani, Beatriz R.</creator><creator>Trarbach, Ericka</creator><creator>Koenigkam-Santos, Marcel</creator><creator>Dos Santos, Antonio Carlos</creator><creator>Elias, Lucila L. K.</creator><creator>Moreira, Ayrton C.</creator><creator>Latronico, Ana Claudia</creator><creator>De Castro, Margaret</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>200702</creationdate><title>Clinical assessment and molecular analysis of GnRHR and KAL1 genes in males with idiopathic hypogonadotrophic hypogonadism</title><author>Versiani, Beatriz R. ; Trarbach, Ericka ; Koenigkam-Santos, Marcel ; Dos Santos, Antonio Carlos ; Elias, Lucila L. K. ; Moreira, Ayrton C. ; Latronico, Ana Claudia ; De Castro, Margaret</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4352-527c173eb15d2f62ccd7bcfe6c74a8a8305743aa82c9206e0decd83c50e8c6b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Endocrinopathies</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Deletion</topic><topic>Gene Frequency</topic><topic>Humans</topic><topic>Hypogonadism - diagnosis</topic><topic>Hypogonadism - genetics</topic><topic>Hypothalamus. Hypophysis. Epiphysis (diseases)</topic><topic>Kallmann Syndrome - diagnosis</topic><topic>Kallmann Syndrome - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mutation, Missense</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Olfaction Disorders - diagnosis</topic><topic>Olfaction Disorders - genetics</topic><topic>Receptors, LHRH - genetics</topic><topic>Sequence Analysis, DNA</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Versiani, Beatriz R.</creatorcontrib><creatorcontrib>Trarbach, Ericka</creatorcontrib><creatorcontrib>Koenigkam-Santos, Marcel</creatorcontrib><creatorcontrib>Dos Santos, Antonio Carlos</creatorcontrib><creatorcontrib>Elias, Lucila L. K.</creatorcontrib><creatorcontrib>Moreira, Ayrton C.</creatorcontrib><creatorcontrib>Latronico, Ana Claudia</creatorcontrib><creatorcontrib>De Castro, Margaret</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical endocrinology (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Versiani, Beatriz R.</au><au>Trarbach, Ericka</au><au>Koenigkam-Santos, Marcel</au><au>Dos Santos, Antonio Carlos</au><au>Elias, Lucila L. K.</au><au>Moreira, Ayrton C.</au><au>Latronico, Ana Claudia</au><au>De Castro, Margaret</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical assessment and molecular analysis of GnRHR and KAL1 genes in males with idiopathic hypogonadotrophic hypogonadism</atitle><jtitle>Clinical endocrinology (Oxford)</jtitle><addtitle>Clin Endocrinol (Oxf)</addtitle><date>2007-02</date><risdate>2007</risdate><volume>66</volume><issue>2</issue><spage>173</spage><epage>179</epage><pages>173-179</pages><issn>0300-0664</issn><eissn>1365-2265</eissn><coden>CLECAP</coden><abstract>Summary
Objective The pathogenesis of idiopathic hypogonadotrophic hypogonadism (IHH) is mostly unclear. We characterized the clinical findings and molecular analysis of GnRHR and KAL1 genes in 26 Brazilian males with IHH with and without hyposmia/anosmia.
Design Clinical assessment was performed for endocrine status, olfactory structure and function, renal lesion, and mirror movement. The diagnosis of Kallmann syndrome (KS) included HH and the clinical complaint of hyposmia/anosmia or decreased olfactory acuity obtained by the Smell Identification Test™ (SIT). We analysed GnRHR and KAL1 genes using the polymerase chain reaction (PCR) direct sequencing method.
Results A variable degree of HH was observed, including various clinical abnormalities, such as cryptorchidism, hearing loss, strabismus, cleft lip/palate, high‐arched palate, dental agenesis, psychiatric disorders, learning dysfunction, and bimanual synkinesia. Twenty‐two out of 26 patients with IHH (85%) were classified as KS. Abnormalities of olfactory bulbs/sulci were observed in 79% of KS patients. One‐third of KS patients had renal defects and 45·5% had a positive family history. GnRHR gene sequence analysis showed no mutations. KAL1 sequence analysis identified two novel missense mutations: c.1061A to G in exon 7 (N304S) and c.1583C to A in exon 10 (S478X). We also observed a 14‐bp deletion within exon 11 that caused a premature termination. According to the National Center for Biotechnology Information (NCBI)‐Single Nucleotide Polymorphism (SNP) database, two previously described polymorphisms (rs808119 and rs809446) were detected.
Conclusion KAL1 mutations accounted for 12% of KS patients. This low prevalence of KAL1 mutations indicates that other genes, such as the fibroblast growth factor receptor 1 (FGFR1) gene or other as yet undiscovered genes, epigenetic events and/or environmental factors might be involved in the aetiology and phenotypic variability of KS.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17223984</pmid><doi>10.1111/j.1365-2265.2006.02702.x</doi><tpages>7</tpages></addata></record> |
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| subjects | Adolescent Adult Biological and medical sciences Case-Control Studies Child Child, Preschool Endocrinopathies Extracellular Matrix Proteins - genetics Fundamental and applied biological sciences. Psychology Gene Deletion Gene Frequency Humans Hypogonadism - diagnosis Hypogonadism - genetics Hypothalamus. Hypophysis. Epiphysis (diseases) Kallmann Syndrome - diagnosis Kallmann Syndrome - genetics Male Medical sciences Mutation, Missense Nerve Tissue Proteins - genetics Non tumoral diseases. Target tissue resistance. Benign neoplasms Olfaction Disorders - diagnosis Olfaction Disorders - genetics Receptors, LHRH - genetics Sequence Analysis, DNA Vertebrates: endocrinology |
| title | Clinical assessment and molecular analysis of GnRHR and KAL1 genes in males with idiopathic hypogonadotrophic hypogonadism |
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