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Medical Treatment of Male Infertility
Published in Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh, Male Infertility in Reproductive Medicine, 2019
Marlon P. Martinez, Mohamed Arafa, Haitham Elbardisi
According to the American Association of Clinical Endocrinologists medical guidelines, injections with hCG are recommended to those peripubertal boys with hypogonadotropic hypogonadism and delayed puberty [25]. This will provide the development of secondary sexual characteristics and maximize fertility potential [26]. Testicular size is noted to increase over 6 to 9 months in most boys [27]. hCG monotherapy is effective in the treatment of induction of spermatogenesis in patients with delayed pubertal presentation. In a study by Vicari et al. of 17 males with isolated hypogonadotropic hypogonadism, 70% of patients became sperm positive after the long-term treatment (14–120 months) with hCG. This was more pronounced in patients with testicular volume greater than or equal to 4 cm (90% vs. 60%) [28].
The inherited basis of hypergonadotropic hypogonadism
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Congenital isolated hypogonadotropic hypogonadism (CIHH) is a well-known cause of absent pubertal development in both boys and girls and results from inadequate secretion of the two pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), with consequent impairment of normal testicular or ovarian function. With a prevalence estimation, based on a civilian and military hospital series, of 1/4000 to 1/10, 000 in males,1 CIHH is reported to be between two and five times more common in boys than in girls.2 Patients with CIHH usually come to clinical attention during adolescence or adulthood because of incomplete or absent pubertal development; owing to progress in molecular genetics and clinical practice, the diagnosis can be made earlier in cases where the diagnosis is specifically sought.
Association analysis of KISS1 polymorphisms and haplotypes with polycystic ovary syndrome
Published in British Journal of Biomedical Science, 2021
M Farsimadan, F Moammadzadeh Ghosi, S Takamoli, H Vaziri
KISS1 and KISS1R are the first genes involved in gonadotropin-dependent precocious puberty (GDPP) phenotypes in humans. Patients with KISS1 mutations exhibit typical features of idiopathic GDPP and show an adequate response to conventional GDPP treatment with GnRH agonists [18,19]. Different investigations have studied KISS1 mutations in disorders of puberty. In a very recent study on a large group of girls, Li et al. evaluated the association of KISS1 polymorphism with the risk of central precocious puberty (CPP) and their results suggested that the mutation in rs5780218 increases the risk of CPP [20]. Similarly, the results of another study among Chinese girls diagnosed with CPP uncovered several potentially polymorphisms in KISS1 and reported the frequency of these SNPs to be significantly higher among patients compared with controls [21]. Likewise, Silveira et al. demonstrated two different missense mutations in KISS1 be associated with a higher risk of isolated hypogonadotropic hypogonadism (IHH) and CPP [11]. However, some studies failed to show any relationship between the KISS1 polymorphisms and increased risks of CPP [22,23] and IHH [24].
The Role of testosterone treatment in patients with metabolic disorders
Published in Expert Review of Clinical Pharmacology, 2021
Giovanni Corona, Giulia Rastrelli, Linda Vignozzi, Arcangelo Barbonetti, Alessandra Sforza, Edoardo Mannucci, Mario Maggi
Interestingly, low-grade inflammation is also present in the hypothalamus and it is associated with a disruption of the complex network orchestrating gonadotropin-releasing hormone [GnRH] release and gonadotropin secretion from the anterior pituitary [25,43,44]. In particular, the latter studies demonstrated that metabolic alterations underpinning MetS can bring on an inflammation-induced discrete damage to groups of neurons in the preoptic area of the hypothalamus, finally resulting in gonadotropin deficiency and secondary hypogonadism, very similar to what is often observed in human MetS. Hence, in our opinion, it can be speculated that the MetS-associated T deficiency does have an organic background. We participated in a genomic screening program on rare isolated hypogonadotropic hypogonadism [IHH] gene variants among patients with either classic IHH or with acquired mild adult-onset T deficiency, such that they were associated with MetS [45]. The study found that the same gene variants could frequently predispose a patient to adult-onset-IHH, such as in MetS [45]. This might help in understanding why not all obese subjects are hypogonadal: T deficiency could develop when a metabolic condition, and its associated low-grade inflammation, acts on a genetic background or susceptibility.
Osteonecrosis of Femoral Head is Associated with Congenital Multiple Pituitary Hormone Deficiency: Report of Three Cases and Literature Review
Published in Endocrine Research, 2019
Shuying Li, Jiangfeng Mao, Xi Wang, Min Nie, Xueyan Wu
While sex hormone plays a critical role in bone maturation and bone mineral density, ONFH has not yet been reported in patients with isolated hypogonadotropic hypogonadism. In our medical center, over 800 patients with congenital hypogonadotropic hypogonadism were followed up, and none were found to present with ONFH. In the meantime, only a few cases of ONFH have been reported in patients with hypothyroidism or adrenal deficiency. The above evidence indicates that a deficiency of sex, thyroid, and adrenal hormones may not play an essential role in the pathogenesis of ONFH.