Low Testosterone Treatment
Testicular failure may occur before puberty and present as delayed puberty and the eunuchoid phenotype, or after puberty, with the development of infertility, impotence, or decreased libido in otherwise fully virilized males. The source of hypogonadism can be testicular, as occurs in primary hypogonadism, or it may result from abnormalities of the hypothalamic-pituitary axis, as in secondary hypogonadism. Prepuberal Hypogonadism Prepuberal hypogonadism is often unsuspected until a delay in male sexual development is noticed at the time
The most characteristic features of this syndrome are chronic mucocutaneous candidiasis, hypoparathyroidism, Addison's disease, and T1ADM other features include other autoimmune endocrinopathies (such as hypothyroidism or hypogonadism), malabsorption syndromes, pernicious anemia, and alopecia. The gene for this disorder is the autoimmune regulator or AIRE (OMIM 607358), which appears to be a transcription factor. The exact mechanism by which it causes the syndrome is not known (131,132).
The role of NO in the physiology of male sexual function establishes its importance as the principal modulator of penile erection. An increase in cGMP activates specific protein kinases, which in turn phospho-rylate certain proteins, activate ion channels, and through intermediary biochemical events lead to reduction in cytosolic calcium and relaxation of smooth muscles. Following an erection or the return to a flaccid state, cGMP is hydrolyzed to GMP by phosphodi-esterase type 5 (PD-5). Although other types of phos-phodiesterases are present in the corpus cavernosum, they do not appear to play a significant physiological role in erection.
Female Hypogonadism Female hypogonadism, especially prepuberal, may be an indication for androgen therapy. Androgens are necessary for normal pubic hair induction and long bone growth in both sexes. In prepuberal females with hy-popituitarism in whom all other hormonal deficiencies (estrogen, progesterone, thyroid, adrenal, and growth hormone) have been corrected, normal sexual development and long bone growth are not complete without androgen hormone replacement. Estrogen administration during adolescence is necessary for the development of the breast, the gynecoid pelvis, and other female characteristics. However, maximal long bone growth and development of axillary and pubic hair will not occur without small amounts of androgen replacement. The use of methyltestosterone (Android) and di-ethylstilbestrol in combination has been demonstrated to be very effective in inducing complete secondary sexual development in these females. Finally, low doses of androgens have been used to...
Sources and medical uses of folliclestimulating hormone luteinizing hormone and human chorionic gonadotrophin
FSH and hCG also find application in the treatment of male subfertility or related conditions. Both are administered to males exhibiting hypogonadotrophic hypogonadism to stimulate sperm synthesis and normal sexual function. hCG has found limited application in the treatment of pre-pubertal cryptorchidism (a condition characterized by failure of the testes to descend fully into the scrotum from the abdomen). The ability of this hormone to stimulate testosterone production also caught the attention of some athletes, and, as a result, the International Olympic Committee has banned its use.
When stimulation of gonadotropin production is needed, the pituitary gland is usually capable of responding to appropriately administered GnRH, even in cases of hypogonadotropic hypogonadism, when LH and FSH levels are always low. Therefore, GnRH therapy can be substituted for gonadotropin therapy by administering GnRH (Lutrepulse) pulses intravenously via an indwelling pump. GnRH itself is used, since the short half-life is important to prevent accumulation between pulses. The advantage of this procedure compared with intramuscular injections of gonadotropins
Chronic administration of many drugs, especially anti-convulsant medications, glucocorticoids, and GnRH agonists, are known to produce osteopenia and osteoporosis. The anticonvulsants inhibit formation of active D3 chronic glucocorticoid therapy increases bone turnover by altering osteoblast differentiation and inhibiting collagen synthesis and the GnRH agonists induce chemical hypogonadism.
SHBG levels are known to be influenced by a variety of clinical conditions. In females, the high estrogen levels of pregnancy or the use of oral contraceptives result in increased SHBG concentrations. In males, elevated levels of SHBG are seen most commonly in individuals with liver cirrhosis or during normal aging. Elevated SHBG levels are also seen in hyperthyroidism and hypogonadism. All of these conditions are associated with elevated estrogen levels, which result in increased hepatic SHBG synthesis. SHBG levels are suppressed by androgen replacement or chronic glucocorticoid therapy. Elevations of SHBG do not necessarily result in a fall in free testosterone levels. When assessing the androgenic status of an individual, whether male or female, it is necessary to measure both total and free testosterone plasma levels. Plasma testosterone levels also exhibit age-associated changes. The levels of the hormone are very low throughout childhood and until early adolescence, when...
There are four important features about a control parameter. Firstly, when it is linearly scaled beyond some critical value, it may induce stochastic behaviour in the order parameter followed by a discontinuous change to another qualitatively different state. Secondly, it is completely aspecific with regard to the change it induces. Thus, a control parameter does not contain prescriptions as to how a system should change unlike its symbolic counterparts such as genetic programmes or schemata. Thirdly, different mechanisms can serve as control parameters at different ages (e.g., hormonal at one age, neural at another and cognitive at yet another). Fourthly, some form of experimental manipulation is required to identify such age-specific control parameters with any confidence. The last two points are brought into relief by a study of testosterone effects in seagulls (Groothuis & Meeuwissen 1992). When administered to young chicks, it induced precociously complete agonistic displays....
Normal prostate cells and tumor cells are sensitive to androgens, which are produced by two major sources the testicles, which produce testosterone (95 of all androgens), and the adrenal glands, which produce dehydroandrosterone, dehy-droandrosterone sulfate, and androstenedione. Both are under the influence of luteinizing hormone (LH), which in turn is controlled by GnRH produced by the hypothalamus. Testosterone levels have a negative feedback effect on GnRH release from the hypothalamus. Targeted endocrine medical treatment of prostate cancers aims to decrease the activity of androgens on the AR, either with antiandrogens (i.e., nonsteroidal agents such as flutamide, biclutamide) that competitively block dihydrotestosterone (DHT) binding to AR, and subsequent activation of AR-regulated genes, or by suppression of LH secretion (i.e., using specific LH agonists that ultimately inhibit LH secretion, thus reducing androgen production).
Prader-Willi syndrome is a disorder with many manifestations related to hypothalamic insufficiency. The major features include infantile hypotonia, hypogonadism, dysmorphic appearance, small hands and feet, hyperpha-gia and obesity, developmental delay and MR, and characteristic behavior such as temper outbursts, rigidity, and repetitive thoughts and behavior. In infancy, the differential diagnosis includes neuromuscular disorders associated with hypotonia such as congenital myotonic dystrophy. The differential diagnosis in children and adults includes disorders with MR and obesity such as Bardet-Biedl, Cohen, and fragile X syndromes as well as acquired hypothalmic injury.
The aim of treatment is to restore gonadal function. This is accomplished by replacing gonadal steroids and, when indicated, restoring fertility potential by the administration of gonadotropins or gonadotropin-releasing hormone. The latter is not a priority in critical care conditions. In contrast, the catabolic effects of testosterone deficiency in men may contribute to the loss of protein from vital organs and tissues, and, in particular, aggravate muscle wasting. The critical condition in itself is associated with profound hypoandrogenemia, and treatment with testosterone or anabolic testosterone analogs has been shown to improve nitrogen balance without having the potential to normalize it.
Posterior to the rectum is the mesorectum, which contains both blood vessels and lymphatics that supply and drain the rectum. This is loosely bound down the front of the sacrum and coccyx by connective tissue known as the fascia propria. The lateral ligaments, which attach the rectum to the pelvic walls, are condensations of the fascia propria and contain loose areolar tissue, nerves, and small blood vessels. Thus, the mesorectum can be mobilized by dissection in the mesorectal plane leaving the mesorec-tum invested in this thin layer of fascia. The sacrum and coccyx are also covered in a thicker fascia, which extends downward and forward, just superficial to the anococ-cygeal ligament known as Waldeyer's fascia. Anteriorly the rectum is covered with a layer of visceral fascia that extends from the anterior peritoneal reflection to the urogenital diaphragm. This is Denonvilliers fascia and lies between the rectum and vagina (or prostate in men). Nerves important to bladder control and...
Androgen deficiency can lead to decreases in nocturnal erections and libido. Hypogonadism is associated with impotence, yet erection in response to visual stimulation is preserved in men with hypogonadism, suggesting that androgens are not essential for erection. Although androgens can enhance male sexual function, testosterone therapy for the treatment of ED should be discouraged unless the cause is clearly related to hypogo-nadism. Androgen therapy in normal men may enhance sexual behavior but is without significant effect upon erectile function. Usefulness of oral methyltestosterone is limited in men with hypogonadal impotence. Improvement following transdermal testosterone may require several months of therapy. Androgen replacement regimens for treating male hypogonadism include long-acting intramuscular injections (e.g., testosterone enanate, testosterone cypi-onate) and oral preparations (e.g. methyltestosterone, fluoxymesterone). Transdermal patches (Testoderm, Androderm) and...
The primary care physician must consider genetic syndromes and endocrine conditions as possible explanations for a child's obesity. Prader-Willi syndrome is characterized by a rapid increase in weight from ages 1 to 6, hypotonia and poor feeding in infancy, hypogonadism, and cognitive delay 13 . The majority of children with Cushing syndrome are obese and short in stature 14 , which contrasts with children who are obese from eating excess calories and are commonly taller than their peers. Other medical conditions like hypothyroidism or growth hormone deficiency can cause a child to be obese, which would be suggested by clinical findings like a goiter, short stature, or delayed puberty. After a complete history and physical examination, in the vast majority of obese patients the physician can reassure the parents that their child does not have a genetic disorder or a metabolic syndrome. The one laboratory test all obese patients need is a thyroid-stimulating hormone (TSH) test....
Recombinant host systems, particularly mammalian cell lines. rhFSH produced in CHO cells has proven clinically effective. Although exhibiting an amino acid sequence identical to the human molecule, its carbohydrate composition differs slightly. When administered to humans, the preparation is well tolerated and yields no unexpected side effects. It does not elicit an immunological response, and its plasma half-life is similar to the native hormone. rhFSH has proven efficacious in stimulating follicular growth in females suffering from hypogonadotrophic hypogonadism and is effective in the treatment of males suffering from similar conditions. rhFSH was amongst the first biopharmaceutical substances to be approved for general medical use in Europe by the European Medicines Agency via the centralized application procedure (Chapter 4). Recombinant gonadotropins approved for general medical use are listed in Table 11.10 and additional details of one representative product (Ovitrelle) are...
The hypothalamic-pituitary-gonadal (HPG) axis is markedly disturbed by chronic renal failure, and this is manifest in diminished testosterone levels and impaired spermatogenesis. These patients often present with complaints of diminished libido, erectile dysfunction (ED), and infertility. Upon evaluation, they have low serum testosterone levels and elevated follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels.1 Interestingly, these patients usually retain a normal response to clomiphene citrate stimulation. Clomiphene citrate has antiestrogenic properties which result in a decrease in negative feedback by
PD patients also suffer from disturbances in the peripheral autonomic nervous system. In line with this are the findings of Braak and Del Tredici (2005) showing that first signs of PD occur in the dorsal nucleus of vagus nerve. Most patients with PD, and all people suffering from PD-associated orthostatic hypotension, have a loss of cardiac sympathetic innervation, probably due to overproduction of a-synuclein. It remains to be established, but there are some indications that rotenone, due to its general complex I inhibition, can mimic these peripheral symptoms of PD too. The low testosterone concentrations which are typical for PD, are mimicked by rotenone in the rat (Alam and Schmidt, 2004b) as well as the DA-cell loss in the retina.
Various medical genetic causes of obesity must also be considered. Endocrine conditions associated with weight gain include hypothyroidism, Cushing's syndrome, hypogonadism in the male, polycystic ovary syndrome (PCOS) in the female and growth hormone deficiency (42). Rare genetic causes of obesity include Prader-Willi syndrome, Bardet-Biedl syndrome and Cohen's syndrome. Diabetes can be an obvious consequence of the severe obesity associated with such syndromes.
Luteinizing hormone is secreted in a pulsatile fashion by the pituitary gland and stimulates testicular secretion of testosterone in men. Testosterone levels fall promptly within 24 h of the onset of severe illness, but there is no compensatory rise in gonadotropins. Instead there is a fall in levels which persists for the duration of illness. In postmenopausal women, severe illness is also associated with relatively low concentrations of gonadotropins which correlate directly with outcome. These findings are compatible with an illness-induced hypogonadal syndrome. In men, testosterone is the most important of the endogenous anabolic steroids and various catabolic states result in low testosterone concentrations. It is interesting to speculate that the changes in gonadal steroids, unlike those observed with the thyroid hormones, reflect actual deficiency states and that the lack of testosterone estrogen contributes to the catabolism of critical illness.
Testosterone from blood is correlated with sensation seeking, particularly that of the experience seeking and disinhibitory types (Aluja & Torrubia, in press Daitzman & Zuckerman, 1980), although Bogaert and Fisher (1995) and Dabbs (2000) found only nonsignificant tendencies toward association using salivary testosterone. Hypogonadal men with very low testosterone referred for complaints of erectile dysfunction were lower on sensation seeking than men with normal levels of testosterone (O'Carroll, 1984). Testosterone in young males correlates with their sexual experience, as defined by the number of sexual partners they have had (Bogaert & Fisher, 1995 Dabbs, 2000 Daitzman & Zuckerman, 1980). Other corelates of testosterone in males include assertiveness, impulsivity, and low self-control. A history of antisocial behavior, beginning in childhood, is found in men with high testosterone levels (Dabbs, 2000).
Antisocial personality disorder may be used as an example. The ECA study revealed that antisocial personality disorder declined from a 1-month prevalence of 0.9 per cent for individuals between 25 and 44 years of age to 0 per cent for those over the age of 65. When considering men only, the rate fell from 1.5 per cent in those aged 22 to 44 to 0.1 per cent in those over 65. (2,9 Supporting this decline in antisocial personality disorder with ageing is a study revealing the decline in lifetime prevalence in antisocial personality disorder from between 2.1 and 3.3 per cent to between 0.2 and 0.8 per cent in those aged 65 and older. (21) In addition, antisocial traits, as measured by the Minnesota Multiphasic Personality Index, reveal a decline with ageing. (22 Similarly, a study in a forensic psychiatric centre revealed that, although antisocial personality disorder declined after the age of 27, one-third remained criminally active throughout their lives. There have been several...
Result in early onset of obesity, together with red hair color (suggesting a role for melanocortins in hair pigmentation in humans), and in deficiency of adrenal corticoid synthesis as a result of defective ACTH biosynthesis. A decrease in the activity of prohormone convertase 1 (PC 1 an important enzyme in POMC processing) has been reported in a woman with childhood obesity and a mutation of the PC 1 gene. This patient exhibited several endocrine abnormalities, including adrenal insufficiency, hypogonadotrophic hypogonadism, impaired glucose tolerance and reactive hypoglycemia, presumably due to impaired processing of POMC and proinsulin.
Woof, P., Hamill, R., and McDonald, J., Transient hypogonadism caused by critical illness, J. Clin. Endocrinol. Metab, 60, 494-500, 1985. Matsumoto, A., Andropause clinical implications of the decline in serum testosterone levels with aging in man, J. Gerontol. Biol. Sci. Med. Sci., 57, 76-99, 2002. Morley, J., Baumgartner, R., Roubenoff, R. et al., Sarcopenia, J. Lab. Clin. Med., 127, 231-243, 2001.
Gonadotropins are used to induce spermatogenesis in hypogonadotropic hypogonadal men a lengthy treatment is required to obtain mature sperm. For several weeks hCG is injected to increase testosterone levels, followed by injections of menotropins for several months. Prepubertal cryptorchidism can be treated by injections of hCG for up to several months.
Adverse reactions to zinc include nausea, vomiting, anorexia, and hyperamylasemia. The reciprocal relationship of zinc and molybdenum to copper must also be respected, particularly because copper can be depressed with zinc loading over long periods of time. The sideroblastic anemia that results is manifested by an iron-like microcytic, hypochromic anemia, and neutropenia. Other zinc deficiency signs and symptoms include skin lesions, dermatological anergy, growth retardation, impaired taste, immu-nological impairment, glucose intolerance (similar to chromium deficiency), alopecia, hypogonadism, hypospermia, mental depression, and diarrhea. Serum testosterone concentrations, seminal volume, and total seminal zinc loss per ejaculate are sensitive to short-term zinc depletion in young men. Diseases (sickle cell anemia, malignancies, diabetes, inflammatory or infectious conditions) and medications (e.g., estrogens, caffeine, theophylline, and corticosteroids) can result in greater zinc...
Addison disease is rare with an estimated annual incidence of 0.8 cases per 100,000 of the population in Western societies. It is due to bilateral destruction of the adrenal cortex. Formerly, the most common cause was tuberculosis. Most cases now are due to organ-specific auto-immune destruction and opportunistic infections such as histoplasmosis in patients with AIDS. Due to this, it is likely that the number of patients with Addi-son disease will increase significantly. Addison disease may be associated with autoimmune polyglandular deficiency type I (Addison disease, chronic mucocutaneous candidosis, hypoparathyroidism) and autoimmune polyglandular deficiency type II (Addison disease, primary hypothyroidism, primary hypogonadism, insulin-dependent diabetes, pernicious anaemia, vitiligo) 130 .
Medroxyprogesterone acetate is the primary hormonal agent that has been used in the United States, since initially reported by Heller et al.(56 Its effect results from the acceleration of testosterone-A-reductase in the liver which accelerates testosterone metabolism and thereby reduces testosterone levels. Medroxyprogesterone acetate also reduces plasma testosterone through the pituitary axis. It is not an antiandrogen. Significant side-effects have included liver damage, fatigue, weight gain, hot and cold flushes, headaches, gallbladder disease, diabetes, and thrombophlebitis. Historically, the dose was 300 to 400 mg of the injectable form of medroxyprogesterone acetate, but in recent years lower doses have been found to be equally effective without causing so many side-effects that the medication is discontinued by the paraphiliac. An alternative to injectable medroxyprogesterone acetate can be administered orally. Generally doses of less than 200 mg daily by mouth are effective at...
This syndrome, also known as HHHO (hypotonia, hypogonadism, hypomentia, obesity) syndrome, was first described by Prader, Labhart, and Willi in 1956. (26) The syndrome is characterized by neonatal hypotonia, mental retardation, short stature, obesity, and cryptorchidism. This is a rare condition with an estimated population prevalence of approximately 1.2 to 1.3 per 10 000 with a boy-to-girl ratio of 1.6 1.2.(27) In approximately 50 to 70 per cent of cases cytogenetic tests can detect deletion of chromosome 15 (q11q13) which is of paternal origin in subjects with Prader-Willi syndrome. This genetic abnormality could be detected either by high-resolution chromosome analysis or fluorescence in situ hybridization using specific probes. However, this condition appears to be genetically heterogeneous, in that it is caused by inheritance of two chromosome 15 from mothers (maternal disomy) in some cases, but in others by a paternal gene mutation. The patients with chromosome deletion is...
As noticed above, the first-generation aromatase inhibitor, aminoglute-thimide, was an unsuccessful, adrenotoxic antiepileptic compound implemented for breast cancer therapy in an attempt to achieve a medical adrenalectomy. While the drug was found to be an effective antitumor agent, meticulous work by Santen et al. identified aminoglutethimide as an aromatase inhibitor in vivo (21). Thus, despite interacting with several enzymes involved in adrenal steroid synthesis, circulating androgen levels were found preserved despite profound suppression of circulating estrogens (22). The reason why plasma androstenedione and testosterone levels were not affected (although there were changes in the ratio of several adrenal-derived hormones) was probably due to an increase in ACTH secretion (see (23) for a detailed description of the effects of aminoglutethimide on adrenal enzyme activities). The finding that amino-glutethimide caused estrogen suppression and, thus, antitumor effects through...
Aging in men is associated with decreased testicular function that results in reduced testicular steroidogene-sis, decreased free plasma testosterone levels, decreased 17-ketosteroid excretion, and increased gonadotropin levels. Decreased testicular function has been implicated as a cause of reduced libido, muscle mass, muscle strength, and bone density in elderly men. However, these observations are so variable that a causal relationship between lowered androgen levels has not been firmly established. Androgen replacement in elderly men has not been demonstrated to be beneficial unless there is true androgen deficiency. In addition, it is wise to avoid the indiscriminate use of androgens in this age group because of the high incidence of prostate neoplasms (benign and malignant). Androgen administration in replacement doses has proved to be moderately successful in increasing libido and sexual performance in men who have true testicular failure.
It is clear that testosterone is needed for the wound healing process, because decreased levels impede healing.107-110 Adequate testosterone levels are required for IGF-1 production (IGF-1 being a wound healing agent). However, there are no reliable data that confirm that an increase in testosterone levels above normal improves wound healing. This is not the case with a number of anabolic steroids that have been shown to increase the rate of wound healing even in the absence of hypogonadism. These agents will be discussed next.
In general, ethanol in low to moderate amounts, is relatively benign to most body systems. A moderate amount of ethanol causes peripheral vasodilation, especially of cutaneous vessels, and stimulates the secretion of salivary and gastric fluids the latter action may aid digestion. On the other hand, ethanol consumption in high concentrations, as found in undiluted spirits, can induce hemorrhagic lesions in the duodenum, inhibit intestinal brush border enzymes, inhibit the uptake of amino acids, and limit the absorption of vitamins and minerals. In addition, ethanol can reduce blood testosterone levels, resulting in sexual dysfunction.
Systemic glucocorticoid therapy increases the probability of osteoporosis even with dosages sufficiently low so as not to affect the hypothalamic-pituitary-adrenal axis. By enhancing bone resorption and decreasing bone formation, glucocorticoids decrease bone mass and increase the risk of fractures. The overall effects appear to be due to direct actions of glucocorti-coids on osteoblasts and to indirect effects, such as impaired Ca++ absorption and a compensatory increase in parathyroid hormone secretion. Inhibition of bone growth is a well-known side effect of long-term systemic glucocorticoid therapy in children with bronchial asthma, even in those receiving alternate-day therapy. Glucocorticoids can also augment bone loss, decreasing testosterone levels in men and estrogen levels in women by direct effects on the gonads and inhibition of gonadotropin release. Thus, patients taking glucocorticoids can also develop hypogonadism. It is recommended that all patients who receive...
Itself.97-99 The anabolic properties were defined in the 1930s. These included an increase in muscle size, synthesis, and strength. Increased skin thickness has also been noted with administration to hypogonadal men. The importance of testosterone is evidenced by the complications seen with low testosterone levels, which include sarcopenia or lost lean mass, increased rate of development of osteoporosis, anemia, thinning of skin, and weakness and impaired wound healing98-100 (Table 14.15 and Table 14.16).
Previous researchers failed to document an effect of melatonin on reproductive axis of adult rats(9,16). Moreover, the studied day night moments, different from those we used, may have determined melatonin's failure to influence testosterone and gona-dotropin secretion. In our study, after melatonin treatment, the plasma testosterone concentrations at 10 a.m. were similar to control group (Figure 1), while at 10 p.m. and 2 a.m., were significantly changed. Melatonin treatment induced a biphasic response of testosterone secretion at 10 p.m., 2 hours after the onset of darkness, the high testosterone levels were significantly reduced by melatonin treatment, while at 2 a.m. the low testosterone levels were significantly stimulated. Our studies on adult rats,
'Sickness behaviour' (fever, weakness, malaise, listlessness, inability to concentrate, depression, lethargia, anhedonia and loss of appetite) Panic patients (social phobia) Prolonged wakefulness Behavioural changes (anorexia, adipsia, sleepiness and depression in social, sexual and general activity) Sexual arousal, aggression, emotional tone, cognition, dominant behaviour (especially violent offenders) High testosterone (men women) Low testosterone (men women) Depression Major depression State of health
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