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[PMID]:29183799
[Au] Autor:Xing JS; Bai ZM
[Ad] Endereço:Department of Urinary Surgery, Central South University Xiangya School of Medicine Affiliated Haikou Hospital(Haikou People's Hospital), Haikou 570208, PR China.
[Ti] Título:Is testicular dysgenesis syndrome a genetic, endocrine, or environmental disease, or an unexplained reproductive disorder?
[So] Source:Life Sci;194:120-129, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Progressive increases in the incidence of male reproductive disorders inclusive of hypospadias, cryptorchidism, poor semen quality, and testicular germ cell cancer (TGCC) have been observed in recent times. The central hypothesis of this study asserted that these disorders may all collectively signify testicular dysgenesis syndrome (TDS). This review aimed to provide evidence verifying the reality of TDS based on four key aspects: environmental endocrine-disrupting chemicals (EDCs), genetic factors, intrauterine growth disorders and lifestyle factors. Although TDS might result from genetic polymorphisms or aberration, recent evidence has highlighted links indicating the conditions associations to both environmental and lifestyle factors due to the rapid temporal changes in the clinical symptoms observed over recent decades. Based on our review of genetic and environmental factors, a key observation of our study suggested that there is an urgent need to prioritize research in reproductive physiology and pathophysiology, particularly in highly industrialized countries facing decreasing populations. At present, current research has yet to elucidate the mechanisms of TDS, in addition to the lack of genuine consideration of a variety of potentially key factors and TDS mechanisms. In conclusion, our study revealed that environmental exposures owing to modern lifestyles are primary factors involved in the associated trends of the syndrome, which are capable of affecting the adult endocrine system via direct means or through epigenetic mechanisms.
[Mh] Termos MeSH primário: Disgenesia Gonadal/etiologia
Infertilidade Masculina/etiologia
Doenças Testiculares/etiologia
Testículo/patologia
[Mh] Termos MeSH secundário: Animais
Disruptores Endócrinos/efeitos adversos
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/patologia
Disgenesia Gonadal/genética
Disgenesia Gonadal/patologia
Seres Humanos
Infertilidade Masculina/genética
Infertilidade Masculina/patologia
Estilo de Vida
Masculino
Neoplasias Embrionárias de Células Germinativas/etiologia
Neoplasias Embrionárias de Células Germinativas/genética
Neoplasias Embrionárias de Células Germinativas/patologia
Polimorfismo Genético
Doenças Testiculares/genética
Doenças Testiculares/patologia
Neoplasias Testiculares/etiologia
Neoplasias Testiculares/genética
Neoplasias Testiculares/patologia
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endocrine Disruptors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


  2 / 1259 MEDLINE  
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[PMID]:28278532
[Au] Autor:Desai S; Rajkovic A
[Ad] Endereço:Department of Obstetrics, Gynecology, and Reproductive Sciences, Magee-Womens Research Institute, University of Pittsburgh, Pittsburgh, Pennsylvania.
[Ti] Título:Genetics of Reproductive Aging from Gonadal Dysgenesis through Menopause.
[So] Source:Semin Reprod Med;35(2):147-159, 2017 Mar.
[Is] ISSN:1526-4564
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reproduction is essential for the survival of the species and is influenced by external factors such as smoking and exposure to chemotherapy as well as chronic disorders such as obesity and autoimmunity. Reproductive senescence, such as menopause, is also dependent on multiple intrinsic genetic factors. Reproductive aging is not isolated from an overall aging process, and several studies strongly support the link between the early age of menopause and mortality. The extreme form of reproductive aging is primary ovarian insufficiency (POI) with prevalence ranging from 1 to 5% of the female population. POI has been shown to have long-term consequences on overall health. POI and age of menopause have a significant hereditary component. The population-based genome-wide association studies have identified 44 genomic loci to associate with age of menopause, and 29 of 44 loci harbor DNA damage response genes. Recent application of whole exome sequencing on carefully selected families with POI has also revealed a significant contribution of DNA damage response genes. The inability to repair the DNA damage in both somatic and germ cells might be a predisposing factor for the link between reproductive and overall aging in a subset of individuals with POI. The aim of this review is to characterize recent advances in the genetics of POI and its link with overall health.
[Mh] Termos MeSH primário: Envelhecimento/genética
Disgenesia Gonadal/genética
Menopausa/genética
Insuficiência Ovariana Primária/genética
Reprodução
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Dano ao DNA
Reparo do DNA
Epistasia Genética
Feminino
Predisposição Genética para Doença
Disgenesia Gonadal/fisiopatologia
Hereditariedade
Seres Humanos
Masculino
Fenótipo
Insuficiência Ovariana Primária/fisiopatologia
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1055/s-0037-1599086


  3 / 1259 MEDLINE  
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[PMID]:28160395
[Au] Autor:Rossi M; Vasiljevic A; Labalme A; Dijoud F; Mallet-Motak D; Petcu CA; Touraine R; Vianey-Saban C; Guibaud L; Edery P; Sanlaville D; Morel Y
[Ad] Endereço:Service de Génétique, Centre de Référence Anomalies du Développement, Hospices Civils de Lyon, Bron, France.
[Ti] Título:A novel disorder of sex development, characterized by progressive regression of testicular function and cystic leukoencephalopathy.
[So] Source:Am J Med Genet A;173(3):654-660, 2017 Mar.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report a novel syndromic disorder of sex development observed in three male siblings, presenting with the association of micropenis without hypospadias, cryptorchidism, very low level of antimüllerian hormone in the neonatal period, and no persistent müllerian duct structures, suggesting a progressive regression of testicular function. The patients described here showed a striking neurological involvement including bilateral periventricular cysts observed in the anterior part of the frontal horns prenatally and increasing in size and number over time, associated with infra and supratentorial parenchymal atrophy, dilated ventricular system, corpus callosum hypoplasia, severe intellectual disability, and epilepsy. Associated features included a distinctive facies, joint contractures, retinopathy, and hearing loss. Pathological examination was consistent with testicular dysgenesis and leukoencephalopathy with spongiosis and microcalcifications. To the best of our knowledge, this disease, characterized by a recognizable pattern of malformations, has not been previously reported. An exhaustive genetic and metabolic evaluation was normal. Autosomal recessive inheritance was considered to be likely, on the basis of SNP studies. We hope that the detailed description provided here of the clinical, radiological, and pathological findings observed in this family will help to identify further unrelated patients, and ultimately, to clarify the genetic basis of this condition. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Transtornos do Desenvolvimento Sexual/diagnóstico
Transtornos do Desenvolvimento Sexual/genética
Disgenesia Gonadal/diagnóstico
Disgenesia Gonadal/genética
Leucoencefalopatias/diagnóstico
Leucoencefalopatias/genética
Fenótipo
Testículo/anormalidades
[Mh] Termos MeSH secundário: Encéfalo/patologia
Pré-Escolar
Facies
Evolução Fatal
Doenças dos Genitais Masculinos/patologia
Hormônios Esteroides Gonadais/sangue
Seres Humanos
Recém-Nascido
Imagem por Ressonância Magnética
Masculino
Pênis/anormalidades
Pênis/patologia
Irmãos
Síndrome
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gonadal Steroid Hormones)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170205
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.38093


  4 / 1259 MEDLINE  
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[PMID]:27967308
[Au] Autor:Smirin-Yosef P; Zuckerman-Levin N; Tzur S; Granot Y; Cohen L; Sachsenweger J; Borck G; Lagovsky I; Salmon-Divon M; Wiesmüller L; Basel-Vanagaite L
[Ad] Endereço:Genomic Bioinformatics Laboratory, Department of Molecular Biology, Ariel University, Ariel 40700, Israel.
[Ti] Título:A Biallelic Mutation in the Homologous Recombination Repair Gene SPIDR Is Associated With Human Gonadal Dysgenesis.
[So] Source:J Clin Endocrinol Metab;102(2):681-688, 2017 Feb 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Primary ovarian insufficiency (POI) is caused by ovarian follicle depletion or follicle dysfunction, characterized by amenorrhea with elevated gonadotropin levels. The disorder presents as absence of normal progression of puberty. Objective: To elucidate the cause of ovarian dysfunction in a family with POI. Design: We performed whole-exome sequencing in 2 affected individuals. To evaluate whether DNA double-strand break (DSB) repair activities are altered in biallelic mutation carriers, we applied an enhanced green fluorescent protein-based assay for the detection of specific DSB repair pathways in blood-derived cells. Setting: Diagnoses were made at the Pediatric Endocrine Clinic, Clalit Health Services, Sharon-Shomron District, Israel. Genetic counseling and sample collection were performed at the Pediatric Genetics Unit, Schneider Children's Medical Center Israel, Petah Tikva, Israel. Patients and Intervention: Two sisters born to consanguineous parents of Israeli Muslim Arab ancestry presented with a lack of normal progression of puberty, high gonadotropin levels, and hypoplastic or absent ovaries on ultrasound. Blood samples for DNA extraction were obtained from all family members. Main Outcome Measure: Exome analysis to elucidate the cause of POI in 2 affected sisters. Results: Analysis revealed a stop-gain homozygous mutation in the SPIDR gene (KIAA0146) c.839G>A, p.W280*. This mutation altered SPIDR activity in homologous recombination, resulting in the accumulation of 53BP1-labeled DSBs postionizing radiation and γH2AX-labeled damage during unperturbed growth. Conclusions: SPIDR is important for ovarian function in humans. A biallelic mutation in this gene may be associated with ovarian dysgenesis in cases of autosomal recessive inheritance.
[Mh] Termos MeSH primário: Disgenesia Gonadal/diagnóstico por imagem
Disgenesia Gonadal/genética
Insuficiência Ovariana Primária/diagnóstico por imagem
Insuficiência Ovariana Primária/genética
Proteínas/genética
[Mh] Termos MeSH secundário: Adolescente
Alelos
Criança
Consanguinidade
Exoma
Feminino
Heterozigoto
Seres Humanos
Israel
Mutação
Linhagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KIAA0146 protein, human); 0 (Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161215
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-2714


  5 / 1259 MEDLINE  
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[PMID]:27861765
[Au] Autor:Rossetti R; Ferrari I; Bonomi M; Persani L
[Ad] Endereço:Department of Endocrine and Metabolic Diseases, IRCCS Istituto Auxologico Italiano, Milan, Italy.
[Ti] Título:Genetics of primary ovarian insufficiency.
[So] Source:Clin Genet;91(2):183-198, 2017 Feb.
[Is] ISSN:1399-0004
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Primary ovarian insufficiency (POI) is characterized by a loss of ovarian function before the age of 40 and account for one major cause of female infertility. POI relevance is continuously growing because of the increasing number of women desiring conception beyond 30 years of age, when POI prevalence is >1%. POI is highly heterogeneous and can present with ovarian dysgenesis and primary amenorrhea, or with secondary amenorrhea, and it can be associated with other congenital or acquired abnormalities. In most cases POI remains classified as idiopathic. However, the age of menopause is an inheritable trait and POI has a strong genetic component. This is confirmed by the existence of several candidate genes, experimental and natural models. The variable expressivity of POI defect may indicate that, this disease may frequently be considered as a multifactorial or oligogenic defect. The most common genetic contributors to POI are the X chromosome-linked defects. Here, we review the principal X-linked and autosomal genes involved in syndromic and non-syndromic forms of POI with the expectation that this list will soon be upgraded, thus allowing the possibility to predict the risk of an early age at menopause in families with POI.
[Mh] Termos MeSH primário: Amenorreia/genética
Doenças Genéticas Ligadas ao Cromossomo X/genética
Disgenesia Gonadal/genética
Insuficiência Ovariana Primária/genética
[Mh] Termos MeSH secundário: Adulto
Amenorreia/patologia
Feminino
Genes Ligados ao Cromossomo X/genética
Doenças Genéticas Ligadas ao Cromossomo X/patologia
Disgenesia Gonadal/patologia
Seres Humanos
Menopausa/genética
Ovário/metabolismo
Ovário/patologia
Insuficiência Ovariana Primária/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1111/cge.12921


  6 / 1259 MEDLINE  
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[PMID]:28621097
[Au] Autor:Keskin M; Savas-Erdeve S; Kurnaz E; Çetinkaya S; Karaman A; Apaydin S; Aycan Z
[Ti] Título:Gonadoblastoma in a patient with 46, XY complete gonadal dysgenesis.
[So] Source:Turk J Pediatr;58(5):538-540, 2016.
[Is] ISSN:0041-4301
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:46, XY complete gonadal dysgenesis (Swyer syndrome) is a rare cause of 46, XY sexual development disorder. The patient presented to our clinic with absence of breast development and lack of periods at the age of 17 years. Her history and familial history involved no relevant conditions. She had Tanner stage 1 thelarche, and Tanner stage 2 pubic hair development with no axillary hair development. External genital structure appearance was consistent with female phenotype and the patient had no palpable gonad. The patient diagnosed as 46, XY complete gonadal dysgenesis after evaluation of laboratory analyses, radiological methods and karyotype. The Sexual Orientation and Gender Identity Committee concluded that gonadectomy should be performed. Histopathologic analysis demonstrated gonadoblastoma. Gonad structures should be sought laparoscopically and once diagnosed, streak gonads should be removed prophylactically in patients with 46, XY complete gonadal dysgenesis.
[Mh] Termos MeSH primário: Disgenesia Gonadal 46 XY/complicações
Disgenesia Gonadal/complicações
Gonadoblastoma/complicações
[Mh] Termos MeSH secundário: Adolescente
Feminino
Seres Humanos
Cariótipo
Laparoscopia
Imagem por Ressonância Magnética
Neoplasias Ovarianas/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE


  7 / 1259 MEDLINE  
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[PMID]:28222406
[Au] Autor:Soerensen RR; Johannsen TH; Skakkebaek NE; Rajpert-De Meyts E
[Ad] Endereço:Department of Growth and Reproduction, and International Center for Research and Research Training on Endocrine Disrupting Effects on Male Reproduction & Child Health (EDMaRC), Copenhagen University Hospital (Rigshospitalet), Copenhagen, Department of Pathology, University Hospital Herlev, Herle
[Ti] Título:Leydig cell clustering and Reinke crystal distribution in relation to hormonal function in adult patients with testicular dysgenesis syndrome (TDS) including cryptorchidism.
[So] Source:Hormones (Athens);15(4):518-526, 2016 Oct.
[Is] ISSN:1109-3099
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Testicular dysgenesis syndrome (TDS) comprises testicular germ cell cancer, cryptorchidism and some cases of male infertility and hypospadias, which can be linked to impairment of intrauterine gonadal development. Among histological signs of TDS, large Leydig cell (LC) clusters (micronodules) are frequently present. This study aimed to investigate possible associations of LC micronodules with the presence of Reinke crystals and hormonal function of LCs, the latter primarily reflected by serum concentrations of luteinising hormone (LH) and testosterone, in patients with TDS. DESIGN: A retrospective study of 101 andrological patients with TDS (infertility with and without a history of cryptorchidism or presence of germ cell neoplasia in situ) and 20 controls with normal testis histology and LC-function. Archived testicular biopsies were re-evaluated for the presence of LC micronodules and Reinke crystals and the findings were correlated with testis size and serum concentrations of LH, follicle-stimulating hormone (FSH), testosterone, inhibin B, estradiol and sex hormone binding globulin (SHBG). RESULTS: TDS patients with bilateral LC micronodules had significantly lower concentrations of LH, FSH and inhibin B, a lower testosterone/LH-ratio and smaller testis sizes compared to TDS-patients lacking this feature. Presence of LC micronodules was correlated with a lower number of Reinke crystals, while cryptorchid testes had a significantly higher number of crystals than normally descended TDS testes. CONCLUSION: LC micronodules appear to be a compensatory mechanism caused by androgenic failure and are presumably driven by high concentrations of LH. A relative paucity of Reinke crystals in LCs within micronodules in normally descended TDS testes may be a feature of recently renewed immature Leydig cells. The increased number of Reinke crystals in LCs in testes that were either undescended at birth or are persistently undescended could indicate an impairment of LC renewal in cryptorchidism.
[Mh] Termos MeSH primário: Disgenesia Gonadal/sangue
Disgenesia Gonadal/patologia
Células Intersticiais do Testículo/patologia
Doenças Testiculares/sangue
Doenças Testiculares/patologia
[Mh] Termos MeSH secundário: Adulto
Criptorquidismo/sangue
Criptorquidismo/patologia
Seres Humanos
Masculino
Neoplasias Embrionárias de Células Germinativas/sangue
Neoplasias Embrionárias de Células Germinativas/patologia
Neoplasias Testiculares/sangue
Neoplasias Testiculares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.14310/horm.2002.1708


  8 / 1259 MEDLINE  
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[PMID]:27978845
[Au] Autor:Buonocore F; Achermann JC
[Ad] Endereço:Genetics and Genomic Medicine, UCL Great Ormond Street Institute for Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
[Ti] Título:Human sex development: targeted technologies to improve diagnosis.
[So] Source:Genome Biol;17(1):257, 2016 Dec 15.
[Is] ISSN:1474-760X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A new study of disorders of sex development presents an improved targeted next-generation sequencing approach for their diagnosis.Please see related Research article: http://genomebiology.biomedcentral.com/articles/10.1186/s13059-016-1105-y .
[Mh] Termos MeSH primário: Transtornos do Desenvolvimento Sexual/genética
Disgenesia Gonadal/genética
Sequenciamento de Nucleotídeos em Larga Escala
Processos de Determinação Sexual
[Mh] Termos MeSH secundário: Transtornos do Desenvolvimento Sexual/patologia
Feminino
Testes Genéticos
Disgenesia Gonadal/patologia
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


  9 / 1259 MEDLINE  
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[PMID]:27876298
[Au] Autor:Diamond DA
[Ad] Endereço:Children's Hospital Boston, Boston, MA 02115, United States. Electronic address: david.diamond@childrens.harvard.edu.
[Ti] Título:Commentary to 'Gonadal dysgenesis in disorders of sex development (DSD): Diagnosis and surgical management'.
[So] Source:J Pediatr Urol;12(6):417, 2016 Dec.
[Is] ISSN:1873-4898
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Disgenesia Gonadal
Desenvolvimento Sexual
[Mh] Termos MeSH secundário: Transtornos do Desenvolvimento Sexual
Seres Humanos
Síndrome de Turner
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE


  10 / 1259 MEDLINE  
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[PMID]:27824615
[Au] Autor:Narayanan VK; Kharbanda M; Donaldson M
[Ti] Título:A case of 46,XX dysgenesis and marked tall stature; the need for caution in interpreting array comparative genomic hybridization (CGH).
[So] Source:J Pediatr Endocrinol Metab;29(12):1407-1412, 2016 Dec 01.
[Is] ISSN:2191-0251
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gonadal dysgenesis with an apparently normal 46,XX karyotype is a rare cause of hypergonadotrophic hypogonadism. Tall stature is not a widely recognized association. CASE REPORT: A 15-year-old girl presented with primary amenorrhoea. Examination showed a non-dysmorphic girl of normal intellect with no breast development (Tanner stage B1P4A1) who was tall compared with her parents: height standard deviation score (SDS) +1.56 vs. midparental height of +0.23 SDS, and slim build (weight -0.13 SDS). Investigations showed a 46,XX karyotype, elevated gonadotropins (FSH 119 and LH 33.7 IU/L), serum estradiol <5 pmol/L, uterine length 3.75 cm with cylindrical shape, and absent ovaries on ultrasound. Initially, a 364055-bp deletion on Xp21.2 was reported on array CGH. However, repeat analysis using BlueGnome CytoChip ISCA 4x180k v2.0 array was normal. With oral ethinyl estradiol induction puberty progressed to B4P4A2 but aged 18.4 years, the patient was remarkably tall with height SDS +2.88, weight SDS +0.97. CONCLUSIONS: Caution is needed in interpreting small changes with array CGH, particularly with the older assays. We postulate that the genetic change causing 46,XX gonadal dysgenesis in our patient may have also resulted in unsuppressed somatic growth. More critical height assessment, including parental height measurement, of future patients with 46,XX gonadal dysgenesis is recommended in order to determine whether or not a true association with tall stature may be present in certain cases.
[Mh] Termos MeSH primário: Estatura/genética
Hibridização Genômica Comparativa/métodos
Disgenesia Gonadal/fisiopatologia
[Mh] Termos MeSH secundário: Adolescente
Feminino
Seres Humanos
Prognóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161109
[St] Status:MEDLINE



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