Genomic Imprinting in Turner Syndrome: Effects on Response to Growth Hormone and on Risk of Sensorineural Hearing Loss
Context: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,Xmaternal and 45,Xpaternal individuals. Objective and Design: We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-s...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 91; no. 8; pp. 3002 - 3010 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Bethesda, MD
Oxford University Press
01.08.2006
Copyright by The Endocrine Society Endocrine Society |
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| Online Access | Get full text |
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| Abstract | Context: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,Xmaternal and 45,Xpaternal individuals.
Objective and Design: We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height.
Methods and Results: Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an Xmaternal, whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact Xpaternal. No significant differences were noted between Xmaternal and Xpaternal subjects for parents’ heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with Xmaternal, baseline height sd score correlated with midparental height (all: r = 0.511, P < 0.001; Xmaternal: r = 0.535, P = 0.001) and with mother’s height (all: r = 0.510, P < 0.001; Xmaternal: r = 0.574, P < 0.001) but only weakly with father’s height (all: r = 0.334, P = 0.015; Xmaternal: r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with Xmaternal had a greater mean height gain than those with Xpaternal (sd score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04–0.82, P = 0.030, and for 45,X was +0.64 and 0.06–1.21, P = 0.031); X-linked imprinting explained 36–53% of the GH response. After pure tone audiometry testing, Xmaternal subjects were also less likely (P = 0.040) to have sensorineural hearing loss than Xpaternal subjects.
Conclusion: This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. |
|---|---|
| AbstractList | Context: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,Xmaternal and 45,Xpaternal individuals.
Objective and Design: We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height.
Methods and Results: Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an Xmaternal, whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact Xpaternal. No significant differences were noted between Xmaternal and Xpaternal subjects for parents’ heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with Xmaternal, baseline height sd score correlated with midparental height (all: r = 0.511, P < 0.001; Xmaternal: r = 0.535, P = 0.001) and with mother’s height (all: r = 0.510, P < 0.001; Xmaternal: r = 0.574, P < 0.001) but only weakly with father’s height (all: r = 0.334, P = 0.015; Xmaternal: r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with Xmaternal had a greater mean height gain than those with Xpaternal (sd score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04–0.82, P = 0.030, and for 45,X was +0.64 and 0.06–1.21, P = 0.031); X-linked imprinting explained 36–53% of the GH response. After pure tone audiometry testing, Xmaternal subjects were also less likely (P = 0.040) to have sensorineural hearing loss than Xpaternal subjects.
Conclusion: This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. Context: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,Xmaternal and 45,Xpaternal individuals. Objective and Design: We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height. Methods and Results: Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an Xmaternal, whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact Xpaternal. No significant differences were noted between Xmaternal and Xpaternal subjects for parents’ heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with Xmaternal, baseline height sd score correlated with midparental height (all: r = 0.511, P < 0.001; Xmaternal: r = 0.535, P = 0.001) and with mother’s height (all: r = 0.510, P < 0.001; Xmaternal: r = 0.574, P < 0.001) but only weakly with father’s height (all: r = 0.334, P = 0.015; Xmaternal: r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with Xmaternal had a greater mean height gain than those with Xpaternal (sd score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04–0.82, P = 0.030, and for 45,X was +0.64 and 0.06–1.21, P = 0.031); X-linked imprinting explained 36–53% of the GH response. After pure tone audiometry testing, Xmaternal subjects were also less likely (P = 0.040) to have sensorineural hearing loss than Xpaternal subjects. Conclusion: This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X(maternal) and 45,X(paternal) individuals. We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height. Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an X(maternal), whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact X(paternal). No significant differences were noted between X(maternal) and X(paternal) subjects for parents' heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with X(maternal), baseline height sd score correlated with midparental height (all: r = 0.511, P < 0.001; X(maternal): r = 0.535, P = 0.001) and with mother's height (all: r = 0.510, P < 0.001; X(maternal): r = 0.574, P < 0.001) but only weakly with father's height (all: r = 0.334, P = 0.015; X(maternal): r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with X(maternal) had a greater mean height gain than those with X(paternal) (sd score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04-0.82, P = 0.030, and for 45,X was +0.64 and 0.06-1.21, P = 0.031); X-linked imprinting explained 36-53% of the GH response. After pure tone audiometry testing, X(maternal) subjects were also less likely (P = 0.040) to have sensorineural hearing loss than X(paternal) subjects. This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X(maternal) and 45,X(paternal) individuals.CONTEXTEvidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X(maternal) and 45,X(paternal) individuals.We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height.OBJECTIVE AND DESIGNWe evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height.Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an X(maternal), whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact X(paternal). No significant differences were noted between X(maternal) and X(paternal) subjects for parents' heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with X(maternal), baseline height sd score correlated with midparental height (all: r = 0.511, P < 0.001; X(maternal): r = 0.535, P = 0.001) and with mother's height (all: r = 0.510, P < 0.001; X(maternal): r = 0.574, P < 0.001) but only weakly with father's height (all: r = 0.334, P = 0.015; X(maternal): r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with X(maternal) had a greater mean height gain than those with X(paternal) (sd score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04-0.82, P = 0.030, and for 45,X was +0.64 and 0.06-1.21, P = 0.031); X-linked imprinting explained 36-53% of the GH response. After pure tone audiometry testing, X(maternal) subjects were also less likely (P = 0.040) to have sensorineural hearing loss than X(paternal) subjects.METHODS AND RESULTSMicrosatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an X(maternal), whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact X(paternal). No significant differences were noted between X(maternal) and X(paternal) subjects for parents' heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with X(maternal), baseline height sd score correlated with midparental height (all: r = 0.511, P < 0.001; X(maternal): r = 0.535, P = 0.001) and with mother's height (all: r = 0.510, P < 0.001; X(maternal): r = 0.574, P < 0.001) but only weakly with father's height (all: r = 0.334, P = 0.015; X(maternal): r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with X(maternal) had a greater mean height gain than those with X(paternal) (sd score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04-0.82, P = 0.030, and for 45,X was +0.64 and 0.06-1.21, P = 0.031); X-linked imprinting explained 36-53% of the GH response. After pure tone audiometry testing, X(maternal) subjects were also less likely (P = 0.040) to have sensorineural hearing loss than X(paternal) subjects.This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes.CONCLUSIONThis study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. CONTEXT:Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X and 45,X individuals. OBJECTIVE AND DESIGN:We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height. METHODS AND RESULTS:Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an X, whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact X. No significant differences were noted between X and X subjects for parents’ heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with X, baseline height SD score correlated with midparental height (allr = 0.511, P < 0.001; Xr = 0.535, P = 0.001) and with mother’s height (allr = 0.510, P < 0.001; Xr = 0.574, P < 0.001) but only weakly with father’s height (allr = 0.334, P = 0.015; Xr = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with X had a greater mean height gain than those with X (SD score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04-0.82, P = 0.030, and for 45,X was +0.64 and 0.06-1.21, P = 0.031); X-linked imprinting explained 36-53% of the GH response. After pure tone audiometry testing, X subjects were also less likely (P = 0.040) to have sensorineural hearing loss than X subjects. CONCLUSION:This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. CONTEXT: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X super(maternal) and 45,X super(paternal) individuals. OBJECTIVE: and Design: We evaluated the parent-of-origin effect of the intact X chromosome on spontaneous growth, GH-stimulated height gain, and frequency of sensorineural hearing loss in 54 subjects with Turner syndrome recruited from a Canadian randomized, controlled trial of GH supplementation to adult height. METHODS: and Results: Microsatellite analyses revealed that 72% of nonmosaic 45,X subjects retained an X super(maternal), whereas 86% of nonmosaic 46,X,i(Xq) subjects carried an intact X super(paternal). No significant differences were noted between X super(maternal) and X super(paternal) subjects for parents' heights, birth weight and length, and height, age, or bone age at study entry. In all subjects, and in those with X super(maternal), baseline height SD score correlated with midparental height (all: r = 0.511, P < 0.001; X super(maternal): r = 0.535, P = 0.001) and with mother's height (all: r = 0.510, P < 0.001; X super(maternal): r = 0.574, P < 0.001) but only weakly with father's height (all: r = 0.334, P = 0.015; X super(maternal): r = 0.292, P = 0.094). Using a linear model including age and height at GH initiation, subjects with X super(maternal) had a greater mean height gain than those with X super(paternal) (SD score difference and 95% confidence interval for all karyotypes was +0.43 and 0.04-0.82, P = 0.030, and for 45,X was +0.64 and 0.06-1.21, P = 0.031); X-linked imprinting explained 36-53% of the GH response. After pure tone audiometry testing, X super(maternal) subjects were also less likely (P = 0.040) to have sensorineural hearing loss than X super(paternal) subjects. CONCLUSION: This study provides evidence of an X-linked imprinting effect on GH response and on sensorineural hearing loss in Turner syndrome and should fuel the search for candidate genes. |
| Author | Quigley, Charmian A. Deal, Cheri L. Hamelin, Catherine E. Anglin, Greg |
| AuthorAffiliation | Division of Experimental Medicine (C.E.H., C.L.D.), McGill University, Montreal, Québec, Canada H3A 1A3; Endocrinology Service and Research Center (C.E.H., C.L.D.), Hôpital Ste-Justine, Montreal, Québec, Canada H3T 1C5; Statistics (G.A.), Lilly Research Laboratories, Toronto, Ontario, Canada M4G 2P1; Endocrinology (C.A.Q.), Lilly Research Laboratories, US Medical, Indianapolis, Indiana 46258; and Department of Pediatrics (C.L.D.), University of Montreal, Montreal, Québec, Canada H3C 3J7 |
| AuthorAffiliation_xml | – name: Division of Experimental Medicine (C.E.H., C.L.D.), McGill University, Montreal, Québec, Canada H3A 1A3; Endocrinology Service and Research Center (C.E.H., C.L.D.), Hôpital Ste-Justine, Montreal, Québec, Canada H3T 1C5; Statistics (G.A.), Lilly Research Laboratories, Toronto, Ontario, Canada M4G 2P1; Endocrinology (C.A.Q.), Lilly Research Laboratories, US Medical, Indianapolis, Indiana 46258; and Department of Pediatrics (C.L.D.), University of Montreal, Montreal, Québec, Canada H3C 3J7 |
| Author_xml | – sequence: 1 givenname: Catherine E. surname: Hamelin fullname: Hamelin, Catherine E. organization: 1Division of Experimental Medicine (C.E.H., C.L.D.), McGill University, Montreal, Québec, Canada H3A 1A3 – sequence: 2 givenname: Greg surname: Anglin fullname: Anglin, Greg organization: 3Statistics (G.A.), Lilly Research Laboratories, Toronto, Ontario, Canada M4G 2P1 – sequence: 3 givenname: Charmian A. surname: Quigley fullname: Quigley, Charmian A. organization: 4Endocrinology (C.A.Q.), Lilly Research Laboratories, US Medical, Indianapolis, Indiana 46258 – sequence: 4 givenname: Cheri L. surname: Deal fullname: Deal, Cheri L. email: Cheri.L.Deal@umontreal.ca organization: 1Division of Experimental Medicine (C.E.H., C.L.D.), McGill University, Montreal, Québec, Canada H3A 1A3 |
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| Keywords | Chromosomal aberration Dysgenesia Internal ear disease Genital system Somatotropin hormone Auditory disorder Sexual differentiation disorder Turner syndrome Epidemiology Female genital diseases Genomic imprinting Adenohypophyseal hormone Malformation Gonad Risk factor ENT disease Perception hearing loss Sensory hearing loss Endocrinology |
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| PublicationYear | 2006 |
| Publisher | Oxford University Press Copyright by The Endocrine Society Endocrine Society |
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| Snippet | Context: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,Xmaternal and... CONTEXT:Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X and 45,X... Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X(maternal) and... CONTEXT: Evidence exists for X-linked parent-of-origin effects in Turner syndrome, because phenotypic and cognitive profiles differ between 45,X... |
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| SubjectTerms | Age Biological and medical sciences Birth weight Body height Body Height - genetics Chromosomes, Human, X - genetics Endocrinopathies Female Fundamental and applied biological sciences. Psychology Genetic disorders Genetic Linkage Genetic Predisposition to Disease Genomic imprinting Genomic Imprinting - genetics Genotype Growth hormones Hearing loss Hearing Loss, Sensorineural - complications Hearing Loss, Sensorineural - genetics Human Growth Hormone - therapeutic use Humans Karyotypes Karyotyping Medical sciences Microsatellite Repeats - genetics Parents Recombinant Proteins - therapeutic use Turner Syndrome - complications Turner Syndrome - genetics Turner's syndrome Vertebrates: endocrinology |
| Title | Genomic Imprinting in Turner Syndrome: Effects on Response to Growth Hormone and on Risk of Sensorineural Hearing Loss |
| URI | https://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00004678-200608000-00033 https://www.ncbi.nlm.nih.gov/pubmed/16757526 https://www.proquest.com/docview/3164420188 https://www.proquest.com/docview/19364772 https://www.proquest.com/docview/68724746 |
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