Simon Chang1, Daniel Biltoft2, Anne Skakkebæk3, Jens Fedder4, Anders Bojesen5, M Vakur Bor2, Claus H Gravholt6, Anna-Marie B Münster2. 1. Unit for Thrombosis Research, Department of Regional Health Research, University of Southern Denmark, Department of Clinical Biochemistry, Hospital of South West Jutland, Esbjerg, Denmark; Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. Electronic address: simon.chang@rsyd.dk. 2. Unit for Thrombosis Research, Department of Regional Health Research, University of Southern Denmark, Department of Clinical Biochemistry, Hospital of South West Jutland, Esbjerg, Denmark. 3. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark; Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Genetics, Aarhus University Hospital, Aarhus, Denmark. 4. Centre of Andrology and Fertility Clinic, Odense University Hospital, Odense, Denmark. 5. Department of Clinical Genetics, Aarhus University Hospital, Aarhus, Denmark. 6. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark; Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark.
Abstract
BACKGROUND: The background for the increased occurrence of thrombosis seen in Klinefelter syndrome (KS) is unknown. The aim was to compare thrombin generation and coagulation inhibition between men with KS and controls, and to investigate whether coagulation in KS was associated with testosterone treatment (TT), and as such, measures of androgen action. METHODS: Untreated men with KS (U-KS) or testosterone treated men with KS (T-KS) were included. KS groups were matched by age and education to groups of control males with no history of TT. Blood samples were collected after overnight fasting. Low tissue factor (1pM) thrombin generation was expressed as lag time (min), time to peak (min), peak (nmol/L), and endogenous thrombin potential (nmol/L × min, ETP). Coagulation inhibitors, sex hormones, and haematocrit were measured. Matched groups were compared by Student's t-test or Wilcoxon rank sum test. Among KS, TT status as an outcome predictor was evaluated by linear regression. RESULTS: 18 U-KS and 27 T-KS with corresponding controls participated. Thrombin generation was not different comparing U-KS and T-KS with respective control groups. Among KS, ETP was lower in T-KS compared with U-KS and inversely associated with testosterone, LH-testosterone ratio and haematocrit. CONCLUSION: Neither U-KS nor T-KS expressed a pro-coagulant state compared with controls. Thrombin generation among KS was inversely associated with androgen action and lower in T-KS compared with U-KS. Whether TT is capable of lowering thrombotic risk among men with KS needs to be assessed prospectively.
BACKGROUND: The background for the increased occurrence of thrombosis seen in Klinefelter syndrome (KS) is unknown. The aim was to compare thrombin generation and coagulation inhibition between men with KS and controls, and to investigate whether coagulation in KS was associated with testosterone treatment (TT), and as such, measures of androgen action. METHODS: Untreated men with KS (U-KS) or testosterone treated men with KS (T-KS) were included. KS groups were matched by age and education to groups of control males with no history of TT. Blood samples were collected after overnight fasting. Low tissue factor (1pM) thrombin generation was expressed as lag time (min), time to peak (min), peak (nmol/L), and endogenous thrombin potential (nmol/L × min, ETP). Coagulation inhibitors, sex hormones, and haematocrit were measured. Matched groups were compared by Student's t-test or Wilcoxon rank sum test. Among KS, TT status as an outcome predictor was evaluated by linear regression. RESULTS: 18 U-KS and 27 T-KS with corresponding controls participated. Thrombin generation was not different comparing U-KS and T-KS with respective control groups. Among KS, ETP was lower in T-KS compared with U-KS and inversely associated with testosterone, LH-testosterone ratio and haematocrit. CONCLUSION: Neither U-KS nor T-KS expressed a pro-coagulant state compared with controls. Thrombin generation among KS was inversely associated with androgen action and lower in T-KS compared with U-KS. Whether TT is capable of lowering thrombotic risk among men with KS needs to be assessed prospectively.
Authors: Simon Chang; Anne Skakkebaek; Shanlee M Davis; Claus H Gravholt Journal: Am J Med Genet C Semin Med Genet Date: 2020-06-04 Impact factor: 3.908
Authors: Simon Chang; Arkadiusz J Goszczak; Anne Skakkebæk; Jens Fedder; Anders Bojesen; M Vakur Bor; Moniek P M de Maat; Claus H Gravholt; Anna-Marie B Münster Journal: Endocr Connect Date: 2022-05-10 Impact factor: 3.221
Authors: Simon Chang; Christian Fynbo Christiansen; Anders Bojesen; Svend Juul; Anna-Marie B Münster; Claus H Gravholt Journal: Endocr Connect Date: 2020-01 Impact factor: 3.335