Purpose: evaluation of cardiometabolic, liver fibrosis and steatosis indices in patients with KS. Methods: a retrospective single center-study, enrolling 182 patients with KS without testosterone (T) replacement therapy, evaluating general, hormonal, and metabolic parameters. We also evaluated in all patients the indices exposed above. Statistical univariate analysis was performed, calculating Pearson correlation coefficient (r), whilst p values ≤ 0.05 were considered statistically significant. Results: 182 patients with KS were enrolled, aged 32±9 years, with a men BMI of 25.4±5.2 kg/m2 and waist circumference (WC) above normal range (98±16 cm). Gonadic axis parameters were evaluated: total testosterone (TT 10.1±5.4 nmol/l), LH (21±8 U/L), FSH (38±29 U/L), SHBG (34.4±16.14 nmol/L), albumin (47.16±4.2 g/L) and calculated free testosterone with Vermeulen formula (cFT 0.193±0.103 nmol/L). We also evaluated lipid profile (total cholesterol 188 ± 41 mg/dl; HDL 50 ± 14 mg/dl and triglycerides 114±146 mg/dl and cLDL 119±34 mg/dl), 25-OH-D-vitamin (56±28 nmol/L) and homocysteine (16±11 mmol/L). Average HOMA-I was calculated (2.3± 2.3). We further calculated mean cardiometabolic, hepatic fibrosis and hepatic steatosis indices (VAI: 4.03±6.95; TyG: 8.18±0.70; LAP: 48.74±77.64; APRI 0.31±0.13; FIB4 0.74±0.43; THR 2.77±4.66; FLI 39±32; HSI 34.25±7.42; DSI-1.75±1.5). We focused on the association between cFT and the ten indices and, in particular, statistical univariate analysis showed significant (p<0.05) inverse correlation between cFT and the following variables: BMI (r -0.43), WC (r -0.45), VAI (r -0.17), TyG (r -0.26), LAP (r -0.25), FIB4 (r -0.23), NAFLDs (r -0.3), THR (r -0.16), FLI (r -0.39,) HSI (r -0.39) and DSI (r -0.41), but not with between cFT and APRI. Conclusion: This is the first study evaluating cardiometabolic, liver fibrosis and liver steatosis indices in patients with KS. In those patients, T levels might be maintained within normal range by an increase of LH production secondary to higher SHBG levels induced by liver fibrosis or steatosis, requiring the measure of cFT. Our study is the first to examine the possible involvement of liver fibrosis/steatosis and the cardiometabolic indices in patients with KS having also the advantage of considering LH levels as marker of hypothalamus–pituitary function and cFT as a more sensitive marker of hypogonadism than TT. Therefore, hypogonadism in KS might be due to both primary testicular and insufficient pituitary compensation. Limitations of our retrospective study include the lack of data on body composition and fat body distribution besides BMI and the use of indirect scoring systems, instead of abdominal ultrasonography/elastography or liver biopsy

Purpose: evaluation of cardiometabolic, liver fibrosis and steatosis indices in patients with KS. Methods: a retrospective single center-study, enrolling 182 patients with KS without testosterone (T) replacement therapy, evaluating general, hormonal, and metabolic parameters. We also evaluated in all patients the indices exposed above. Statistical univariate analysis was performed, calculating Pearson correlation coefficient (r), whilst p values ≤ 0.05 were considered statistically significant. Results: 182 patients with KS were enrolled, aged 32±9 years, with a men BMI of 25.4±5.2 kg/m2 and waist circumference (WC) above normal range (98±16 cm). Gonadic axis parameters were evaluated: total testosterone (TT 10.1±5.4 nmol/l), LH (21±8 U/L), FSH (38±29 U/L), SHBG (34.4±16.14 nmol/L), albumin (47.16±4.2 g/L) and calculated free testosterone with Vermeulen formula (cFT 0.193±0.103 nmol/L). We also evaluated lipid profile (total cholesterol 188 ± 41 mg/dl; HDL 50 ± 14 mg/dl and triglycerides 114±146 mg/dl and cLDL 119±34 mg/dl), 25-OH-D-vitamin (56±28 nmol/L) and homocysteine (16±11 mmol/L). Average HOMA-I was calculated (2.3± 2.3). We further calculated mean cardiometabolic, hepatic fibrosis and hepatic steatosis indices (VAI: 4.03±6.95; TyG: 8.18±0.70; LAP: 48.74±77.64; APRI 0.31±0.13; FIB4 0.74±0.43; THR 2.77±4.66; FLI 39±32; HSI 34.25±7.42; DSI-1.75±1.5). We focused on the association between cFT and the ten indices and, in particular, statistical univariate analysis showed significant (p<0.05) inverse correlation between cFT and the following variables: BMI (r -0.43), WC (r -0.45), VAI (r -0.17), TyG (r -0.26), LAP (r -0.25), FIB4 (r -0.23), NAFLDs (r -0.3), THR (r -0.16), FLI (r -0.39,) HSI (r -0.39) and DSI (r -0.41), but not with between cFT and APRI. Conclusion: This is the first study evaluating cardiometabolic, liver fibrosis and liver steatosis indices in patients with KS. In those patients, T levels might be maintained within normal range by an increase of LH production secondary to higher SHBG levels induced by liver fibrosis or steatosis, requiring the measure of cFT. Our study is the first to examine the possible involvement of liver fibrosis/steatosis and the cardiometabolic indices in patients with KS having also the advantage of considering LH levels as marker of hypothalamus–pituitary function and cFT as a more sensitive marker of hypogonadism than TT. Therefore, hypogonadism in KS might be due to both primary testicular and insufficient pituitary compensation. Limitations of our retrospective study include the lack of data on body composition and fat body distribution besides BMI and the use of indirect scoring systems, instead of abdominal ultrasonography/elastography or liver biopsy.

Evaluation of new cardiometabolic and liver parameters in patients with Klinefelter Syndrome.

TABIH, NURAN
2022/2023

Abstract

Purpose: evaluation of cardiometabolic, liver fibrosis and steatosis indices in patients with KS. Methods: a retrospective single center-study, enrolling 182 patients with KS without testosterone (T) replacement therapy, evaluating general, hormonal, and metabolic parameters. We also evaluated in all patients the indices exposed above. Statistical univariate analysis was performed, calculating Pearson correlation coefficient (r), whilst p values ≤ 0.05 were considered statistically significant. Results: 182 patients with KS were enrolled, aged 32±9 years, with a men BMI of 25.4±5.2 kg/m2 and waist circumference (WC) above normal range (98±16 cm). Gonadic axis parameters were evaluated: total testosterone (TT 10.1±5.4 nmol/l), LH (21±8 U/L), FSH (38±29 U/L), SHBG (34.4±16.14 nmol/L), albumin (47.16±4.2 g/L) and calculated free testosterone with Vermeulen formula (cFT 0.193±0.103 nmol/L). We also evaluated lipid profile (total cholesterol 188 ± 41 mg/dl; HDL 50 ± 14 mg/dl and triglycerides 114±146 mg/dl and cLDL 119±34 mg/dl), 25-OH-D-vitamin (56±28 nmol/L) and homocysteine (16±11 mmol/L). Average HOMA-I was calculated (2.3± 2.3). We further calculated mean cardiometabolic, hepatic fibrosis and hepatic steatosis indices (VAI: 4.03±6.95; TyG: 8.18±0.70; LAP: 48.74±77.64; APRI 0.31±0.13; FIB4 0.74±0.43; THR 2.77±4.66; FLI 39±32; HSI 34.25±7.42; DSI-1.75±1.5). We focused on the association between cFT and the ten indices and, in particular, statistical univariate analysis showed significant (p<0.05) inverse correlation between cFT and the following variables: BMI (r -0.43), WC (r -0.45), VAI (r -0.17), TyG (r -0.26), LAP (r -0.25), FIB4 (r -0.23), NAFLDs (r -0.3), THR (r -0.16), FLI (r -0.39,) HSI (r -0.39) and DSI (r -0.41), but not with between cFT and APRI. Conclusion: This is the first study evaluating cardiometabolic, liver fibrosis and liver steatosis indices in patients with KS. In those patients, T levels might be maintained within normal range by an increase of LH production secondary to higher SHBG levels induced by liver fibrosis or steatosis, requiring the measure of cFT. Our study is the first to examine the possible involvement of liver fibrosis/steatosis and the cardiometabolic indices in patients with KS having also the advantage of considering LH levels as marker of hypothalamus–pituitary function and cFT as a more sensitive marker of hypogonadism than TT. Therefore, hypogonadism in KS might be due to both primary testicular and insufficient pituitary compensation. Limitations of our retrospective study include the lack of data on body composition and fat body distribution besides BMI and the use of indirect scoring systems, instead of abdominal ultrasonography/elastography or liver biopsy
Dipartimento di Medicina - DIMED
2022
Evaluation of new cardiometabolic and liver parameters in patients with Klinefelter Syndrome.
Purpose: evaluation of cardiometabolic, liver fibrosis and steatosis indices in patients with KS. Methods: a retrospective single center-study, enrolling 182 patients with KS without testosterone (T) replacement therapy, evaluating general, hormonal, and metabolic parameters. We also evaluated in all patients the indices exposed above. Statistical univariate analysis was performed, calculating Pearson correlation coefficient (r), whilst p values ≤ 0.05 were considered statistically significant. Results: 182 patients with KS were enrolled, aged 32±9 years, with a men BMI of 25.4±5.2 kg/m2 and waist circumference (WC) above normal range (98±16 cm). Gonadic axis parameters were evaluated: total testosterone (TT 10.1±5.4 nmol/l), LH (21±8 U/L), FSH (38±29 U/L), SHBG (34.4±16.14 nmol/L), albumin (47.16±4.2 g/L) and calculated free testosterone with Vermeulen formula (cFT 0.193±0.103 nmol/L). We also evaluated lipid profile (total cholesterol 188 ± 41 mg/dl; HDL 50 ± 14 mg/dl and triglycerides 114±146 mg/dl and cLDL 119±34 mg/dl), 25-OH-D-vitamin (56±28 nmol/L) and homocysteine (16±11 mmol/L). Average HOMA-I was calculated (2.3± 2.3). We further calculated mean cardiometabolic, hepatic fibrosis and hepatic steatosis indices (VAI: 4.03±6.95; TyG: 8.18±0.70; LAP: 48.74±77.64; APRI 0.31±0.13; FIB4 0.74±0.43; THR 2.77±4.66; FLI 39±32; HSI 34.25±7.42; DSI-1.75±1.5). We focused on the association between cFT and the ten indices and, in particular, statistical univariate analysis showed significant (p<0.05) inverse correlation between cFT and the following variables: BMI (r -0.43), WC (r -0.45), VAI (r -0.17), TyG (r -0.26), LAP (r -0.25), FIB4 (r -0.23), NAFLDs (r -0.3), THR (r -0.16), FLI (r -0.39,) HSI (r -0.39) and DSI (r -0.41), but not with between cFT and APRI. Conclusion: This is the first study evaluating cardiometabolic, liver fibrosis and liver steatosis indices in patients with KS. In those patients, T levels might be maintained within normal range by an increase of LH production secondary to higher SHBG levels induced by liver fibrosis or steatosis, requiring the measure of cFT. Our study is the first to examine the possible involvement of liver fibrosis/steatosis and the cardiometabolic indices in patients with KS having also the advantage of considering LH levels as marker of hypothalamus–pituitary function and cFT as a more sensitive marker of hypogonadism than TT. Therefore, hypogonadism in KS might be due to both primary testicular and insufficient pituitary compensation. Limitations of our retrospective study include the lack of data on body composition and fat body distribution besides BMI and the use of indirect scoring systems, instead of abdominal ultrasonography/elastography or liver biopsy.
Klinefelter Syndrome
Testosterone
Hypogonadism
Fibrosis index
Cardio metabolic
FERLIN, ALBERTO
GRAZIANI, ANDREA
Lauree magistrali a ciclo unico
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12608/46667