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      Gonadotropin Secretion in Girls with Turner Syndrome Measured by an Ultrasensitive Immunochemiluminometric Assay

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          Abstract

          Background/Aim: Gonadotropin levels measured by radioimmunoassays are high in girls with Turner syndrome (TS), but overlap significantly with those of normal girls. We hypothesized that gonadotropin levels would be above the normal range in TS when measured by ultrasensitive assays. Methods: Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were measured in 68 TS, and 133 control girls using ultrasensitive immunochemiluminometric assays (ICMA). Results: FSH levels in TS and normal girls were highest in early childhood (56.0 ± 39.7 and 2.3 ± 1.8 IU/l, respectively), declined at 6–10 years of age (11.3 ± 13.1 and 1.8 ± 0.9 IU/l, respectively), and then increased again (104.4 ± 68.9 and 4.9 ± 2.4 IU/l, respectively). FSH was in the normal range on 11 of 27 occasions in TS girls with ages 5–10 years, and on 3 of 44 occasions in >10 years. Although average LH values were higher than those of controls, they often overlapped the normal range. Conclusion: A significant number of TS girls have normal gonadotropins by ICMA. Spontaneous gonadotropin levels are not an adequate screening test for the diagnosis of TS but may prove useful for predicting the gonadal function and determining the appropriate timing of estrogen replacement therapy.

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          Impaired endothelial function in young women with premature ovarian failure: normalization with hormone therapy.

          D Sideris, Maria Kravariti, Evangelos Papanikolaou … (2004)
          Normal menopause is associated with vascular endothelial dysfunction, an early stage of atherosclerosis. The effect of premature ovarian failure (or premature menopause) on endothelial function in young women is unknown. Endothelial function was assessed in 18 women with premature ovarian failure before and after 6 months of hormone therapy and was compared with the endothelial function of 20 age- and body mass index-matched premenopausal women. Brachial artery diameter was measured both during hyperemia (an index of endothelium-dependent vasodilation) and in response to glyceryl trinitrate (an index of endothelium-independent vaso-dilation). Flow-mediated dilation was significantly lower in women with premature ovarian failure at baseline (increase in brachial artery diameter during hyperemia by 3.06 +/- 4.33%) than in control women (increase by 8.84 +/- 2.15%; P < 0.0005). Glyceryl trinitrate-induced vasodilation did not differ between the groups. After hormone therapy for 6 months, flow-mediated dilation was improved in women with premature ovarian failure, increasing by more than 2-fold (7.41 +/- 3.86%; P < 0.005 compared with pretreatment) and reaching normal values (P not significant compared with control women). Glyceryl trinitrate-induced vasodilation did not change after treatment in women with premature ovarian failure. Young women with premature ovarian failure have significant vascular endothelial dysfunction. Early onset of endothelial dysfunction associated with sex steroid deficiency may contribute to the increased risk of cardiovascular disease and mortality in young women with premature ovarian failure. Hormone therapy restores endothelial function within 6 months of treatment.
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            A diphasic pattern of gonadotropin secretion in patients with the syndrome of gonadal dysgenesis.

            F. Conte, S. Kaplan, Jacob Grumbach (1975)
            Cross sectional and longitudinal studies of plasma FSH and LH in 58 patients, age 2 days of 20 yr, with the syndrome of gonadal dysgenesis show a diphasic pattern of gonadotropin secretion. The mean basal plasma FSH level is 43 plus or minus 7 (SE) ng/ml (LER-869) in patients from 2 days to 4 yr, which is strikingly elevated. Thereafter, a decline in plasma FSH to a mean level of 4 plus or minus 0.7 (SE) ng/ml occurs between 4 and 10 yr, followed by a rise after 10 yr to 61 plus or minus 4 (SE) ng/ml. The pattern of LH (LER-960) secretion is qualitatively similar to that of FSH, although quantitatively the values for LH are 1/3 to 1/10 those for FSH. The similarity of pattern of gonadotropin secretion observed between patients with gonadal dysgenesis and normal children suggests that gonadal function does not play a decisive role in the pattern of gonadotropin secretion from infancy through adolescence, but exercises striking effects on the quantity of gonadotropin secreted.
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              Ovarian differentiation and gonadal failure.

              Philippa Simpson, A Rajkovic (1999)
              Ovarian failure can result from several different genetic mechanisms-X chromosomal abnormalities, autosomal recessive genes causing various types of XX gonadal dysgenesis, and autosomal dominant genes. The number and precise location of loci on the X are still under investigation, but it is clear that, in aggregate, these genes are responsible for ovarian maintenance, given that monosomy X shows germ cells that undergo accelerated atresia. Despite recent hypotheses, at present there is no evidence for a gene directing primary ovarian differentiation; this process may be constitutive. Phenotypic/karyotypic correlation and limited molecular confirmation have long shown that proximal Xp and proximal Xq contain regions of the most importance to ovarian maintenance. Terminal deletions at Xp11 result in 50% primary amenorrhea and 50% premature ovarian failure or fertility. Deletions at Xq13 usually produce primary amenorrhea. Terminal deletions nearer the telomeres on either Xp of Xq bring about premature ovarian failure more often than complete ovarian failure. The X-linked zinc finger gene (ZFX) and diaphanous 2 Drosophila homologue (DIAPH2) are the only candidate genes for ovarian maintenance that map to the X chromosome. Additional, as yet unidentified, genes along the X chromosome must be involved. The search for these genes in humans is hampered by the lack of candidate genes that map to the X chromosome, the scarcity of patients with fortuitous autosomal translocations, and small pedigrees, which hinder mapping of the loci. In addition, difficulties with human germ cell research also make it challenging to dissect genes important to ovarian development. Autosomal genes also are involved in ovarian differentiation and gonadal failure. Follicle-stimulating hormone receptor and ataxia telangiectasia are examples of autosomal genes known to cause human ovarian failure. Transgenic mouse models point to many other candidate autosomal genes, and sequencing of the human homologues in affected women should lead to the discovery of new genes responsible for human ovarian failure. Identification, functional analysis, and mapping of novel genes specifically expressed in the ovary of mice and women eventually should lead to fruitful dissection of essential genes in mammalian ovarian development and maintenance. Copyright 2000 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Journal ID (publisher-id): HRE
                Journal ID (nlm-ta): Horm Res Paediatr
                Journal ID (doi): 10.1159/issn.1663-2818
                Title: Hormone Research in Paediatrics
                Publisher: S. Karger AG
                ISSN (Print): 1663-2818
                ISSN (Electronic): 1663-2826
                Publication date Subscription-year: 2006
                Publication date (Print): April 2006
                Publication date (Electronic): 22 May 2006
                Volume: 65
                Issue: 5
                Pages: 261-266
                Affiliations
                aDepartment of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, N.C., USA; bDepartment of Pediatrics, University of Patras, Patras, Greece; cEsoterix Endocrinology, Calabasas Hills, Calif., USA; dDepartment of Pediatrics, University of Bologna, Bologna, Italy
                Article
                Publisher ID: 92516 Other ID: Horm Res 2006;65:261–266
                DOI: 10.1159/000092516
                PubMed ID: 16582569
                SO-VID: db95505f-6ef8-47f1-8f0e-3fb254eebe76
                Copyright © © 2006 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 20 December 2005
                Date accepted : 20 February 2006
                Page count
                Figures: 2, Tables: 1, References: 33, Pages: 6
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
                Keywords: Follicle-stimulating hormone,Luteinizing hormone,X chromosome,Turner syndrome,Gonadal dysgenesis
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes, Neurology, Nutrition & Dietetics, Sexual medicine, Internal medicine, Pharmacology & Pharmaceutical medicine
                Keywords: Follicle-stimulating hormone, Luteinizing hormone, X chromosome, Turner syndrome, Gonadal dysgenesis

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