AUTOIMMUNE DISORDERS IN WOMEN WITH TURNER SYNDROME AND WOMEN WITH KARYOTYPICALLY NORMAL PRIMARY OVARIAN INSUFFICIENCY
Identifieur interne : 004535 ( Main/Exploration ); précédent : 004534; suivant : 004536AUTOIMMUNE DISORDERS IN WOMEN WITH TURNER SYNDROME AND WOMEN WITH KARYOTYPICALLY NORMAL PRIMARY OVARIAN INSUFFICIENCY
Auteurs : Vladimir K. Bakalov ; Liat Gutin ; Clara M. Cheng ; Jian Zhou ; Puja Sheth ; Kavita Shah ; Sruthi Arepalli ; Vien Vanderhoof ; Lawrence M. Nelson ; Carolyn A. BondySource :
- Journal of Autoimmunity [ 0896-8411 ] ; 2012.
Abstract
The higher prevalence of autoimmune diseases in women compared to men could be due to effects of ovarian hormones, pregnancy and/or the presence of a 2nd X chromosome. To elucidate the role of these factors, we investigated the prevalence and spectrum of autoimmune diagnoses in women with primary ovarian insufficiency associated with X chromosome monosomy (Turner syndrome, TS, n=244) and women with karyotypically normal (46,XX) primary ovarian insufficiency (POI, n=457) in a prospective study, conducted at the National Institutes of Health. We compared the study group prevalence to normative data for the U.S. population of women. Chronic lymphocytic (Hashimoto’s) thyroiditis (HT) occurred in 37% of women with TS vs. 15% with POI (P<0.0001); HT prevalence in both ovarian insufficiency groups significantly exceeded that in U.S. population of women (5.8%). Inflammatory bowel (IBD, 4%) and celiac disease (CD, 2.7%) were significantly increased in TS, but not in POI. No other autoimmune diagnosis, including Graves’ disease or Type 1 diabetes appears to be significantly increased in either group. Women with TS had higher pro-inflammatory IL6 and TGF β1 levels (p<0.0001 for both), and lower anti-inflammatory IL10 and TGF β2 levels (p<0.005 for both) compared to POI and to normal volunteers. Lifetime estrogen exposure and parity were significantly lower in TS compared to POI, which were in turn lower than the general population of women. The finding that lymphocytic thyroiditis is greatly increased in both women with TS and POI suggests that factors associated with ovarian insufficiency per se promote this form of autoimmunity. The absence of a normal second X-chromosome further contributes to increased autoimmunity in TS.
Url:
DOI: 10.1016/j.jaut.2012.01.015
PubMed: 22342295
PubMed Central: 3358475
Affiliations:
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">AUTOIMMUNE DISORDERS IN WOMEN WITH TURNER SYNDROME AND WOMEN WITH KARYOTYPICALLY NORMAL PRIMARY OVARIAN INSUFFICIENCY</title>
<author><name sortKey="Bakalov, Vladimir K" sort="Bakalov, Vladimir K" uniqKey="Bakalov V" first="Vladimir K." last="Bakalov">Vladimir K. Bakalov</name>
<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<author><name sortKey="Cheng, Clara M" sort="Cheng, Clara M" uniqKey="Cheng C" first="Clara M" last="Cheng">Clara M. Cheng</name>
<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<author><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name>
<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<author><name sortKey="Sheth, Puja" sort="Sheth, Puja" uniqKey="Sheth P" first="Puja" last="Sheth">Puja Sheth</name>
<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<author><name sortKey="Shah, Kavita" sort="Shah, Kavita" uniqKey="Shah K" first="Kavita" last="Shah">Kavita Shah</name>
<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<author><name sortKey="Arepalli, Sruthi" sort="Arepalli, Sruthi" uniqKey="Arepalli S" first="Sruthi" last="Arepalli">Sruthi Arepalli</name>
<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<author><name sortKey="Vanderhoof, Vien" sort="Vanderhoof, Vien" uniqKey="Vanderhoof V" first="Vien" last="Vanderhoof">Vien Vanderhoof</name>
<affiliation><nlm:aff id="A2">Program on Reproductive and Adult Endocrinology,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
</affiliation>
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<author><name sortKey="Nelson, Lawrence M" sort="Nelson, Lawrence M" uniqKey="Nelson L" first="Lawrence M." last="Nelson">Lawrence M. Nelson</name>
<affiliation><nlm:aff id="A2">Program on Reproductive and Adult Endocrinology,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
<wicri:noCountry code="subfield">20892</wicri:noCountry>
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<affiliation><nlm:aff id="A1">Section on Epigenetics & Development, Program on Developmental Endocrinology and Genetics,<italic>Eunice Kennedy Shriver</italic>
National Institute of Child Health and Human Development, NIH, Bethesda, MD, 20892</nlm:aff>
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<series><title level="j">Journal of Autoimmunity</title>
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<front><div type="abstract" xml:lang="en"><p id="P2">The higher prevalence of autoimmune diseases in women compared to men could be due to effects of ovarian hormones, pregnancy and/or the presence of a 2<sup>nd</sup>
X chromosome. To elucidate the role of these factors, we investigated the prevalence and spectrum of autoimmune diagnoses in women with primary ovarian insufficiency associated with X chromosome monosomy (Turner syndrome, TS, n=244) and women with karyotypically normal (46,XX) primary ovarian insufficiency (POI, n=457) in a prospective study, conducted at the National Institutes of Health. We compared the study group prevalence to normative data for the U.S. population of women. Chronic lymphocytic (Hashimoto’s) thyroiditis (HT) occurred in 37% of women with TS vs. 15% with POI (P<0.0001); HT prevalence in both ovarian insufficiency groups significantly exceeded that in U.S. population of women (5.8%). Inflammatory bowel (IBD, 4%) and celiac disease (CD, 2.7%) were significantly increased in TS, but not in POI. No other autoimmune diagnosis, including Graves’ disease or Type 1 diabetes appears to be significantly increased in either group. Women with TS had higher pro-inflammatory IL6 and TGF β1 levels (p<0.0001 for both), and lower anti-inflammatory IL10 and TGF β2 levels (p<0.005 for both) compared to POI and to normal volunteers. Lifetime estrogen exposure and parity were significantly lower in TS compared to POI, which were in turn lower than the general population of women. The finding that lymphocytic thyroiditis is greatly increased in both women with TS and POI suggests that factors associated with ovarian insufficiency per se promote this form of autoimmunity. The absence of a normal second X-chromosome further contributes to increased autoimmunity in TS.</p>
</div>
</front>
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<affiliations><list></list>
<tree><noCountry><name sortKey="Arepalli, Sruthi" sort="Arepalli, Sruthi" uniqKey="Arepalli S" first="Sruthi" last="Arepalli">Sruthi Arepalli</name>
<name sortKey="Bakalov, Vladimir K" sort="Bakalov, Vladimir K" uniqKey="Bakalov V" first="Vladimir K." last="Bakalov">Vladimir K. Bakalov</name>
<name sortKey="Bondy, Carolyn A" sort="Bondy, Carolyn A" uniqKey="Bondy C" first="Carolyn A." last="Bondy">Carolyn A. Bondy</name>
<name sortKey="Cheng, Clara M" sort="Cheng, Clara M" uniqKey="Cheng C" first="Clara M" last="Cheng">Clara M. Cheng</name>
<name sortKey="Gutin, Liat" sort="Gutin, Liat" uniqKey="Gutin L" first="Liat" last="Gutin">Liat Gutin</name>
<name sortKey="Nelson, Lawrence M" sort="Nelson, Lawrence M" uniqKey="Nelson L" first="Lawrence M." last="Nelson">Lawrence M. Nelson</name>
<name sortKey="Shah, Kavita" sort="Shah, Kavita" uniqKey="Shah K" first="Kavita" last="Shah">Kavita Shah</name>
<name sortKey="Sheth, Puja" sort="Sheth, Puja" uniqKey="Sheth P" first="Puja" last="Sheth">Puja Sheth</name>
<name sortKey="Vanderhoof, Vien" sort="Vanderhoof, Vien" uniqKey="Vanderhoof V" first="Vien" last="Vanderhoof">Vien Vanderhoof</name>
<name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name>
</noCountry>
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