Reduced fibrin clot lysis in Klinefelter syndrome associated with hypogonadism.
Klinefelter syndrome
clinical study
fibrinolysis
obesity
testosterone
Journal
Endocrine connections
ISSN: 2049-3614
Titre abrégé: Endocr Connect
Pays: England
ID NLM: 101598413
Informations de publication
Date de publication:
10 May 2022
10 May 2022
Historique:
received:
18
02
2022
accepted:
31
03
2022
pubmed:
1
4
2022
medline:
1
4
2022
entrez:
31
3
2022
Statut:
epublish
Résumé
Klinefelter syndrome (KS) is associated with increased risk of thrombosis. Hypogonadism and accumulating body fat in KS have a potential impact on fibrinolysis. In this study, we assessed the fibrinolytic system and the association with testosterone levels in KS. This study is a cross-sectional comparison of men with KS and age-matched male controls. Fibrin clot lysis was evaluated by turbidity measurements and by measuring levels of individual fibrinolytic proteins in plasma samples. Fibrin clot structure was evaluated by scanning electron microscopy. Total testosterone was measured by liquid chromatography-tandem mass spectrometry. Body fat was evaluated by dual-energy X-ray absorptiometry. In this study, 45 men with KS and 45 age- and education-matched controls were included. Men with KS had a 24% reduction in fibrin clot lysis compared with controls (46.2 ± 17.1 vs 60.6 ± 18.8 %/h, P = 0.0003) and higher levels of fibrinogen, factor XIII (P ≤ 0.01), and plasminogen activator inhibitor type 1 (P = 0.04). Men with KS had lower total testosterone (P = 0.008) and higher body fat (P = 0.001). In KS, reduced fibrin clot lysability was associated with higher fibrinogen and body fat related to decreasing total testosterone and hypogonadism among men with KS. Fibrin clot structure was not different compared to KS and controls. Fibrin clot lysis in KS was markedly reduced, potentially contributing to a prothrombotic state and increasing thrombotic risk. Hypogonadism in KS was associated with increased fibrinogen and total body fat, predicting reduced fibrin clot lysis.
Identifiants
pubmed: 35358059
doi: 10.1530/EC-21-0490
pii: e210490
pmc: PMC9175611
doi:
pii:
Types de publication
Journal Article
Langues
eng
Références
Endocr Connect. 2020 Jan;9(1):34-43
pubmed: 31829966
Thromb Haemost. 2007 Aug;98(2):339-45
pubmed: 17721616
J Clin Endocrinol Metab. 2006 Apr;91(4):1254-60
pubmed: 16394093
Mol Hum Reprod. 2010 Jun;16(6):396-401
pubmed: 20231162
Am J Mens Health. 2018 Nov;12(6):2152-2156
pubmed: 30334491
Biomaterials. 2015 Aug;61:327-38
pubmed: 26043061
Br J Dermatol. 1997 Mar;136(3):341-4
pubmed: 9115912
J Endocr Soc. 2021 Apr 05;5(6):bvab062
pubmed: 34056502
Metabolism. 1997 Nov;46(11):1287-93
pubmed: 9361687
Dis Model Mech. 2009 May-Jun;2(5-6):231-7
pubmed: 19407331
Curr Opin Hematol. 2012 Sep;19(5):349-56
pubmed: 22759629
Blood. 2005 Feb 1;105(3):1102-5
pubmed: 15466929
J Intern Med. 2015 May;277(5):573-84
pubmed: 25161014
J Clin Endocrinol Metab. 2015 Mar;100(3):E508-17
pubmed: 25514102
J Endocrinol Invest. 2002 Nov;25(10):899-904
pubmed: 12508953
Semin Thromb Hemost. 2018 Nov;44(8):734-746
pubmed: 30267392
Thromb Res. 2019 Oct;182:175-181
pubmed: 31505312
Am J Med Sci. 2013 Aug;346(2):164-5
pubmed: 23377169
J Am Heart Assoc. 2016 May 20;5(5):
pubmed: 27208002
Blood. 2010 Jul 8;116(1):113-21
pubmed: 20385790
J Thromb Haemost. 2018 Oct;16(10):2070-2082
pubmed: 30039577
J Thromb Haemost. 2014 Feb;12(2):197-205
pubmed: 24261582
Sci Rep. 2018 Sep 13;8(1):13740
pubmed: 30213969
Endocr Rev. 2018 Aug 1;39(4):389-423
pubmed: 29438472
J Clin Invest. 2017 Aug 1;127(8):3152-3166
pubmed: 28737512
Surg Obes Relat Dis. 2018 Jul;14(7):918-926
pubmed: 29706497
Eur J Appl Physiol. 2015 Jun;115(6):1331-8
pubmed: 25618791
Endocr Connect. 2019 Sep;8(9):1250-1261
pubmed: 31394497
Semin Thromb Hemost. 2000;26(6):605-18
pubmed: 11140797
Diabetes Care. 2006 Jul;29(7):1591-8
pubmed: 16801584