How to Reverse Testicular Atrophy
Wischusen et al. described a patient with partial 21-hydroxylase deficiency, azoospermia, small testes, normal to high serum testosterone levels, and suppressed serum levels of gonadotropins. After treatment with glucocorticoids for several months, the semen quality improved, and he fathered a child (59). Small testes are incidentally reported in males with CAH, especially in poorly controlled patients, who had low FSH levels (12,14,59). In 101 patients, described in four recent studies, 6 patients had small testes, as measured by ultrasonography (2,5,6,9). Plasma FSH levels in these 6 patients were normal in 2 (5), decreased in 2 (5), just above the normal range in 1 (6), and not documented in 1 (9). Therefore, small testes have been observed in patients with CAH, but not frequently, and they are generally found in men with low FSH levels (hypogonadotropism). Testicular volume is relevant with respect to fertility, because it is positively correlated with semen quality (60,61).
However, when adult testicular volume was evaluated in relation to previous germ cell counts at biopsy in prepubertal boys with cryptorchidism, prepubertal testicular size did not predict adult germ cell count (138). There is also a lack of correlation between testicular volume at orchiopexy and paternity, hormone levels, sperm count, and testicular volume in adulthood when studied in both unilateral and bilateral men with cryptorchidism (115,132,139).
Monkeys resulted in a precipitous decline in testicular size associated with the complete regression of the seminiferous epithelium to the extent that the tissue comprised only type A spermatogonia and Sertoli cells. More recent experiments using monkeys rendered hypogonadotropic, hypogonadal by either surgical or chemical hypophysec-tomy, have confirmed Smith's earlier observation and have extended it by demonstrating that replacement of testosterone stimulates testicular growth to approx 60 of the pretreatment size (43-45). The gonadal growth primarily resulted from stimulation of spermatogenesis by the androgen, but morphometric analysis of the seminiferous epithelium revealed that the smaller testicular size was accounted for by a deficit in the numbers of all type B spermatogonia. FSH replacement in testosterone-
This leads to the classic phenotype of KS long legs, with an arm span frequently greater than height, gynecomastia, decreased muscle mass and increased abdominal adiposity, decreased facial and body hair, and small testes which often measure less than 5 mL in volume (see Fig. 2). The penis may be decreased in size but is often of normal length. Gynecomastia is variable but is often prominent and may require surgical correction. Mosaicism may present more subtly, because affected individuals can appear anywhere along a phenotypic spectrum between classical KS and normal. Infertility is almost universal however, human leukocyte antigen (HLA)-confirmed children fathered by individuals with KS have been reported (19). Moreover, assisted reproductive techniques may allow some men with KS to father children (see section on KS and infertility). The frequency of various symptoms and signs of KS is summarized in Table 2. Small testes 99-100
Dose of GnRH that is required to achieve testosterone levels in the normal adult male range and to stimulate spermatogenesis varies considerably in men with hypogo-nadotropic hypogonadism ranging from 5 to 20 g 120 min or 25-600 ng kg per bolus. The therapeutic dose correlates positively with body weight and negatively with pretreatment testicular size (12). Serum testosterone levels usually normalize within 1-2 mo, and the testes increase in size within 3-6 mo after therapy begins. For adjustments, serum testosterone, gonadotropins, and testicular volume should be monitored closely at 2- to 4-wk intervals. Most patients should be treated for up to 2 yr to maximize testicular growth and achieve spermatogenesis, because it has been shown that the time until appearance of sperm in the ejaculate is quite variable, ranging from 2 to 22 mo of therapy (7). Therapy With hCG Urinary or Highly Purified Urinary Human FSH. Urinary FSH, as well as the highly purified preparation, are effective...
The vasectomy began with the identification of the vas deferens through the scrotal skin. An incision was made, and the vas was gently dissected and retracted through the opening. Each vas was clamped with a small hemostat, and a 1-cm length was resected. Both cut ends were coagulated with electrosurgery and tied independently with a fine-gauge absorbable suture material. The testicles were examined, and the scrotal incision was closed with an absorbable suture material.
Pathophysiology Of Hivinfection In The Reproductive Tract And Potential Mechanisms Of Gonadal Dysfunction
Testicular atrophy is a common finding in autopsy series of patients infected with HIV (8-11). Histological examination of the testes reveals a spectrum of abnormalities, including hypospermatogenesis, spermatogenic arrest, and Sertoli cell-only pheno-types (11). In addition to the loss of germ cells and atrophy, the seminiferous tubules exhibit basement membrane thickening and peritubular fibrosis (8,9). Common abnormalities in semen include leukocytospermia, lower ejaculation volume and total sperm count, and lower percentage of rapidly progressive sperm in comparison to healthy controls (12,13) however, in the majority of HIV-infected patients, these values are within the normal adult male range. The body mass index was the best predictor of testicular atrophy in a retrospective analysis (8) thus, underweight patients are at 3.5-fold higher risk for testicular atrophy than are normal weight patients. Surprisingly, in this small series, CD4+ T-lymphocyte count was not a significant...
Since he is a body builder with small, soft testes, high testosterone levels, and low LH levels, the physician should suspect androgen abuse or possibly androgen-producing tumor (extremely rare). The high androgen levels would suppress LH secretion and reduce intratesticular testosterone levels. The low LH and intratesticular testosterone would correlate well with small testes and low sperm count, respectively.
The prostate gland is dependent on androgens that are produced exogenously by the testicles to facilitate normal development and to maintain normal structure and function (1). Briefly, the testes are stimulated to produce and secrete testosterone and other steroids by an exogenous protein, luteinizing hormone, which is made in the pituitary gland. Testosterone (T) is converted to its reduced form, dihydrotestosterone (DHT), by the enzyme 5a-reductase in the prostate. Both T and DHT bind to and activate the androgen receptor, causing a cascade of events that results in stimulation and maintenance of prostatic epithelial and stromal growth and secretion. DHT has a greater affinity for the androgen receptor than T and is normally the major prostate growth stimulant. Currently, attempts to interrupt or alter the stimulatory effects of exogenous factors that control prostate growth target aspects of the pituitary-testis-prostate axis. One approach is to alter the production and secretion...
Male hypogonadism may result from defects in spermato-genesis, steroidogenesis, or both. It may be a primary defect in the testes or secondary to hypothalamic-pituitary dysfunction, and determining whether the onset of gonadal failure occurred before or after puberty is important in establishing the cause. However, several factors must be considered. First, normal spermatogenesis almost never occurs with defective steroidogenesis, but normal steroidogenesis can be present with defective spermatogenesis. Second, primary testicular failure removes feedback inhibition from the hypothalamic-pituitary axis, resulting in elevated plasma gonadotropins. In contrast, hypothalamic and or pituitary failure is almost always accompanied by decreased gonadotropin and steroid levels and reduced testicular size. Third, gonadal failure before puberty results in the absence of secondary sex characteristics, creating a distinctive clinical presentation called eunuchoidism. In contrast, men with a...
The primary factor mediating gonadal damage in acromegaly is GH excess. GH regulates testicular function, by stimulating the local production of insulin-like growth factor (IGF)-1, which modulates steroidogenesis and spermatogenesis. In fact, GH administration increases Ley dig and Sertoli cell responses to FSH and LH (36,37). However, high GH and IGF-1 levels induce severe testicular alterations and disrupt the hypothalamic-pituitary-testicular axis. Repeated administration of high doses of GH in dogs reduced testicular weight with germ cell degeneration and epithelial atrophy (38). The extent of testicular damage is related to the severity of acromegaly. In fact, serum GH and IGF-1 levels correlate negatively with serum DHT levels (see Fig. 2). Several mechanisms have been proposed to explain these findings, including a change in androgen metabolism (39), FSH and LH suppression by increased somatostatin tone, a decrease in the serum concentration of SHBG, and lactogenic effects of...
Klinefelter, Jr., a native of Baltimore and a graduate of the Johns Hopkins Medical School, spent a year working as a traveling fellow with Dr. Fuller Albright in the Metabolic Ward of the Massachusetts General Hospital in Boston (3). At that time, Dr. Albright was at the height of his formidable academic career and, among many other subjects, was interested in the endocrinology of sexual development and the therapeutic applications of the recently available steroid hormones. Dr. Albright had identified a group of adult men with a previously unchar-acterized syndrome typified by gynecomastia, small testes, and varying degrees of eunuchoidism. Dr. Albright assigned Dr. Klinefelter the task of further describing this syndrome for publication.
Only one totally inactivating mutation of the LHfi gene has so far been detected (27) (Table 1). The proband was a male who presented with delayed puberty at the age of 17 yr and had a family history of male infertility on the father's side, but none on the mother's side. His serum testosterone level was low and immunoreactive LH was high. A normal serum testosterone response was found on challenge with exogenous hCG, but in vitro bioassay of serum LH revealed no activity. These findings, together with a family history of consanguinity, suggested an inherited defect in the LH structure, maintaining its immunoreactivity but abolishing bioactivity. After 2 yr of testosterone treatment, there was no evidence for spontaneous puberty after treatment was withdrawn. Testicular biopsy revealed arrested spermatogenesis and absent Leydig cells. Long-term hCG treatment resulted in testicular enlargement, normal virilization, and spermatogenesis.
Myotonic dystrophy is an inherited disease that begins early in adult life. It is manifested by distal muscle weakness and atrophy. Deep tendon reflexes are reduced. Ptosis may be present, and closure of the eyelids is also weak. Atrophy of the temporalis and sternocleidomastoid muscles is severe. Other clinical features include early frontal alopecia, cataracts, blepharitis, conjunctivitis, and testicular atrophy. Mental retardation may occur. Dystrophic cardiac disease occurs late. The disease can be quite variable, and some patients and affected family members may manifest only one or two features.
Congenital Hypogonadotropic Hypogonadism Caused by Genetic Defects of the Gonadotropin Subunit Genes Mutation in the
Recently, two men with FSH-P subunit mutations have been described. The first subject, a 32-yr-old man, appeared normally virilized with normal LH and T levels but small testes, azoospermia, and undetectable FSH level (100). Genetic analysis revealed a homozygous T to C mutation (Cys 82 to Arg). It was predicted that the lack of cys-teine would result in the inability to form the proper disulfide bond of FSH-P with abnormal tertiary structure. The second reported case of an FSH-P gene mutation is an 18-yr-old man who presented with delayed puberty, small testes (1 and 2 mL), azoospermia, and undetectable FSH levels. The finding of a high LH and low T levels implies an additional unexplained defect in Leydig cell function (101). Genetic analysis demonstrated a homozygous 2 bp deletion in codon 61. The mutation gives rise to an altered amino acid sequence, followed by a premature stop codon. Consequently, the translated FSH-P protein was truncated and unable to associate with the...
Confident face-forward manner in which he approaches other members of his pack. In a similar manner, the dominant rhesus monkey advertises his status by an elaborate posture which includes elevated head and tail, lowered testicles, and slow, deliberate body movements accompanied by an unhesitating but measured scrutiny of other monkeys he encounters. Animals not only utilize visual signals to advertise dominance, but they also use acoustic and chemical signals. For example, dominant European rabbits use a mandibular secretion to mark their territory.
The clinical features of Klinefelter syndrome, found only in males and usually detected at puberty, are sterility, testicular atrophy, hyalinization of the seminiferous tubules, and usually gynecomastia. The cells have 47 chromosomes with a sex chromosomal complement of the XXY type, and a sex chromatin body (Barr body formed by condensation of an inactivated sex chromosome a Barr body is also present in normal females) is found in 80 of cases (Fig. 1.11). The incidence is approximately 1 in 500 males. Nondisjunction of the XX homologues is the most common causative event. Occasionally, patients with Klinefelter syndrome have 48 chromosomes 44 autosomes and four sex chromosomes (XXXY). Although mental retardation is not generally
Constitutively activating mutations of the LH-R gene give rise to FMPP. Inactivating LH-R mutation results in an array of male phenotypes ranging from micropenis and hypospadias to complete sex reversal (XY, pseudohermaphroditism), depending on the completeness of inactivation of the receptor. Inactivating FSHR mutations in men cause a decrease of testicular size and suppressed quality and quantity of spermatogen-esis but not azoospermia. Some affected men may be fertile. FSH inactivation is unlikely to affect pubertal maturation. No unequivocally activating mutations of the FSHR have yet been described in either sex. Studies on candidate syndromes (e.g., precocious puberty and macro-orchia) have yielded negative results.
Virilization in the woman is the most common reaction associated with anabolic steroids, especially when higher doses are used. Acne occurs frequently in all age groups and both sexes. Nausea, vomiting, diarrhea, fluid and electrolyte imbalances (the same as for the androgens, discussed previously), testicular atrophy,
The second male, reported from Israel (35), was an 18-yr-old with slight delay of puberty, small testes, azoospermia, and a plasma FSH concentration below 0.5 IU L. Total testosterone was low (4.5 nmol L), and LH was increased (24.5 IU L), indicating a defect in testosterone biosysthesis. DNA sequencing revealed the same homozygous 2 bp deletion in codon 61 that was found previously in the female patients (34,36,38). The mutation gave rise to a completely altered amino acid sequence between codons 61 and 86 of the FSH3 chain, which was followed by a premature stop codon, and lack of translation of amino acids 87 to 111. Consequently, the translated FSH3 protein was truncated and unable to associate with common -subunit to form bioactive or immunoreactive a 3 dimers.
Men with chronic renal failure exhibit features consistent with classical androgen deficiency reproductive manifestations, including gynecomastia, impotence, testicular atrophy, impaired spermatogenesis, and infertility, as well as somatic disorders of bone, muscle, and other androgen responsive tissues (1,2). However, only a single well-controlled study has examined androgen replacement therapy in men with uremia (34). Nineteen men who were receiving regular hemodialysis were randomized to receive either oral testosterone undecanoate (240 mg d) or placebo for 12 wk. Libido and sexual activity were increased, but hemoglobin was unchanged. There were no adverse clinical effects or hepatotoxicity. Effects on bone, muscle, cognition, and well-being were not reported. Further studies examining physiological androgen replacement therapy in men with chronic renal failure, notably using nonparenteral therapies in view of the increased bleeding risks in men with chronic renal failure, would...
The endocrine system involves internal secretions related to the function of the endocrine glands such as the thyroid, adrenal, pituitary. Hormonal secretions from these glands pass directly into the blood stream. An important part of this system, the pituitary, lies at the base of the brain. This master gland secretes a variety of hormones, including hormones that stimulate the thyroid gland and control its secretion of thyroxine, which dictates the rate at which all cells utilize oxygen control the secretion in the adrenal gland of hormones that influence the metabolism of carbohydrates, sodium, and potassium and control the rate at which substances are exchanged between blood and tissue fluid control the secretion in the ovaries of estrogen and progesterone and the creation in the testicles of testosterone control the rate of development of the skeleton and large interior organs through its effect on the metabolism of proteins and carbohydrates and inhibit insulin a lack of insulin...
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