Literature DB >> 21757513

Further evidence of the clinical, hormonal, and genetic heterogeneity of Klinefelter syndrome: a study of 216 infertile Egyptian patients.

Moheb M Abdel-Razic1, Ibrahim A Abdel-Hamid, Ezzat Elsobky, Faeza El-Dahtory.   

Abstract

This study aims to provide further insight into the phenotypic heterogeneity of Klinefelter syndrome (KS) by presenting clinical, hormonal, and genetic data from a large series of Egyptian infertile patients with KS. A retrospective case series of KS patients was studied over a period from January 2003 to April 2010. All patients underwent a complete history and physical examination; color duplex examination; semen analysis; measurement of total testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), and prolactin (PRL); and chromosomal typing. Mosaic KS diagnosis was confirmed by fluorescence in situ hybridization. The series included 216 KS patients (198 nonmosaic, 16 mosaic, and 2 KS variants). Typical clinical signs of hypoandrogenism were observed in 86% of patients. Gynecomastia affected 20.8% of the patients. Eunuchoidal body proportions, with arm span exceeding height and lower segment length exceeding upper segment length, were detected in 43.9% and 64.4% of the patients, respectively. In all patients, a reduction in testicular size and azoospermia were detected. Normal levels of T, FSH, LH, E2, and PRL were detected in 44.5%, 3.7%, 3.3%, 93.5%, and 91.2% of patients, respectively. Differences were not significant between patients with classic KS and those with mosaic KS in terms of the frequency of clinical signs of hypoandrogenism, gynecomastia, low T concentrations, or high concentrations of FSH, LH, E2, and PRL (all P > .05). The results of the current study emphasize the heterogeneous clinical, hormonal, and genetic phenotype of infertile KS patients. Our findings support the usefulness of cytogenetic studies in infertile patients showing small testicular size and azoospermia, regardless of the presence of other clinical or endocrine findings.

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Year:  2011        PMID: 21757513     DOI: 10.2164/jandrol.110.011536

Source DB:  PubMed          Journal:  J Androl        ISSN: 0196-3635


  5 in total

1.  Single-nucleotide polymorphisms in HORMAD1 may be a risk factor for azoospermia caused by meiotic arrest in Japanese patients.

Authors:  Toshinobu Miyamoto; Akira Tsujimura; Yasushi Miyagawa; Eitetsu Koh; Mikio Namiki; Michiharu Horikawa; Yasuaki Saijo; Kazuo Sengoku
Journal:  Asian J Androl       Date:  2012-03-12       Impact factor: 3.285

2.  Relative hyperestrogenism in Klinefelter Syndrome: results from a meta-analysis.

Authors:  Daniele Santi; Sara De Vincentis; Sara Scaltriti; Vincenzo Rochira
Journal:  Endocrine       Date:  2019-01-30       Impact factor: 3.633

Review 3.  The Fate of Leydig Cells in Men with Spermatogenic Failure.

Authors:  Daria Adamczewska; Jolanta Słowikowska-Hilczer; Renata Walczak-Jędrzejowska
Journal:  Life (Basel)       Date:  2022-04-12

4.  5-α reductase inhibitors, benign prostatic hyperplasia, and risk of male breast cancer.

Authors:  David Robinson; Hans Garmo; Lars Holmberg; Pär Stattin
Journal:  Cancer Causes Control       Date:  2015-06-25       Impact factor: 2.506

5.  Obesity and Hyperglycemia in Korean Men with Klinefelter Syndrome: The Korean Endocrine Society Registry.

Authors:  Seung Jin Han; Kyung Soo Kim; Wonjin Kim; Jung Hee Kim; Yong Ho Lee; Ji Sun Nam; Ji A Seo; Bu Kyung Kim; Jihyun Lee; Jin Ook Chung; Min Hee Kim; Tae Seo Sohn; Han Seok Choi; Seong Bin Hong; Yoon Sok Chung
Journal:  Endocrinol Metab (Seoul)       Date:  2016-12
  5 in total

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