Increased urinary 6-sulfatoxymelatonin excretion in women with non-classical steroid 21-hydroxylase deficiency
To determine melatonin production in hyperandrogenic women. Seventeen women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) and 15 control women were studied in early follicular phase of the menstrual cycle. Fasting serum levels of luteinizing hormone (LH), follicle-stim...
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Veröffentlicht in: | Neuro-endocrinology letters 2001-10, Vol.22 (5), p.332-336 |
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creator | Luboshitzky, R Qupti, G Ishay, A Shen-Orr, Z Herer, P |
description | To determine melatonin production in hyperandrogenic women.
Seventeen women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) and 15 control women were studied in early follicular phase of the menstrual cycle. Fasting serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, dihydroepiandrosterone sulfate (DHEA-S), 17-hydroxyprogesterone (17-OHP) as well as the peak 17-OHP response to ACTH (250 microg IV) and 24h urinary 6-sulfatoxymelatonin (aMT6s) were determined in all participants.
All 17 hyperandrogenic women were carrying mutations of the CYP21 gene. Women with LOCAH had significantly higher serum testosterone, DHEA-S, 17-OHP and ACTH stimulated 17-OHP values compared with controls. Their aMT6s values (44.6+/-20.3 microg/24h) were significantly higher than the values in control women (31.5+/-20.3) (p |
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Seventeen women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) and 15 control women were studied in early follicular phase of the menstrual cycle. Fasting serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, dihydroepiandrosterone sulfate (DHEA-S), 17-hydroxyprogesterone (17-OHP) as well as the peak 17-OHP response to ACTH (250 microg IV) and 24h urinary 6-sulfatoxymelatonin (aMT6s) were determined in all participants.
All 17 hyperandrogenic women were carrying mutations of the CYP21 gene. Women with LOCAH had significantly higher serum testosterone, DHEA-S, 17-OHP and ACTH stimulated 17-OHP values compared with controls. Their aMT6s values (44.6+/-20.3 microg/24h) were significantly higher than the values in control women (31.5+/-20.3) (p<0.03). The urinary aMT6s values were positively correlated with testosterone (p<0.04), DHEA-S (p<0.02) and peak 17-OHP (p<0.04).
Women with LOCAH have increased melatonin production. There is a relationship between adrenal androgens and melatonin in these women.</description><identifier>ISSN: 0172-780X</identifier><identifier>PMID: 11600882</identifier><language>eng</language><publisher>Sweden</publisher><subject>17-alpha-Hydroxyprogesterone - blood ; Adolescent ; Adrenal Hyperplasia, Congenital ; Adrenocorticotropic Hormone ; Adult ; Dehydroepiandrosterone Sulfate - blood ; Estradiol - blood ; Fasting ; Female ; Follicle Stimulating Hormone - blood ; Follicular Phase ; Humans ; Hyperandrogenism - enzymology ; Hyperandrogenism - genetics ; Luteinizing Hormone - blood ; Melatonin - analogs & derivatives ; Melatonin - urine ; Mutation ; Steroid 21-Hydroxylase - genetics ; Testosterone - blood</subject><ispartof>Neuro-endocrinology letters, 2001-10, Vol.22 (5), p.332-336</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11600882$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luboshitzky, R</creatorcontrib><creatorcontrib>Qupti, G</creatorcontrib><creatorcontrib>Ishay, A</creatorcontrib><creatorcontrib>Shen-Orr, Z</creatorcontrib><creatorcontrib>Herer, P</creatorcontrib><title>Increased urinary 6-sulfatoxymelatonin excretion in women with non-classical steroid 21-hydroxylase deficiency</title><title>Neuro-endocrinology letters</title><addtitle>Neuro Endocrinol Lett</addtitle><description>To determine melatonin production in hyperandrogenic women.
Seventeen women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) and 15 control women were studied in early follicular phase of the menstrual cycle. Fasting serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, dihydroepiandrosterone sulfate (DHEA-S), 17-hydroxyprogesterone (17-OHP) as well as the peak 17-OHP response to ACTH (250 microg IV) and 24h urinary 6-sulfatoxymelatonin (aMT6s) were determined in all participants.
All 17 hyperandrogenic women were carrying mutations of the CYP21 gene. Women with LOCAH had significantly higher serum testosterone, DHEA-S, 17-OHP and ACTH stimulated 17-OHP values compared with controls. Their aMT6s values (44.6+/-20.3 microg/24h) were significantly higher than the values in control women (31.5+/-20.3) (p<0.03). The urinary aMT6s values were positively correlated with testosterone (p<0.04), DHEA-S (p<0.02) and peak 17-OHP (p<0.04).
Women with LOCAH have increased melatonin production. There is a relationship between adrenal androgens and melatonin in these women.</description><subject>17-alpha-Hydroxyprogesterone - blood</subject><subject>Adolescent</subject><subject>Adrenal Hyperplasia, Congenital</subject><subject>Adrenocorticotropic Hormone</subject><subject>Adult</subject><subject>Dehydroepiandrosterone Sulfate - blood</subject><subject>Estradiol - blood</subject><subject>Fasting</subject><subject>Female</subject><subject>Follicle Stimulating Hormone - blood</subject><subject>Follicular Phase</subject><subject>Humans</subject><subject>Hyperandrogenism - enzymology</subject><subject>Hyperandrogenism - genetics</subject><subject>Luteinizing Hormone - blood</subject><subject>Melatonin - analogs & derivatives</subject><subject>Melatonin - urine</subject><subject>Mutation</subject><subject>Steroid 21-Hydroxylase - genetics</subject><subject>Testosterone - blood</subject><issn>0172-780X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kD1rwzAYhDW0NGnav1A0dTNIsmVJYwn9CAS6tNDNyNIroiJLqWXT-N9X0GS547iHG-4KrQkVrBKSfK3Qbc7fhDDFWX2DVpS2hEjJ1ijuohlBZ7B4Hn3U44LbKs_B6SmdlgFC8egjhlPBJp8iLuE3DVDUTwccU6xM0Dl7owPOE4zJW8xodVjsWBZKBdiC88ZDNMsdunY6ZLg_-wZ9vjx_bN-q_fvrbvu0r46MiKniqgGqwFnRO9tL1TJqaqN4T2tnnG1ly3XNuOwd145IZVjDBVOEStGwntf1Bj3-7x7H9DNDnrrBZwMh6Ahpzp1gTNJGtAV8OINzP4DtjqMfygnd5aH6D6M9Y3Q</recordid><startdate>20011001</startdate><enddate>20011001</enddate><creator>Luboshitzky, R</creator><creator>Qupti, G</creator><creator>Ishay, A</creator><creator>Shen-Orr, Z</creator><creator>Herer, P</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20011001</creationdate><title>Increased urinary 6-sulfatoxymelatonin excretion in women with non-classical steroid 21-hydroxylase deficiency</title><author>Luboshitzky, R ; Qupti, G ; Ishay, A ; Shen-Orr, Z ; Herer, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p207t-594e19efd7bfdb89621c3c95b13fcfd6865a3258bf5af089c245729018742b533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>17-alpha-Hydroxyprogesterone - blood</topic><topic>Adolescent</topic><topic>Adrenal Hyperplasia, Congenital</topic><topic>Adrenocorticotropic Hormone</topic><topic>Adult</topic><topic>Dehydroepiandrosterone Sulfate - blood</topic><topic>Estradiol - blood</topic><topic>Fasting</topic><topic>Female</topic><topic>Follicle Stimulating Hormone - blood</topic><topic>Follicular Phase</topic><topic>Humans</topic><topic>Hyperandrogenism - enzymology</topic><topic>Hyperandrogenism - genetics</topic><topic>Luteinizing Hormone - blood</topic><topic>Melatonin - analogs & derivatives</topic><topic>Melatonin - urine</topic><topic>Mutation</topic><topic>Steroid 21-Hydroxylase - genetics</topic><topic>Testosterone - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luboshitzky, R</creatorcontrib><creatorcontrib>Qupti, G</creatorcontrib><creatorcontrib>Ishay, A</creatorcontrib><creatorcontrib>Shen-Orr, Z</creatorcontrib><creatorcontrib>Herer, P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Neuro-endocrinology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luboshitzky, R</au><au>Qupti, G</au><au>Ishay, A</au><au>Shen-Orr, Z</au><au>Herer, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased urinary 6-sulfatoxymelatonin excretion in women with non-classical steroid 21-hydroxylase deficiency</atitle><jtitle>Neuro-endocrinology letters</jtitle><addtitle>Neuro Endocrinol Lett</addtitle><date>2001-10-01</date><risdate>2001</risdate><volume>22</volume><issue>5</issue><spage>332</spage><epage>336</epage><pages>332-336</pages><issn>0172-780X</issn><abstract>To determine melatonin production in hyperandrogenic women.
Seventeen women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) and 15 control women were studied in early follicular phase of the menstrual cycle. Fasting serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, dihydroepiandrosterone sulfate (DHEA-S), 17-hydroxyprogesterone (17-OHP) as well as the peak 17-OHP response to ACTH (250 microg IV) and 24h urinary 6-sulfatoxymelatonin (aMT6s) were determined in all participants.
All 17 hyperandrogenic women were carrying mutations of the CYP21 gene. Women with LOCAH had significantly higher serum testosterone, DHEA-S, 17-OHP and ACTH stimulated 17-OHP values compared with controls. Their aMT6s values (44.6+/-20.3 microg/24h) were significantly higher than the values in control women (31.5+/-20.3) (p<0.03). The urinary aMT6s values were positively correlated with testosterone (p<0.04), DHEA-S (p<0.02) and peak 17-OHP (p<0.04).
Women with LOCAH have increased melatonin production. There is a relationship between adrenal androgens and melatonin in these women.</abstract><cop>Sweden</cop><pmid>11600882</pmid><tpages>5</tpages></addata></record> |
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subjects | 17-alpha-Hydroxyprogesterone - blood Adolescent Adrenal Hyperplasia, Congenital Adrenocorticotropic Hormone Adult Dehydroepiandrosterone Sulfate - blood Estradiol - blood Fasting Female Follicle Stimulating Hormone - blood Follicular Phase Humans Hyperandrogenism - enzymology Hyperandrogenism - genetics Luteinizing Hormone - blood Melatonin - analogs & derivatives Melatonin - urine Mutation Steroid 21-Hydroxylase - genetics Testosterone - blood |
title | Increased urinary 6-sulfatoxymelatonin excretion in women with non-classical steroid 21-hydroxylase deficiency |
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