madman
Super Moderator
ABSTRACT
Objective: We aimed to investigate the role of testosterone to estradiol ratio in predicting the effectiveness of human chorionic gonadotropin and testosterone treatments in male hypogonadism.
Materials and methods: Thirty-six male patients with hypogonadotropic hypogonadism were included in the study. Seventeen (47.2%) patients received weekly recombinant human choriogonadotropin alpha (hCG) treatment (group-1) and 19 (52.8%) received testosterone replacement therapy (T treatment) every 21 days (group-2). Under these treatments, adequate frequency of morning erection (≥3/week), testosterone to estradiol ratio (T/E), and testicular volume changes was analyzed.
Results: The mean age of the patients was 28.5 ± 8.7 years. When the frequency of morning erection (≥3/week) was specified as adequate, the cut-off value for effective T/E ratio was found to be 12.0 (sensitivity 93.8%, specificity 90.0%). There was no significant difference between the treatment groups in terms of total testosterone levels, T/E ratio, or frequency of morning erections (≥3/week) (p > 0.05). However, there was a statistically significant difference between the groups in terms of median left-right testicular volume in favor of group-1 (p < 0,05).
Conclusion: In patients with hypogonadism who are under treatment, elevated estradiol-induced erectile dysfunction symptoms may persist even if serum testosterone levels are normal. Testosterone to estradiol ratio can be used as a predictive value in the effective treatment of hypogonadotropic hypogonadism with hCG and T.
INTRODUCTION
Hypogonadism is a gonadal dysfunction that can occur as a result of disruption in one or both of the gametogenesis and gonadal hormone secretions (1). Gonadal functions are under the control of hypothalamic gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormones (LH). LH stimulation induces testosterone production in the testicle and FSH stimulates spermatogenesis (2). Dysfunction due to gonadal failure is called primary hypogonadism (hypergonadotropic hypogonadism) and hypogonadism caused by the lack of hypophyseal hormones is known as secondary hypogonadism (hypogonadotropic hypogonadism).
The diagnosis of androgen insufficiency in men is considered in the presence of low testosterone levels consistent with symptoms and signs of hypogonadism. The most common symptoms and signs are decreased libido, sexual activity, and spontaneous erection; gynecomastia decreased body hair or shaving frequency, small or shrunken testicle, infertility, and absence or low count of sperms (1,3). Today, expanded knowledge about normal male sexual function and the causes of sexual impairment has led to the development of effective treatments. The main goals of treatment in male hypogonadism are to correct the symptoms of testosterone deficiency and maintain secondary sex characteristics. In healthy adult men, the target of the treatment is to keep the testosterone level at the lower limit of the normal range (280-300 ng/dL [9.7-10.4 nmol/L]) (4). Hormone replacement is the preferred treatment option in hypogonadotropic hypogonadism (5) and has evolved to comprise various options, including recombinant human FSH, recombinant human LH, and pulsatile gonadotropin-releasing hormone (GnRH), in addition to human chorionic gonadotropin (hCG), human menopause gonadotropin (hMG), and testosterone (T) treatments (6,7). According to the current state of the literature, the effectiveness of these different treatment strategies remains controversial (8,9). Besides, it is not clear what role estrogen hormone plays as a factor in regulating sexual dysfunction in men. In this regard, the effect of imbalance between testosterone and estradiol on sexuality has not yet been clearly determined (10). It has been suggested that rather than the direct effect of estrogens on erectile dysfunction and decreased libido, the testosterone-estradiol (T/E) ratio may be correlated with these symptoms (11). The aim of this study is to evaluate the role of the T/E ratio in estimating the effectiveness of hCG and T treatment in male hypogonadism.
*Due to the retrospective and single-center design, the bias of selection is our main limitation. The second limitation is the relatively small sample size and the lack of a control group.
In conclusion, in patients with hypogonadism who are under treatment, elevated estradiol-induced erectile dysfunction symptoms may persist even if serum testosterone levels are normal. Keeping testosterone to estradiol ratio around 12.0 may increase the frequency of spontaneous erections in the morning. To better understand the role of the T/E ratio in this disease, randomized double-blind placebo-control (RDBPC) studies involving large numbers of patients are needed.
Objective: We aimed to investigate the role of testosterone to estradiol ratio in predicting the effectiveness of human chorionic gonadotropin and testosterone treatments in male hypogonadism.
Materials and methods: Thirty-six male patients with hypogonadotropic hypogonadism were included in the study. Seventeen (47.2%) patients received weekly recombinant human choriogonadotropin alpha (hCG) treatment (group-1) and 19 (52.8%) received testosterone replacement therapy (T treatment) every 21 days (group-2). Under these treatments, adequate frequency of morning erection (≥3/week), testosterone to estradiol ratio (T/E), and testicular volume changes was analyzed.
Results: The mean age of the patients was 28.5 ± 8.7 years. When the frequency of morning erection (≥3/week) was specified as adequate, the cut-off value for effective T/E ratio was found to be 12.0 (sensitivity 93.8%, specificity 90.0%). There was no significant difference between the treatment groups in terms of total testosterone levels, T/E ratio, or frequency of morning erections (≥3/week) (p > 0.05). However, there was a statistically significant difference between the groups in terms of median left-right testicular volume in favor of group-1 (p < 0,05).
Conclusion: In patients with hypogonadism who are under treatment, elevated estradiol-induced erectile dysfunction symptoms may persist even if serum testosterone levels are normal. Testosterone to estradiol ratio can be used as a predictive value in the effective treatment of hypogonadotropic hypogonadism with hCG and T.
INTRODUCTION
Hypogonadism is a gonadal dysfunction that can occur as a result of disruption in one or both of the gametogenesis and gonadal hormone secretions (1). Gonadal functions are under the control of hypothalamic gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormones (LH). LH stimulation induces testosterone production in the testicle and FSH stimulates spermatogenesis (2). Dysfunction due to gonadal failure is called primary hypogonadism (hypergonadotropic hypogonadism) and hypogonadism caused by the lack of hypophyseal hormones is known as secondary hypogonadism (hypogonadotropic hypogonadism).
The diagnosis of androgen insufficiency in men is considered in the presence of low testosterone levels consistent with symptoms and signs of hypogonadism. The most common symptoms and signs are decreased libido, sexual activity, and spontaneous erection; gynecomastia decreased body hair or shaving frequency, small or shrunken testicle, infertility, and absence or low count of sperms (1,3). Today, expanded knowledge about normal male sexual function and the causes of sexual impairment has led to the development of effective treatments. The main goals of treatment in male hypogonadism are to correct the symptoms of testosterone deficiency and maintain secondary sex characteristics. In healthy adult men, the target of the treatment is to keep the testosterone level at the lower limit of the normal range (280-300 ng/dL [9.7-10.4 nmol/L]) (4). Hormone replacement is the preferred treatment option in hypogonadotropic hypogonadism (5) and has evolved to comprise various options, including recombinant human FSH, recombinant human LH, and pulsatile gonadotropin-releasing hormone (GnRH), in addition to human chorionic gonadotropin (hCG), human menopause gonadotropin (hMG), and testosterone (T) treatments (6,7). According to the current state of the literature, the effectiveness of these different treatment strategies remains controversial (8,9). Besides, it is not clear what role estrogen hormone plays as a factor in regulating sexual dysfunction in men. In this regard, the effect of imbalance between testosterone and estradiol on sexuality has not yet been clearly determined (10). It has been suggested that rather than the direct effect of estrogens on erectile dysfunction and decreased libido, the testosterone-estradiol (T/E) ratio may be correlated with these symptoms (11). The aim of this study is to evaluate the role of the T/E ratio in estimating the effectiveness of hCG and T treatment in male hypogonadism.
*Due to the retrospective and single-center design, the bias of selection is our main limitation. The second limitation is the relatively small sample size and the lack of a control group.
In conclusion, in patients with hypogonadism who are under treatment, elevated estradiol-induced erectile dysfunction symptoms may persist even if serum testosterone levels are normal. Keeping testosterone to estradiol ratio around 12.0 may increase the frequency of spontaneous erections in the morning. To better understand the role of the T/E ratio in this disease, randomized double-blind placebo-control (RDBPC) studies involving large numbers of patients are needed.
