Background: Gonadotropin therapy in boys with congenital isolated hypogonadotropic hypogonadism helps to increase testes volume and induce spermatogenesis in comparison with testosterone therapy. However, difficulties with dose titration, partial therapy success, absence of generally accepted regimen protocols don't allow to use this therapy in order to induce puberty in adolescents with Kallmann syndrome or normosmic hypogonadotropic hypogonadism.
Aim: To assess the effectiveness of combination hormonal replacement therapy via human chorionic gonadotropin and recombinant follicle stimulation hormone in adolescents with congenital isolated normosmic hypogonadotropic hypogonadism and with Kallmann syndromeMATERIALS AND METHODS: This is an open single-center prospective non-controlled study. Boys with hypogonadotropic hypogonadism were receiving hormonal replacement therapy for 12 months. Initial dose of human chorionic gonadotropin was 500 IU per week. Initial dose of recombinant follicle stimulation hormone was 37.5 IU per week. Doses were doubled in 6 months. Antropometric data, Tanner stage, testes volumes, inhibin B and anti-Mullerian hormone (AMH) levels were evaluated in all the patients before the treatment, after 6 and 12 months of the therapy.
Results: 8 boys with hypogonadotropic hypogonadism were included into the study. Median age before therapy initiation was 15.7 years [15.33; 16.41]. In 12 months after the therapy initiation puberty development, testosterone increase from 0.44 [0.34;0.62] to 4.39 [0.88;10.51] nmol/l (p=0.012), AMH decrease from 35.70 [18.00;59.00] to 14.41 [11.60;16.65] ng/ml were noted in all the patients (p=0.017). Testes volumes increase and inhibin B level increase were not statistically significant.
Conclusion: Gonadotropin therapy is effective in order to puberty initiation in adolescents with congenital hypogonadotropic hypogonadism. In helps to achieve not only androgenization, but also to Sertoli cells maturation.
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http://dx.doi.org/10.14341/probl13141 | DOI Listing |
Ginekol Pol
January 2025
Department of Clinical Dietetics, Faculty of Health Sciences, Medical University of Warsaw, Poland, Poland.
Anti-Müllerian hormone (AMH), also known as Müller duct inhibitory factor and primarily known for its role in sexual differentiation. In female fetuses, AMH production by granulosa cells begins around the 36th week of gestation and continues in women until menopause. It is becoming more significant in the endocrine and gynecological diagnosis of adult women.
View Article and Find Full Text PDFJ Cell Biol
April 2025
Department of Genetics and Cell Biology, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
TBC1D20 deficiency causes Warburg Micro Syndrome in humans, characterized by multiple eye abnormalities, severe intellectual disability, and abnormal sexual development, but the molecular mechanisms remain unknown. Here, we identify TBC1D20 as a novel Rab11 GTPase-activating protein that coordinates vesicle transport and actin remodeling to regulate ciliogenesis. Depletion of TBC1D20 promotes Rab11 vesicle accumulation and actin deconstruction around the centrosome, facilitating the initiation of ciliogenesis even in cycling cells.
View Article and Find Full Text PDFJ Sex Marital Ther
January 2025
Clinical Research Department, Elexial Research, Urology, Boston Medical Group, Bogotá, Colombia.
In this study, data from 7,440 patients from six Ibero-American countries were analyzed, focusing on men who consulted for erectile dysfunction (ED). Participants were queried about infidelity in their relationships. Results showed a negative correlation between infidelity and the severity of ED, suggesting that the likelihood of infidelity decreases as the severity of ED increases.
View Article and Find Full Text PDFBackground: Differential diagnosis of hypogonadotropic hypogonadism (HH) and constitutional delay of puberty (CDP) is extremely important since with the latter puberty begins and completes without any medical intervention and in the case of HH puberty does not occur or is incomplete. Failure to start treatment on time leads to medical and psychosocial maladjustment of the patient.
Aim: Development of a method for differential diagnosis of hypogonadotropic hypogonadism and constitutional delay of puberty in boys 13.
Introduction: CarboxypeptidaseE (CPE) is an enzyme involved in the neuropepetides/hormones processing. Its deficiency is associated with endocrinopathies comparable to those caused by proprotein convertase1/3(PC1/3) deficiency. In this case report we expand the clinical features of CPE deficiency by examining the index case's clinical/laboratory results, which are also indicative of PC1/3 deficiency.
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