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Reproductive system
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
During fetal development the testes descend from their point of origin on the posterior abdominal wall, and the descent may be arrested at any point along the pathway. In over two-thirds of cases the testicular descent arrests in the inguinal region, thus ultrasound is the optimum initial imaging test to locate the ‘missing’ testis.
Urology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Testicular descent occurs during the 5th to 7th months of pregnancy, the left descending before the right. An undescended testis is observed in 1 in 50–100 term infants and in up to one-third of premature babies. Descent after birth does occur spontaneously but is rare after the first few months of life.
Testis and scrotum
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The mechanisms that result in testicular descent are poorly understood but probably involve Mullerian inhibiting substance. Maternal chorionic gonadotrophin stimulates growth of the testis and may stimulate its migration. Imperfectly developed testes tend to descend incompletely.
What are the pharmacological considerations for male congenital hypogonadotropic hypogonadism?
Published in Expert Opinion on Pharmacotherapy, 2022
Giulia Rastrelli, Mario Maggi, Giovanni Corona
The objective of the treatment in CHH patients depends on patient’s age and requests. In adolescence, the main aim of the treatment is to induce the development of secondary sexual characteristics. In young adults with a fertility wish, spermatogenesis is the pivotal aim. Lastly, in middle-aged/elderly men, fertility loses its primary importance and sexual function, muscle strength, and body composition are the most important outcomes. It is also important to mention that, when red flags are identified in neonates or infants and CHH is suspected and/or diagnosed early in life, a short course treatment (3–6 months) with gonadotropins or GnRH may be attempted to induce testicular descent and development as well as to improve penile length [4]. However, there is still no consensus on this early treatment mainly due to a limited amount of data on the topic that have been recently reviewed [4].
New mutation causing androgen insensitivity syndrome – a case report and review of literature
Published in Gynecological Endocrinology, 2019
Marzena Maciejewska-Jeske, Patrycja Rojewska-Madziala, Karolina Broda, Karolina Drabek, Anna Szeliga, Adam Czyzyk, Stanislaw Malinger, Anna Kostrzak, Agnieszka Podfigurna, Gregory Bala, Blazej Meczekalski, Agnieszka Malcher, Maciej Kurpisz
CAIS is an X-linked disease manifesting as a result of the impaired functioning of cellular androgen receptors. Despite possessing a male karyotype, affected patients develop a female habitus, short and blind-ended vagina, the absence of uterus and ovaries, and normal-appearing testes which do not descend. These structurally normal testes may instead be found anywhere along the embryonic path of testicular descent [9]. In adolescence, regular breast development and a lack of pubic and axillary hair is observed, while stature approaches the expected mean male height [10,11]. While certain characteristics such as lack of pubic and axillary hair are a consequence of androgen insensitivity during puberty, the absence of structures developing from the Müllerian ducts arise from prenatal hormone abnormalities [5]. Elevated anti-Müllerian hormone (AMH) levels are typical for infant males [12]. Low levels of LH and T are characteristic for male newborns and infants, increasing significantly after puberty [13,14].
Testicular developmental impairment caused by flutamide-induced and DEHP-induced cryptorchid rat models is mediated by excessive apoptosis and deficient autophagy
Published in Toxicology Mechanisms and Methods, 2018
Yi Wei, Yu Zhou, Xiang-Liang Tang, Bin Liu, Lian-Ju Shen, Chun-lan Long, Tao Lin, Da-wei He, Sheng-de Wu, Guang-hui Wei
Cryptorchidism has become one of the important reasons for male infertility, but the mechanism of cryptorchid impairment has not been fully elucidated. Until now, to clarify the mechanism of testicular descent or evaluate the testicular function, various experimental cryptorchidism models have been reported, such as surgical induction of cryptorchidism(Shikone et al. 1994; Watts et al. 2000) and hormonal inducted cryptorchid rat model (Nomura and Kanzaki 1977). To our knowledge, most of the experiment-induced cryptorchid rats models are made by surgical methods which could not be denied to have a risk of infection (Ohta et al. 1996; Wang et al. 1998). In addition, EDs (particularly DEHP and Flu) have been linked to developmental problems in the testis and reproductive tract. These EDs were observed to induce abnormalities in the formation of external genitalia, including agenesis of the epididymis, hypospadias and cryptorchidism (Gray et al. 2000). Then Flu and DEHP were chosen to induced cryptorchid rats.