3% of male babies; about 30% of premature male babies. ... see also overview of Undescended Testicle.
approx 1 in 66 or 1.50% or 4.1 million people in USA [Source statistic for calcuation: "3% of male babies; about 30% of premature male babies." -- see also general information about data sources]
4,080,000 per year, 340,000 per month, 78,461 per week, 11,178 per day, 465 per hour, 7 per minute, 0 per second. [Source statistic for calculation: "3% of male babies; about 30% of premature male babies." -- see also general information about data sources]
16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the prevalence and/or incidence of Undescended Testicle.
Primary hypogonadism results directly from interstitial (Leydig’s cell) cellular or seminiferous tubular damage due to faulty development or mechanical damage. This causes increased secretion of gonadotropins by the pituitary in an attempt to increase the testicular functional state and is therefore termed hypergonadotropic hypogonadism. This form of hypogonadism includes Klinefelter syndrome, Reifenstein’s syndrome, Turner syndrome, Sertoli-cell-only syndrome, anorchism, orchitis, and sequelae of irradiation.
Secondary hypogonadism is due to faulty interaction within the hypothalamic-pituitary axis, resulting in failure to secrete normal levels of gonadotropins, and is therefore termed hypogonadotropic hypogonadism. This form of hypogonadism includes hypopituitarism, isolated follicle-stimulating hormone deficiency, isolated luteinizing hormone deficiency, Kallmann’s syndrome, and Prader-Willi syndrome. Depending on the patient’s age at onset, hypogonadism may cause eunuchism (complete gonadal failure) or eunuchoidism (partial failure).
Medications, such as exogenous testosterone or anabolic steroids, can also cause of hypogonadism, resulting in infertility.
Hypogonadism is rare, and it has no racial predilection.
Source: Professional Guide to Diseases (Eighth Edition), 2005
The mechanism whereby the testes descend into the scrotum is still unexplained. Some evidence is available to implicate hormonal factors — most likely androgenic hormones from the placenta, maternal or fetal adrenals, or the immature fetal testis and, possibly, maternal progesterone or gonadotropic hormones from the maternal pituitary.
Researchers have linked undescended testes to the development of the gubernaculum, a fibromuscular band that connects the testes to the scrotal floor. In the normal male fetus, testosterone stimulates the formation of the gubernaculum. This band probably helps pull the testes into the scrotum by shortening as the fetus grows. Thus, cryptorchidism may result from inadequate testosterone levels or a defect in the testes or the gubernaculum.
Because the testes normally descend into the scrotum during the eighth month of gestation, cryptorchidism most commonly affects premature neonates. (It occurs in 30% of premature male neonates but in only 3% to 4% of those born at term.) In about 80% of affected infants, the testes descend spontaneously during the first year; in the rest, the testes may descend later.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Source: The 5-Minute Pediatric Consult, 2008
The term 'prevalence' of Undescended Testicle usually refers to the estimated population of people who are managing Undescended Testicle at any given time. The term 'incidence' of Undescended Testicle refers to the annual diagnosis rate, or the number of new cases of Undescended Testicle diagnosed each year. Hence, these two statistics types can differ: a short-lived disease like flu can have high annual incidence but low prevalence, but a life-long disease like diabetes has a low annual incidence but high prevalence. For more information see about prevalence and incidence statistics.
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