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Klinefelter syndrome, insulin resistance, metabolic syndrome, and diabetes: review of literature and clinical perspectives

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journal contribution
posted on 05.06.2018, 13:11 authored by Andrea Salzano, Roberta D'Assante, Liam HeaneyLiam Heaney, Federica Monaco, Giuseppe Rengo, Pietro Valente, Daniela Pasquali, Eduardo Bossone, Daniele Gianfrilli, Andrea Lenzi, Antonio Cittadini, Alberto M. Marra, Raffaele Napoli
Klinefelter syndrome (KS), the most frequent chromosomic abnormality in males, is associated with hypergonadotropic hypogonadism and an increased risk of cardiovascular diseases (CVD). The mechanisms involved in increasing risk of cardiovascular morbidity and mortality are not completely understood. Insulin resistance, metabolic syndrome, and type 2 diabetes are more frequently diagnosed in KS than in the general population; however, the contribution of hypogonadism to metabolic derangement is highly controversial. Whether this dangerous combination of risk factors fully explains the CVD burden of KS patients remains unclear. In addition, testosterone replacement therapy only exerts a marginal action on the CVD system. This review summaries the current understandings of the complex relationship between KS, metabolic syndrome and cardiovascular risk in order to plan future studies and improve current strategies to reduce mortality in this high-risk population. Since fat accumulation and distribution seem to play a relevant role in triggering metabolic abnormalities, an early diagnosis and a tailored intervention strategy with drugs aimed at targeting excessive visceral fat deposition appear necessary in patients with KS.

Funding

Dr. Salzano receives research grant support from Cardiopath.

History

School

  • Sport, Exercise and Health Sciences

Published in

Endocrine

Citation

SALZANO, A. ... et al., 2018. Klinefelter syndrome, insulin resistance, metabolic syndrome, and diabetes: review of literature and clinical perspectives. Endocrine, 61(2), pp. 194–203.

Publisher

© Springer

Version

AM (Accepted Manuscript)

Publisher statement

This work is made available according to the conditions of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. Full details of this licence are available at: https://creativecommons.org/licenses/by-nc-nd/4.0/

Acceptance date

15/03/2018

Publication date

2018-03-23

Notes

This is a post-peer-review, pre-copyedit version of an article published in Endocrine. The final authenticated version is available online at: https://doi.org/10.1007/s12020-018-1584-6.

ISSN

1355-008X

eISSN

1559-0100

Language

en