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MP35-18 ULTIMATE TIME TO IMPROVEMENT IN SEMEN QUALITY AFTER SUBINGUINAL VARICOCELECTOMY
THE JOURNAL OF UROLOGYâ
Vol. 197, No. 4S, Supplement, Saturday, May 13, 2017
CONCLUSIONS: Post-varicocele repair outcomes in men with sperm EM abnormalities appear to be non-inferior to those without identified abnormalities. Certainly, it will be more challenging for these men with severe asthenospermia to approach normal parameters, but this small series demonstrates that the presence of EM abnormalities should not preclude a discussion about varicocelectomy.
e465
MP35-20 THE UTILITY OF ALKALINE PHOSPHATASE AS A MARKER FOR RESPONSE TO TESTOSTERONE REPLACEMENT THERAPY IN HYPOGONADAL MEN John Sheng*, Ari Sapin, Michael Benson, Hossein Sadeghi-Nejad, Newark, NJ
Source of Funding: None.
MP35-18 ULTIMATE TIME TO IMPROVEMENT IN SEMEN QUALITY AFTER SUBINGUINAL VARICOCELECTOMY Ahmed M. Ragheb*, Ayman S. Moussa, Taha A. Ahmed, Amr M. Massoud, Giza, Egypt WITHDRAWN
MP35-19 PRIMARY, SECONDARY, AND COMPENSATED HYPOGONADISM: A NOVEL RISK STRATIFICATION FOR INFERTILE MEN Eugenio Ventimiglia*, Paolo Capogrosso, Milan, Italy; Luca Boeri, Milano, Italy; Walter Cazzaniga, Filippo Pederzoli, Nicola Frego, , Franco Gaboardi, Milan, Italy; Davide Oreggia, Federico Deho Vincenzo Mirone, Naples, Italy; Francesco Montorsi, Andrea Salonia, Milan, Italy INTRODUCTION AND OBJECTIVES: Recently, the cohort of men from the European Male Ageing Study (EMAS) has been stratified into different categories distinguishing primary, secondary and compensated hypogonadism. A similar classification has not yet been applied to infertile men, traditionally younger than those usually considered for population studies. We aimed to investigate the prevalence of different forms of hypogonadism and the eventual association of clinical, semen and hormonal parameters in a homogeneous cohort of white-European men presenting for primary couple’s infertility. METHODS: We performed a cross-sectional study enrolling 786 consecutive Caucasian-European primary infertile men segregated into: eugonadal [normal serum total testosterone (tT >¼ 3.03 ng/mL) and normal LH (¼<9.4 mU/mL)]; secondary (low tT; low/normal LH); primary (low tT; elevated LH); and, compensated hypogonadism (normal tT; elevated LH). Logistic regression models tested the association between semen parameters, clinical characteristics and the defined gonadal status. RESULTS: Eugonadism, secondary, primary, and compensated hypogonadism were found in 80%, 15%, 2%, and 3% of men, respectively. Secondary hypogonadal men were at highest risk for obesity (OR [95% CI] 3.56 [2.03-6.13]). Primary hypogonadal men were those at highest risk for non-obstructive azoospermia (NOA) (23.5 [6.25-152.96]) and testicular volume <15ml (12.78 [3.42-82.91]). Compensated had a similar profile to primary hypogonadal men, though their risk of NOA (6.27 [2.79-14.81]) and small testicular volume (8.94 [3.57-27.19]) was lower. The risk of small testicular volume (1.6 [1.052.44]) and NOA (1.83 [1.15-2.89]) was increased, though in a milder fashion, in secondary hypogonadal men as well. CONCLUSIONS: Overall, primary and compensated hypogonadism depicted the worst clinical picture in terms of impaired fertility. Though not specifically designed for infertile men, EMAS’ categories might serve as a clinical stratification tool even in this setting. Source of Funding: none
INTRODUCTION AND OBJECTIVES: Osteopenia and osteoporosis may be adverse sequelae of hypogonadism. In a recent publication, Dabaja, et al (2015) found elevated alkaline phosphatase (AP) in men with total testosterone (T) <250ng/dl, suggesting increased bone turnover. Following T therapy, decreased AP was associated with increased bone mineral density, suggesting that AP levels may be used as a marker of response to T therapy. We evaluated the association between T and AP levels in an outpatient setting in an effort to replicate these findings. METHODS: A retrospective chart review of 88 men who presented to our reproductive medicine clinic with symptomatic or clinical features of hypogonadism was performed. Men with total testosterone levels <350ng/dL were followed for 2 years with AP levels measured at baseline, 6, 12, and 24 months. 15 of the 88 men had both T and AP measured before treatment, and at 6, 12, and 24 months. Men were either treated with transdermal testosterone, intramuscular testosterone, or testosterone long-acting pellets. RESULTS: Mean age (SD) of the patients was 61 (18) years, with an age range of 27 to 84. The mean (SD) testosterone level was 217 (75) ng/dL at baseline and 675 (538), 652 (373), 716 (516) ng/dL at 6, 12, and 24 months, respectively. AP levels decreased from a mean (SD) of 67 (14) U/L to 65 (14) U/L (P¼0.353), 65 (12) U/L (P¼.421), and 61 (14) U/L (P¼.111), at 6, 12, and 24 months respectively. CONCLUSIONS: We found no correlation between testosterone replacement therapy and AP levels. Specifically, the significant decrease in AP levels following T therapy noted in the Dabaja study were not observed in this small cohort. There were significant differences between the two studies, including mean age (41 vs 61 years), mean initial level of AP (87 u/L vs 67 u/L), mean decrease in AP after two years of treatment (32 u/L vs 6 u/L), and mean testosterone level prior to treatment (264 ng/dL vs 217 ng/dL). The significant age difference between the two studies is noteworthy, suggesting that younger patients may be more susceptible to increased bone turnover as a result of T deficiency. Further investigation may be needed to determine whether AP can be used as a marker of response to T replacement therapy in a select group of patients.
Source of Funding: None
Vol. 197, No. 4S, Supplement, Saturday, May 13, 2017
CONCLUSIONS: Post-varicocele repair outcomes in men with sperm EM abnormalities appear to be non-inferior to those without identified abnormalities. Certainly, it will be more challenging for these men with severe asthenospermia to approach normal parameters, but this small series demonstrates that the presence of EM abnormalities should not preclude a discussion about varicocelectomy.
e465
MP35-20 THE UTILITY OF ALKALINE PHOSPHATASE AS A MARKER FOR RESPONSE TO TESTOSTERONE REPLACEMENT THERAPY IN HYPOGONADAL MEN John Sheng*, Ari Sapin, Michael Benson, Hossein Sadeghi-Nejad, Newark, NJ
Source of Funding: None.
MP35-18 ULTIMATE TIME TO IMPROVEMENT IN SEMEN QUALITY AFTER SUBINGUINAL VARICOCELECTOMY Ahmed M. Ragheb*, Ayman S. Moussa, Taha A. Ahmed, Amr M. Massoud, Giza, Egypt WITHDRAWN
MP35-19 PRIMARY, SECONDARY, AND COMPENSATED HYPOGONADISM: A NOVEL RISK STRATIFICATION FOR INFERTILE MEN Eugenio Ventimiglia*, Paolo Capogrosso, Milan, Italy; Luca Boeri, Milano, Italy; Walter Cazzaniga, Filippo Pederzoli, Nicola Frego, , Franco Gaboardi, Milan, Italy; Davide Oreggia, Federico Deho Vincenzo Mirone, Naples, Italy; Francesco Montorsi, Andrea Salonia, Milan, Italy INTRODUCTION AND OBJECTIVES: Recently, the cohort of men from the European Male Ageing Study (EMAS) has been stratified into different categories distinguishing primary, secondary and compensated hypogonadism. A similar classification has not yet been applied to infertile men, traditionally younger than those usually considered for population studies. We aimed to investigate the prevalence of different forms of hypogonadism and the eventual association of clinical, semen and hormonal parameters in a homogeneous cohort of white-European men presenting for primary couple’s infertility. METHODS: We performed a cross-sectional study enrolling 786 consecutive Caucasian-European primary infertile men segregated into: eugonadal [normal serum total testosterone (tT >¼ 3.03 ng/mL) and normal LH (¼<9.4 mU/mL)]; secondary (low tT; low/normal LH); primary (low tT; elevated LH); and, compensated hypogonadism (normal tT; elevated LH). Logistic regression models tested the association between semen parameters, clinical characteristics and the defined gonadal status. RESULTS: Eugonadism, secondary, primary, and compensated hypogonadism were found in 80%, 15%, 2%, and 3% of men, respectively. Secondary hypogonadal men were at highest risk for obesity (OR [95% CI] 3.56 [2.03-6.13]). Primary hypogonadal men were those at highest risk for non-obstructive azoospermia (NOA) (23.5 [6.25-152.96]) and testicular volume <15ml (12.78 [3.42-82.91]). Compensated had a similar profile to primary hypogonadal men, though their risk of NOA (6.27 [2.79-14.81]) and small testicular volume (8.94 [3.57-27.19]) was lower. The risk of small testicular volume (1.6 [1.052.44]) and NOA (1.83 [1.15-2.89]) was increased, though in a milder fashion, in secondary hypogonadal men as well. CONCLUSIONS: Overall, primary and compensated hypogonadism depicted the worst clinical picture in terms of impaired fertility. Though not specifically designed for infertile men, EMAS’ categories might serve as a clinical stratification tool even in this setting. Source of Funding: none
INTRODUCTION AND OBJECTIVES: Osteopenia and osteoporosis may be adverse sequelae of hypogonadism. In a recent publication, Dabaja, et al (2015) found elevated alkaline phosphatase (AP) in men with total testosterone (T) <250ng/dl, suggesting increased bone turnover. Following T therapy, decreased AP was associated with increased bone mineral density, suggesting that AP levels may be used as a marker of response to T therapy. We evaluated the association between T and AP levels in an outpatient setting in an effort to replicate these findings. METHODS: A retrospective chart review of 88 men who presented to our reproductive medicine clinic with symptomatic or clinical features of hypogonadism was performed. Men with total testosterone levels <350ng/dL were followed for 2 years with AP levels measured at baseline, 6, 12, and 24 months. 15 of the 88 men had both T and AP measured before treatment, and at 6, 12, and 24 months. Men were either treated with transdermal testosterone, intramuscular testosterone, or testosterone long-acting pellets. RESULTS: Mean age (SD) of the patients was 61 (18) years, with an age range of 27 to 84. The mean (SD) testosterone level was 217 (75) ng/dL at baseline and 675 (538), 652 (373), 716 (516) ng/dL at 6, 12, and 24 months, respectively. AP levels decreased from a mean (SD) of 67 (14) U/L to 65 (14) U/L (P¼0.353), 65 (12) U/L (P¼.421), and 61 (14) U/L (P¼.111), at 6, 12, and 24 months respectively. CONCLUSIONS: We found no correlation between testosterone replacement therapy and AP levels. Specifically, the significant decrease in AP levels following T therapy noted in the Dabaja study were not observed in this small cohort. There were significant differences between the two studies, including mean age (41 vs 61 years), mean initial level of AP (87 u/L vs 67 u/L), mean decrease in AP after two years of treatment (32 u/L vs 6 u/L), and mean testosterone level prior to treatment (264 ng/dL vs 217 ng/dL). The significant age difference between the two studies is noteworthy, suggesting that younger patients may be more susceptible to increased bone turnover as a result of T deficiency. Further investigation may be needed to determine whether AP can be used as a marker of response to T replacement therapy in a select group of patients.
Source of Funding: None