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Hypogonadismagonadism and hypoactive sexual desire

Although there are currently no established models of female sexual dysfunction in rats, there are several reasons to believe that such models could exist. The most obvious would be the consequences of hypogonadism induced by ovariectomy followed by maintenance with different doses of estrogen alone, or estrogen and progesterone. Ovariectomized rats treated with estrogen and progesterone display a complete pattern of procep-tive and receptive behaviors, whereas those treated with estrogen alone display no proceptive behaviors, low levels of lordosis, and high rates of rejection responses. Certain pharmacologic treatments (e.g. apomorphine, oxytocin, PT-141), are able to increase proceptive behaviors and reduce rejection responses in ovariectomized females treated or maintained on estrogen alone. This pattern of data suggests that such drugs may be useful in the treatment of hypoactive sexual desire disorder, with or without accompanying hypogonadism.

Prevalence of hypogonadism

Serum T is more often than not normal in ED. It was below 3ng mL in 12 of 7000 ED patients compiled from nine large series (including in 4 of 944 men 50 years, and 14.7 of 4342 men 50) 18-20 . The real prevalence of hypogonadism is probably lower because most of these patients had a single T determination. A repeat determination is recommended in cases of subnormal value, since it proves to be normal in as many as one-third of the patients 18-21 . In addition, some studies did not sample blood in the morning in every case even though the T level decreases after 11 am in normal men, at least up to the age of 40 6 . In one series of over 1000 ED patients in which the diagnosis of hypogonadism was based on two consecutive values

Clinical picture of hypogonadism

Androgen production is minimal and hypogonadism will not manifest itself. Hypogonadism at the normal time of puberty will result in a typical syndrome of eunuchoidism. Epiphyseal cartilage does not stop growing, so the long bones continue to grow, resulting in a ratio of upper to lower body

Screening for hypogonadism in sexual dysfunctions

Several varieties of sexual dysfunction, mainly ED, may be the presenting symptom of hypogonadism, a condition that can reveal diseases with serious nonsexual consequences, such as pituitary tumors. In addition, missing a hypogonadism responsible for sexual dysfunction would deprive the patient of an etiologic therapy that would give him the best chance of success. This has led to the advocating of routine determination of T in several dysfunctions. Several authors question the recommendation of routine T determination in ED because of the cost of hormone determinations, the low prevalence of hy-pogonadism in this population, and the limited success rate of T therapy in the hypogonadal ED patient 18,54 . They recommend screening only patients with low sexual desire or abnormal physical examination (small and soft testes, reduced body hair, and so on). However, in a study of routine determinations of TT in over 1000 ED patients, the specificity, sensitivity, and efficiency of low...

Nature and prevalence of late onset hypogonadism

In late onset hypogonadism (LOH) there is a variable decline predominantly involving non-SHBG-bound T. Several studies document that androgen levels decline with aging (for review see 75 ). Longitudinal studies 76-78 have documented a statistical decline of serum T by approximately 30 in healthy men between the ages of 25 and 75 years. Since serum levels of SHBG increase with aging, plasma T not bound to SHBG decreases even more, by about 50 , over that period. Studies in twins have shown that genetic factors account for 63 of the variability of serum T levels, and for 30 of the variability in SHBG levels 79 . Also systemic diseases, increasing with age, are a cause of declining serum levels of T 78,80 . While it now has been shown beyond doubt, that serum T, and in particular BT and FT, decline with aging, it remains uncertain what percentage of men actually become T-deficient with aging, in the sense that they will suffer the clinical consequences of T deficiency, and will...

Responsibility of hypogonadism

Sexual function of men with severe organic hypogonadism The effects of T upon male sexual function are dose-dependent up to a serum level close to the lower limit of the normal adult range, at which they are maximum. Below this threshold sexual function is impaired. This threshold level is consistent within an Data from experiments in men In human males the main sites of the action of T upon sexual function are considered to be located in the brain. Positron emission tomography (PET) studies have begun to map them 47,48 . Until now a critical impact on the peripheral mechanisms of erection had not been demonstrated in men. However there are androgen receptors in the human corpus cavernosum 49 , and some recent studies suggest T may modulate the vascular mechanisms of erection also in men. Peak systolic velocity was measured at the level of the cavernosal arteries with penile color Doppler ultrasound (CDU), following intracavernosal injection of alprostadil in ED patients with severe...


In male rats, castration or the administration of androgen synthesis inhibitors, like cyproterone acetate, disrupt and ultimately eliminate copulatory behaviors and penile reflexes progressively over time. They also shrink androgen sensitive peripheral tissues (e.g. penis and prostate). Although the degree of disruption depends on the amount of androgen synthesis inhibition that is induced (e.g. moderate following low doses of cyproterone acetate to total disruption following castration), the amount of time it takes to reach an asymptotic level of behavioral or reflexive performance depends on the level of sexual experience male rats have prior to treatment. In each case, subsequent exogenous administration of androgens or estrogens can restore sexual interest and copulatory behavior, with nonaromatizable androgens (such as dihydrotes-tosterone) restoring peripheral tissues, and aro-matizable androgens (e.g. testosterone) restoring behavioural measures. As with hypogonadal men,...


Responds to that of male sexual potency and activity. However the possibility of minimally-impaired sexual function in men with very low levels of testosterone (T), as well as the often disappointing results of T therapy used alone in men with sexual dysfunction and moderate hypogonadism, have cast doubt on the importance of androgens in sexual function. Actually the androgen deficiency that may be found during the work-up of a sexual dysfunction more often than not is only one element of a multifactorial causality.

Contemporary Endocrinology

Battaglia, 2005 Male Hypogonadism Basic, Clinical, and Therapeutic Principles, edited by Stephen J. Winters, 2004 Androgens in Health and Disease, edited by Carrie J. Bagatell and William J. Bremner, 2003 Endocrine Replacement Therapy in Clinical Practice, edited by A. Wayne Meikle, 2003

Injury of the Hypothalamic Pituitary Axis in Patients with Cancer

GH deficiency is commonly believed to be the first hypothalamic-pituitary deficiency to emerge after injury to the HPA, followed by deficiencies of gonadotropin, ACTH and TSH 60,65 however, these deficiencies can occur in any order 11,21,35,54,67 . Although the most common neuroendocrinologic abnormality in survivors of childhood cancer is GH deficiency, hypothyroidism is at least as prevalent when sensitive testing methods are used 54 . The next most common alteration is in pubertal timing (precocious, rapid, delayed, or absent). ACTH deficiency, although less common than the other disorders, has more serious consequences if it is not detected. Osteopenia may result from hypothalamic-pituitary deficiency, particularly GH deficiency, hypothyroidism and hypogonadism. Hypothalamic injury resulting from tumor, surgery, or irradiation can result in unrelenting weight gain, termed hypothalamic obesity.

Hypothalamopituitary dysfunction

Secondary hypogonadism results from deficiency of luteinizing hormone (LH) and follicular stimulating hormone (FSH). The primary deficiency arises from the pituitary or hypothalamus. Hypopituitarism may be idio-pathic or secondary to tumours of, or adjacent to, the hypothalamic-pituitary axis. In childhood and adolescence, these include craniopharyngiomas, germ cell tumours and adenomas. Radiotherapy to the central nervous system for the treatment of brain tumours or leukaemia may result in acquired failure of the hypothalamic-pituitary axis with secondary infertility.

Clinical Presentation of Dyskeratosis Congenita

DC is also known as Zinsser-Engman-Cole syndrome (Zinsser 1906, Engman 1926, Cole et al. 1930). Classically DC is characterized by the triad of abnormal skin pigmentation, nail dystrophy, and mucosal leukoplakia. A variety of other noncutaneous abnormalities have also been reported since its first description (Table 5.1), including dental caries, tooth loss, esophageal webs, epiphora, short stature, developmental delay, hypogonadism, osteoporosis, pulmonary disease, premature grey hair, and hair loss (Trowbridge et al. 1977, Womer et al. 1983, Wiedemann et al. 1984, Zijlmans et al. 1997, Knight et al. 1998, Solder et al. 1998, Dokal 2000, Mason et al. 2005). Hypogonadism

Gender Specific Behavior

In addition to their influence on reproductive behaviors, the gonadal hormones also may have organizing and triggering effects on other types of behavior. For example, aggression between males is positively related to testosterone levels, whether the males are competing for a female. These effects may be related to neural events taking place in the medial and preoptic hypothalamus. Aggressive play is much more prevalent in male animals, and the incidence of this form of play is sharply reduced in male rats if they are castrated before postnatal day 6, but not if they are castrated later in life. Conversely, female rats given large doses of testosterone within the first 6 days of life exhibit as much aggressive play as males when this activity develops several weeks later. Similar findings have been reported for monkeys, but the manipulations must be made prenatally.

Mutations in Nuclear Genes Affecting mtDNA Stability

Autosomal dominant progressive external ophthalmoplegia (adPEO) and mitochondrial neurogastrointestinal encephalomyopathy syndrome (MNGIE) are diseases caused by defective interplay of the mitochondrial and nuclear genome. Most of the adPEO patients carry mutations in one of three genes ANT1 (muscle-heart specific isoform of mitochondrial adeni-nenucleotide translocator), Twinkle (mtDNA helicase), or POLG1 (catalytic subunit of mtDNA polymerase) 38 . On the molecular level adPEO is associated with multiple mtDNA mutations 39 .AdPEO is clinically characterized by ophthalmoplegia (progressive muscle weakness affecting eye muscle), very often associated with ataxia, hypogonadism, severe depression, endocrine dysfunction, hearing loss, and peripheral neuropathy 39, 40 . Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is associated with a loss of thymidine phosphorylase (TP) and is characterized by PEO, severe gastrointestinal syndrome, peripheral neuropathy,...

Testicular Function Following Total Body Irradiation

Or 1500 cGy in 125 cGy t.i.d. fractionation) prior to puberty as part of a transplantation regimen for leukemia 69 . Fourteen of seventeen patients (82 ) entered puberty spontaneously, with 13 having normal testosterone levels. Of the three that did not enter puberty spontaneously, one had received a 1200 cGy testicular boost, in addition to the TBI, and in the remaining two, the levels of FH and LH were very low, consistent with a prepubertal state. Costo-Silva followed 29 boys who received TBI for different malignancies in association with a variety of chemotherapy regimens 18 .The TBI was given as a single 1000 cGy fraction in twelve patients and in 200 cGy x 6 fractions (1200 cGy) in 17 patients. At the last follow-up, 19 29 (66 ) had tubular failure associated with elevated FSH. Eight (28 ) also had Leydig cell failure. There was no relationship between the age at BMT and serum FSH, LH or testosterone levels. Bakker et al. followed 25 boys who were prepuber-tal at the time of...

Method to Minimize Testicular Radiation Dose

As discussed above, in most cases, the testicular dose from a radiation treatment is due to internal scatter, not direct irradiation. Internal scatter is difficult to prevent, but methods have been developed to decrease the dose. Frass et al. reported on a gonadal shield that formed a cup around the testes to reduce the testicular dose 23, 74 . They found that this led to a 3-10-fold reduction in the dose to the testes, depending on the distance from the proximal edge of the field. In almost all cases, the measured dose to the testes was less than 1 of the prescription dose. Therefore, for a patient receiving 5000 cGy to a pelvic field, the dose to the testes would be less than 50 cGy. This most likely would prevent permanent azoosper-mia, and it almost certainly would prevent a decline in testosterone levels.

Chromosomal Anomalies

Mothers of infants with the Prader-Willi syndrome note decreased in utero fetal activity, and often these neonates are born in breech presentation. The affected individuals are of short stature and have small hands and feet and a narrowed cranial bifrontal diameter. 9 Their eyes are almond-shaped, and they often have strabismus. The face is long, and nearly 50 percent of patients have hypopigmentation of the skin. Other common features include a small phallus, cryptorchidism, and hypogonadism with a small flat scrotum. Affected infants have a feeble suck and severe hypotonia, which commonly requires the use of a feeding tube. Near the end of the first year of life, however, the hypotonia may become less severe. The degree of mental retardation may seem more prominent in early life and may be correlated with the severity of the hypotonia. At 1 to 3 years of age the patients gain considerable weight and become obese because of hyperphagia. As the hypotonia becomes less severe, they also...

Autosomal Recessive Inheritance

Erythematous skin lesions in early life followed by telangiectasias, atrophy, hypo- and or hyperpigmentation, ectodermal dysplasia body hair is sparse or absent cataracts, short stature, hypogonadism, and skeletal abnormalities are common intelligence is normal lcthyosis and hypogonadism are major features microcephaly, sensorineural deafness, polyneuropathy, and hypoplastic teeth and nails are less frequent

Autosomal Recessive Disease

Patients with AT also demonstrate progeric changes of the hair and skin, including early graying of the hair and atrophic, hidebound facial skin. Pigmentary changes are also frequent and consist of hyperpigmentation and hypopigmentation with cutaneous atrophy. A few patients may demonstrate partial albinism, vitiligo, and cafe au lait spots. Seborrheic dermatitis occurs in nearly all patients, and senile keratoses, atopic dermatitis, and eczema are also reported. Another prominent feature of AT is frequent sinopulmonary infections. These may range from infection of the ears, nose, and sinuses to chronic bronchitis and recurrent pneumonia. The latter two may result in bronchiectasis and pulmonary fibrosis. Chronic infections are typically due to common bacteria however, they are sometimes poorly responsive to antibiotic therapy. The predisposition to infection is associated with the presence of an abnormal thymus and a marked deficiency of IgA, which is the predominant immunoglobulin...

Other daytime symptoms

This is partly due to EDS resulting from sleep fragmentation and partly to reduced testosterone levels due to a reduction in gonadotrophin secretion during sleep. There are also fewer penile erections during sleep because of REM sleep fragmentation.

The Developmental Instability Model

The concept of fluctuating asymmetry as related to developmental instability actually refers to asymmetry of morphological characters, not to behavioral phenomena. Thus proponents of the developmental instability model presumably regard handedness as being isomorphic with structural asymmetry of the brain. The theory proposes that extreme handedness in either direction represents deviation from the norm of moderate (modal) right-handedness. Saying this does not explain why right-handedness is the norm the bias toward the right still has to be explained. Degrees of handedness can be readily accommodated by the theory as it incorporates the notion of fluctuating asymmetry. The theory requires little in the way of additional postulates to explain the sex difference in handedness, if it is accepted that an HLA allele may influence prenatal testosterone levels (Gangestad et al., 1996). What is less clear is that it can explain the observation that variation in hand skill concerns mainly...

Hypoactive Sexual Desire Disorder

There are currently no empirically validated treatments for HSDD. Sex therapy techniques generally consist of 15 to 45 sessions of cognitive therapy aimed at restructuring thoughts or beliefs that may adversely impact sexual desire (e.g., women should not initiate sexual activities, sex is dirty ) and to address negative underlying relationship issues. Behavioral approaches are utilized to teach patients to express intimacy and affection in both nonsexual (e.g., holding hands, hugging) and sexual ways, to incorporate new techniques into their sexual repertoire that may enhance their sexual pleasure, and to increase sexual communication. Testosterone is effective in restoring sexual desire in women with abnormally low testosterone levels (e.g., secondary to removal of the adrenal glands, bilateral removal of the ovaries, menopause).

Benefits of androgen therapy

Clinical studies examining T monotherapy for the treatment of ED have yielded varying results. Meta-analysis, including trials in young organic hypogonadal patients, has shown a 57 response rate for T therapy in patients with ED, ranging from 64 for primary hypogonadism to 44 for secondary hypogonadism 14 . Morales et al. showed that T therapy is an effective treatment for hypogonadal impotence, with improvement in sexual attitudes and performance in 61 of patients 56 . In another study, T monotherapy has been observed to improve erectile function in only 36 of the hypogonadal patients consulting for ED 18 (see also pp. 203-2). T therapy may have more significant effects on libido than on erectile function 170 . In one study, normalization of serum T levels in hypogonadal men with ED resulted in only short-term improvement (one month) in erectile function and sexual satisfaction, while improvement of sexual desire was statistically significant for the six months of the study, making...

Autosomal Dominant Cerebellar Ataxia

There are a number of rare types of early-onset cerebellar ataxia of unknown etiology that resemble EOCA in many respects but have characteristic additional features. These disorders include early-onset cerebellar ataxia with hypogonadism (Holmes' syndrome), with optic atrophy and spasticity (Behr's syndrome), with cataract and mental retardation (MarinescoSjogren's syndrome), with retinal degeneration and deafness( Hallgren's syndrome), with spasticity, amyotrophy, and bladder dysfunction (autosomal recessive spastic ataxia Charlevoix-Saguenay), and with myoclonus in the absence of severe epilepsy and dementia (Ramsay Hunt syndrome).

Routine laboratory tests

Free testosterone, testosterone, prolactin and dehydroepiandrosterone sulfate (DHEAS) are the specific hormones that may be part of the ED evaluation. These hormones have been associated with sexual desire. Luteinizing hormone (LH), follicle-stimulating hormone (FSH) and sex hormone-binding globulin (SHBG) are determined for further differential diagnosis in the case of low testosterone values, to ascertain primary or secondary hypo-gonadism. Estradiol, growth hormone or, better, insulin-like growth factor 1 (IGF-1) and thyroid parameters are determined in individual cases to diagnose further hormonal deficits. It is recognized that serum testosterone levels decrease below the eugonadal range in some men with advancing age. Restoration of testosterone levels to the eugonadal range (300-1000 ng dL) appear to correct many of the clinical abnormalities (impaired sexual function, negative changes in body composition, etc.) commonly associated with hypogonadism 24 . With respect to...

Sexual Response Sexual Desire

Sexual desire refers to the broad interest in sexual objects or experiences and is generally inferred by self-reported frequency of sexual thoughts, fantasies, dreams, wishes, and interest in initiating and or engaging in sexual experiences. Definition of this construct is complicated by factors such as attitudes, opportunity partner availability, mood, and health. Relationship factors, individual preferences for sexual variety and emotional intimacy are closely linked to sexual desire. Androgens appear to also play a role. In males, about 95 of androgens (e.g., testosterone) are produced by the testes the remainder is produced by the outer adrenal glands. In females, androgens are produced by the ovaries and adrenal glands in quantities much lower than in males (about 20-40 times less Rako, 1996). In both males and females, decreased testosterone levels due to, for example, orchidectomy (removal of testes) or oophorectomy (removal of ovaries) have been linked to impaired sexual...

Assessment of Testicular Function

Hormone analysis involves measurement of plasma FSH, LH and sex steroids (Table 14.5). In prepubertal children, however, this is an unreliable predictor of gonadal damage, since the prepubertal hypothalamic pituitary-testicular axis is quiescent. In post-pubertal boys, elevated LH and diminished testosterone levels are indicative of Leydig cell dysfunction, while elevated FSH and diminished inhibin B suggest germ cell failure. HCG may be given to confirm the diagnosis of end organ failure as a cause of hypogonadism. An abnormal response to HCG is suggestive of disturbed Leydig cell function. Patients with hypogonadotrophic hypogonadism should have a brisk response, while those with decreased Leydig cell function will have little or no response. GnRH may be administered to determine whether the primary defect is in the hypothalamus or in the pituitary. If it's in the hypothalamus, the pituitary and testicles themselves should respond normally to exogenous GnRH. Alternatively, if the...

Hypoactive Sexual Desire Disorder HSDD

The three major etiological factors for low sexual desire that have been proposed are hormonal problems, affective-cognitive models, and relationship dynamic theories. Although evidence of hormonal influence on sexual desire in females is inconsistent, research continually shows a relationship between androgens and sexual desire in males (Beck, 1995). Androgens, particularly testosterone, seem to be essential for normal levels of sexual desire in males (Bancroft, 1988). However, testosterone deficiency does not account for all cases of HSDD in males (Schover & LoPic-colo, 1982).

Alternatives to testosterone therapy

Vat Calculations And The Vat Returns

Another potential method of the treatment of hypogonadism is the use of agents that increase the endogenous production of T in men with hypog-onadotropic hypogonadism. Shabsigh et al. reported on a study on 36 men with hypogonadism defined as serum T level less than 3ng mL. Each patient was treated with a daily dose of 25 mg clomiphene citrate, and followed prospectively. The mean age was 39 years with the mean pretreatment T and estrogen levels of 2.47 0.39ng mL and 32.3 10.9pg mL, respectively. By the first follow-up visit (four to six weeks), the mean T level rose to 6.1 1.78ng mL (P 0.00001). Moreover, the T E ratio improved from 8.7 to 14.2 (P 0.001). This therapy may represent an alternative to T therapy by stimulating the endogenous androgen production pathway 211 , and allowed Guay et al. to improve T secretion Indications for testosterone supplementation Clinical symptoms Psychologic symptoms Somatovegetative symptoms Laboratory tests Total testosterone Fig. 18.4 Algorithm...

History and Epidemiology of Male Sexual Dysfunction

Perhaps made possible by this sexual revolution, progress in male sexual medicine accelerated in the 1970s. Prior to this time, sexual dysfunction was considered to be an endocrine or a psychologic problem. The usual treatments were testosterone therapy for men with hypogonadism, and psychotherapy. In the early 1970s, Vaclav Michal, a vascular surgeon from Prague, began to investigate the role of penile revas-cularization techniques for the treatment of vasculo-genic erectile dysfunction 9,10 . Interest in Michal's surgical techniques led Adrian Zorgniotti in 1978 to organize the First International Conference on Corpus Cavernosum Revascularization in New York. This conference evolved into biennial conferences, which expanded to cover the entire field of sexual medicine. By 1984, these conferences became the meetings of the International Society for Impotence Research (ISIR). ISIR has since been renamed the International Society for Sexual Medicine (ISSM).

Biochemical diagnosis

What hormone should be measured The laboratory reference values of T and FT show a wider range than those for most other hormones (for instance, thyroid hormones), which makes it difficult to establish whether measured values of T in patients are normal or abnormal. Is a patient whose plasma levels of T fall from the upper to the lower range of normal T levels (a drop of as much as 50 ), T deficient T levels may well remain within the reference range but may be inappropriately low for that particular individual or his particular age. In thyroid pathophysiology, plasma thyroid-stimulating hormone (TSH) proves to be a better criterion of thyroid hyper hypofunction than plasma T4 or T3, but it is uncertain whether plasma LH is a reliable indicator of male hypogonadism in the elderly man. With aging there are reductions in LH pulse frequency and amplitude. Several studies have found that LH levels are elevated in response to the decline of T levels with aging, but less so than is observed...

Risks of androgen therapy

With clinical features of symptomatic LOH (SLOH) is controversial. Pechersky et al. found that prostate growth can be retarded or even reversed with androgen therapy 177 . Others found that prostate volume, as determined by ultrasonography, increases significantly during T therapy, mainly during the first six months, to a level equivalent to that of men without hypogonadism. However, urine flow rates, post-voiding residual urine volumes, and prostate voiding symptoms did not change significantly in these studies. This apparent paradox is explained by the poor correlation between prostate volume and urinary symptoms. Clinicians should nevertheless be aware that individual men with hypogonadism may occasionally have increased voiding symptoms with T therapy. et al. found prostate cancer on sextant prostate biopsy in 14 of men (median age 64 years) with hypogonadism who had normal prostate serum antigen (PSA) levels and normal results on digital rectal examinations before receiving T...

The importance of receptivity

Many of the changes associated with aging, such as loss of bone and muscle mass, increased fat mass, and deterioration of physical, cognitive, and sexual capacities, are similar to the symptoms of classical hypogonadism in younger men. The decline in circulating T is not universal in elderly men and is of a lesser magnitude than in classical hypogonadism. To explain the androgen deficiency-like symptoms in aging in the presence of relatively mildly reduced T levels, it has been hypothesized that the efficacy of androgen action at the level of receptor and postreceptor mechanisms is diminished in old age compared to younger age. Arguing against this is that, with regard to the anabolic actions of T, elderly men are as responsive to T as young men 8 . While male sexual functioning in (young) adulthood can be maintained with lower-than-normal values 9,10 , there are indications that the threshold required for behavioral effects of T increases with aging 11 . The fact that libido and...

Treatment of Hypoactive Sexual Desire

Testosterone replacement can be of benefit if the patient has hypogonadism 45 . In any event, testosterone replacement therapy should be established with the criteria outlined in the chapter Hormones, Metabolism, Aging and Men's Health of this book. Likewise, cases of hyperprolactinemia should be further studied and treated the same chapter in this book offers guidelines for this treatment.

Abnormalities of Secretion by the Ovaries

Less than normal secretion by the ovaries can result from poorly formed ovaries, lack of ovaries, or genetically abnormal ovaries that secrete the wrong hormones because of missing enzymes in the secretory cells. When ovaries are absent from birth or when they become nonfunctional before puberty, female eunuchism occurs. In this condition, the usual secondary sexual characteristics do not appear, and the sexual organs remain infantile. Especially characteristic of this condition is prolonged growth of the long bones because the epiphyses do not unite with the shafts as early as they do in a normal woman. Consequently, the female eunuch is essentially as tall as or perhaps even slightly taller than her male counterpart of similar genetic background. Hypogonadism. As pointed out in the preceding discussion of menopause, the quantity of estrogens produced by the ovaries must rise above a critical value in order to cause rhythmical sexual cycles. Consequently, in...

Recommendations for screening and therapy

Currently there is no basis for androgen therapy in older men, unless they have overt androgen deficiency with symptoms and low testosterone 2 . Testosterone levels needed for normal sexual function may vary between individuals. Some men may have normal sexual function even if their T levels fall into the age-adjusted lower normal range 221 . However, in patients with ED and or hypoactive sexual desire, T testing is recommended to screen for hypogonadism. T therapy is appropriate when clinical indications and biochemical evidence of hypogonadism exist 168,222 . In men with ED, determining T levels only in case of either low sexual desire or abnormal physical examination overlooks many patients with low T who do not have these symptoms but may benefit from androgen therapy 18 . Testosterone monotherapy may correct sexual dysfunction caused by hypogonadism, but absence of an adequate response after appropriate therapy may require further evaluation to exclude associated co-morbidities,...

General reviews on animal models

McKenna KE, Adams MA, Baum M, Bivalacqua T, Coolen L, Gonzalez-Cadavid N, Hedlund P, Park K, Pescatori E, Rajfer J, Sato Y. Experimental models for the study of male sexual function. In Lue TF, Basson R, Rosen R, Giuliano F, Khoury S, Montorsi F, eds. Sexual Medicine. Health Publications, 2004. Meisel RD, Sachs BD. The physiology of male reproduction. In Knobil E. Neil JD, eds. The Physiology of Reproduction. New York Raven Press, 1994, vol. 2. pp. 3-105. Pfaus JG, Kippin TE, Coria-Avila G. What can animal models tell us about human sexual response Ann Rev Sex Res 2003 14 1-63.

Leydig Cell Function Following Radiotherapy

In the study of men treated for sarcomas by Shapiro et al. discussed above 74 , maximal increases in LH levels relative to baseline were seen at six months following radiation,but these elevations were statistically significant only in the group that received 200 cGy of scatter irradiation to the testes, not for the groups that received 50-200 cGy or 200cGy, the elevation in LH levels persisted until the last follow-up, 30 months out. No statistically significant changes in testosterone levels were seen for any of these three dose levels. Higher doses to the testes result in more marked Leydig cell damage. In one study, 18 men who had undergone orchiectomy for a unilateral testicular cancer were subsequently found to have carcinoma in situ for which they received 2000 cGy in ten fractions to the remaining testis 24 . Eight of the men already had evidence of Leydig cell dysfunction even before they received radiation, a finding previously described in patients...

Treatment Induced Leydig Cell Failure from Chemotherapy

In androgen insufficiency and requiring testosterone replacement therapy is rare. However, studies suggest that Leydig cell dysfunction may be observed following treatment with alkylator-based regiments. In fact, raised plasma concentrations of LH, combined with low levels of testosterone, are the hallmarks of Leydig cell dysfunction. When Leydig cell dysfunction occurs prior to or during puberty, affected individuals will experience delayed and or arrested pubertal maturation and the failure to develop secondary sexual characteristics 76 . If the insult follows completion of normal pubertal development, observed symptoms include loss of libido,erectile dysfunction, decreased bone density and decreased muscle mass 76 . Measurements of testosterone and gonado-tropin concentrations are, therefore, warranted following chemotherapy treatment. Males with a raised LH concentration in the presence of a low testosterone level should be considered for androgen replacement therapy.

The Testosterone Theory

Most work carried out within the framework of the GBG hypothesis has looked at two- or three-way associations between handedness, dyslexia, and immune disorders (see Bryden et al., 1994a). It was not until ten years after its initial proposal that the major postulate was directly tested. Amniotic testosterone levels measured at 16 weeks gestational age were found by Grimshaw et al. (1995) to predict handedness in girls and language lateralization (assessed by dichotic listening) in boys at age 10 years. However, the results were in the opposite direction to that predicted by the GBG hypothesis (and thus in the direction proposed by Witelson, 1991 see below). That is, higher levels of prenatal testosterone were associated with stronger right-handedness and stronger left language lateralization. It has also been found (Moffat & Hampson, 1996) that adult right-handers show higher levels of salivary testosterone than left-handers. This, too, contradicts the GBG hypothesis unless low...

Cushings Syndrome Cushings Disease

Growth hormone (GH somatotropin) is secreted by the anterior pituitary in response to hypothalamic GH-releasing hormone (GHRH). GH promotes linear growth and has both anabolic and catabolic effects. Hypersecretion of GH causes gigantism when it occurs before epiphyseal closure and acromegaly when it begins afterward. Hyposecretion causes short stature in childhood and possibly a chronic fatigue-like syndrome in adults. GH acts indirectly through insulin-like growth factors (IGFs, somatomedins), with IGF-1 (formerly somatomedin C) being the most important for growth. Prolonged exposure to elevated levels of GH and IGF-1 results in the insidious onset of skeletal and soft tissue overgrowth, the latter of which is most pronounced in tissues containing large amounts of cartilage proteoglycans. '109 Cortical bone density is increased and trabecular bone (e.g., vertebral) density is decreased, probably because of coexistent hypogonadism. '109 Soft tissue hypertrophy may result in...

Role of Telomere Length and Telomerase in Human Disease

Strikingly, DC patients show increased chromosomal instability with age, consistent with a faster rate of telomere loss, suggesting that DC may be a chromosomal instability syndrome produced by a defect in telomerase activity and the proper maintenance of telomeres (see Du et al., this volume). DC patients develop many of the pathologies shown for the telomerase-deficient mouse model, such as short stature, hypogonadism and infertility, defects of the skin and the hematopoietic system, bone marrow failure, and premature death. Similarly to telomerase-deficient mice, human DC is characterized by showing disease anticipation in affected progeny, demonstrating that short telomeres directly contribute to disease presentation (Vulliamy et al. 2004). In addition, a number of patients diagnosed with aplastic anemia also show mutations in the telomerase Terc and Tert genes, resulting in accelerated telomere shortening and premature death (Yamaguchi et al. 2005, Marrone et al. 2004). However,...

Other Segmentation And Cleavage Disorders

Absence of the olfactory bulbs and tracts, or arrhinencephaly, is also considered in the midline defects, although the pathogenesis may be distinct. Arrhinencephaly can be found as an isolated malformation or in conjunction with a variety of malformation syndromes. Clinically, bilateral arrhinencephaly manifests as anosmia. Although arrhinencephaly is frequently included in the midline dysplasias and can represent a mild manifestation of the holoprosencephaly spectrum, it would be incorrect to conclude that every isolated case of arrhinencephaly belongs with this spectrum. Possibly, arrhinencephaly can result from a number of independent mechanisms. One example of a non-holoprosencephaly-sequence syndrome associated with arrhinencephaly is Kallmann's syndrome. This syndrome is characterized by a combination of arrhinencephaly, resulting in anosmia, and hypogonadotropic hypogonadism, resulting from gonadotropin-releasing hormone

Cardiovascular function

Low testosterone level in coronary artery disease Premenopausal women, in comparison to men, are felt to be protected against cardiovascular disease by estrogens. It is then paradoxical that in cross-sectional studies of men, elevated levels of estrogens 115 and relatively low levels of T 116,122,123 appear to be associated with coronary disease and myocar-dial infarction. These studies suggest the intriguing possibility that, in spite of the prior assumption of overall negative effects of androgens on lipid profiles, a lower-than-normal androgen level in aging men is associated with an increase of atherosclerotic disease. In a study of geriatric male patients who had suffered a myocardial infarction, it was found that these patients had low T levels 116 . In addition four trials have found that pharmacologic doses of T relax coronary arteries when injected intraluminally, and modest but consistent improvement of exercise-induced angina and electrocardiographic ischemia have been...

Pharmacologic profile

Apomorphine is a central dopamine receptor agonist with effects on D1 and D2 receptors (dominantly on D2). Predominant sites of action are located in the paraventricular nucleus, stria terminalis, medial preoptic area, and amygdaloid nucleus 19,20 . Apomorphine-induced erections are both testosterone and NO dependent 21,22 , i.e. the erection-triggering effects of apomorphine diminish or may even be absent in the case of a clinically-relevant NO or testosterone deficiency withdrawal. Following stimulation of the cerebral dopamine receptors the apomorphine-induced erections are mainly transmitted via parasympathetic oxytocinergic nerve fibers, and lead to an increase of arterial blood supply in the penis 23 as well as in the clitoris and vaginal wall 24 . In addition to its known cerebral

Candidates for androgen therapy

It is generally accepted in clinical practice that any male with any form of classical hypogonadism and inadequately low T for his age will require androgen therapy if hypogonadism occurred before the age of 50 213 . Even in men who have proceeded normally through puberty, and who experience no or only minor symptoms (e.g. fatigue, reduced libido), T therapy may be recommended, to prevent long-term sequelae such as osteoporosis 1 . Conversely, there is much debate concerning the validity of this therapy in men with sexual dysfunction and low normal T levels, those with chronic illness and low T, and those with LOH, even if the decline in BT may be partially responsible for the frailty syndrome seen in the aging male 214 . The recommendation common to

Growth Hormone Hypersecretion Museuloskeletal Increas

Other Arthralgias, slight kyphosis, visceromegaly, reproductive problems (women amenorrhea, galactorrhea, anovulatory problems men decreased libido, hypogonadism), hyperprolactinemia, adenomatous polyps and colon cancer, esophageal and gastric cancer, parathyroid and pancreatic islet cell adenomas (MEN-I syndrome)

The mTerc Wrn Compound Mutant Mouse as a Model of Human Werner Syndrome

Interestingly, despite the wide-ranging activities of the WRN helicase in human cells, Wrn null mice do not exhibit any cellular or clinical phenotypes characteristic of human WS (Lombard et al. 2000). The observations that WRN is required for telomere maintenance, and that laboratory mice normally possess very long telom-eres, suggest that manifestation of premature aging phenotypes in Wrn-null mice may require the presence of critically short telomeres. This hypothesis has since received genetic support from studies of mice lacking both telomerase and Wrn (Chang et al. 2004, Du et al. 2004). Strikingly, these late-generation mTerc ' Wrn ' mice display clinical symptoms resembling human WS, including early onset of age-related disorders such as impaired wound repair, osteoporosis and skeletal fractures, hypogonadism, cataract formation, type II diabetes, and premature death. These mice also exhibit an elevated incidence of mesenchymal cancers compared with control mice (Chang et al....

Human Studies of Behavioral Effects of Androgens and Estrogens

Findings from females with CAH have been confirmed in other ways. For example, girls exposed to masculinizing hormones because their mothers took medication during pregnancy are more likely than their unexposed sisters to report using aggression in conflict situations. Converging evidence for these special cases comes from normal individuals with typical variations in prenatal hormones 7-year-old girls who had high testosterone in utero (determined from amniotic fluid at prenatal weeks 14 to 16) had better spatial ability than girls who had low testosterone.

Neuromuscular conditions

In this disorder, obesity, hypogonadism and mental retardation are combined with hypotonia and hypo-thalamic abnormalities. Excessive daytime sleepiness is seen in around 70 of subjects. The sleepiness may be partly due to an intrinsic hypersomnia related to hypothalamic abnormalities, but obstructive sleep apnoeas are frequent and often contribute. They may

Other Changes

Estrogen loss can affect other parts of your sex life as well. Your libido may actually increase because testosterone levels can rise when estrogen levels drop. (The general rule is that your levels of testosterone will either stay the same or increase.) However, women who do experience an increase in sexual desire will also be frustrated that their vaginas are not accommodating their needs. First, there is the lubrication problem more stimulation is required to lubricate the vagina naturally. Second, a decrease in estrogen means that less blood flows to the vagina and clitoris, which means that orgasm may be more difficult to achieve or may not last as long as it normally has in the past. Other changes involve the breasts. Normally, estrogen causes blood to flow into the breasts during arousal, which makes the nipples more erect, sensitive, and responsive. Estrogen loss causes less blood to flow to the breasts, which makes them less sensitive. And finally, since the vagina shrinks as...


17 -Estradiol is the main estrogen synthesized and secreted by normal female ovaries. Its oxidized analog, estrone, is secreted to a significantly lesser degree by premenopausal ovaries. The hormonal effect of estrogens on target tissues is based on a complex mechanism that includes their reaction with specific estrogenic cytoplasmic receptors. After binding with these receptors, a conformational change occurs, which results in the estrogen-receptor complex penetrating into the nucleus, where it disassociates and returns to its native condition. Estrogens are used for insufficient ovary function. Estrogen replacement therapy is used in agonadal, menopausal, hypothalamic, and amenorrheal conditions (i.e. in cases of primary hypogonadism and hormone therapy in postmenopausal women). Estrogens are also recommended for other clinical endocrine diseases if hypoestrogenism has been established. Estrogens are most widely used in combination with progestins in a number of oral contraceptive...

Bone Mineral Density

There are increasing data on the effects of HSCT upon bone mineral density. Factors that may impact BMD include prior therapy for malignancies, conditioning regimens, lack of physical activity, poor nutrition and post-HSCT therapy with calcineurin inhibitors and corticosteroids. Post-HSCT hypogonadism may also impact bone mineral density. One recent study showed nadir BMD at month 24 for total body and femoral neck 37 in patients who received allogeneic HSCT. BMD continuously declined at the femoral neck sites. Steroids and cyclosporine use, as well as loss of muscle mass, were associated with low BMD. Only very young patients were protected from bone loss. The relationship between BMD changes and fracture risk is not yet established post HSCT.


Hypogonadism in men is deficient function of the testes. In this chapter its reproductive aspects will not be considered. This term will be used in the sense of deficiency of the testicular secretion of androgens mainly needed for virilization, anabolic effects, and expression of male sexual behavior. If the cause of hypogonadism lies in the testis itself, this is referred to as primary or hypergonadotropic hypogonadism. Hypothalamic or pituitary disorders of testicular dysfunction are grouped together under the term secondary or hypogonadotropic hypogonadism 1 . Late onset hypogonadism (LOH) is the term recommended by the International Society for the Study of the Aging Male (ISSAM), the International Society of Andrology (ISA), and the European Association of Urology (EAU), to replace the previous terminology of andropause, androgen deficiency of the aging male (ADAM), and partial androgen deficiency of the aging male (PADAM) 2 . It is a clinical and biochemical syndrome associated...

Metabolic syndrome

Although opinions have been mixed, there seems to be more data that indicates a certain relationship between T and the metabolic syndrome. The TT assay is the one most commonly used in clinical practice and the level is significantly affected by SHBG. Laaksonen etal. followed 702 middle-aged men participating in a population-based cohort study 409 . After 11 years 147 men developed the metabolic syndrome and 57 men developed diabetes. Men with TT, calculated FT, and SHBG levels in the lower fourth had a several-fold increased risk of developing the metabolic syndrome and diabetes. This has been confirmed in a recent analysis of the MMAS data 129 . The conclusion was that hypogonadism was an early marker for insulin and glucose metabolism. Kalme etal. confirmed the known fact that increased insulin downregulates SHBG production, which in turn decreases total T levels 410 . They followed 1711 men longitudinally. They found that low SHBG and IGF-binding protein-1 were both associated...

Future therapies

Selective androgen receptor modulators The discovery and development of selective androgen receptor modulators (SARMs) provides the opportunity to design molecules that are not only orally active, but that target androgen receptors in different tissues to elicit the specific desired activity 223 . The desired activity profile of novel SARMs is described in Table 18.5. An ideal SARM for the treatment of primary or secondary male hypogonadism would have the following profile orally active, with a pharmacokinetic profile consistent with once a day administration capable or incapable of stimulating the prostate, seminal vesicles, and other sex accessory tissues at doses equipotent to those needed to provide increases in muscle mass and strength along with fat-free mass support bone growth and maintain restore erectile function, libido, virilization, and male habitus. Unlike testosterone, these SARMs are not substrates for 5a-reductase activity. Other activities that are considered...

Drug induced ED

Several classes of medications and recreational drugs have been linked to the manifestation of ED (Table 5.3). This list is not meant to be inclusive of all medications that could cause ED. Drugs exhibit their adverse effects either through central inhibitory neuroendocrine mechanisms and or local neu-rovascular actions, or they have an impact on the hormonal milieu (testosterone, prolactin). Psy-chotropic medications may exert their inhibitory effects through their effect on central neurotrans-mitter pathways (serotonergic, adrenergic or dopaminergic). Beta-adrenergic blockers may exhibit central inhibitory effects or allow predominance of peripheral a-mediated vasoconstrictive effects 57 . Antiandrogens may suppress libido. Almost all recreational drugs have been reported to be associated with sexual dysfunctions, including Marijuana, opiates and cocaine 58,59 . In addition to the central nervous system (CNS) inhibitory effect, opiates have demonstrated an acute suppression of...


Treatment of the hypogonadism that is often seen in diabetes may correct many of the symptoms of androgen deficiency, and may improve ED, depending, of course, on how many other medical co-factors there are. Boyanov etal. treated hypogonadism in diabetic men with T undecanoate, 120 mg per day for three months 392 . The androgen replacement had a positive effect on visceral obesity, with a significant reduction in body weight, waist-hip ratio, and body fat. It significantly improved metabolic control, by decreasing blood glucose levels as mean as HbA1C levels from 10.4 to 8.6 . There was a reversal in the symptoms of androgen deficiency, including ED.

Skeletal System

Osteoporosis is most typical in post-menopausal women, who have low blood levels of the hormones estrogen and progesterone. Men can get osteoporosis, too, but their testosterone supports building greater bone mass. Though their risk is less than women's, men can get osteoporosis as their testosterone levels decline with age.


In males, the Sertoli and germ cells are more vulnerable to radiation and chemotherapy than the Leydig cells. FSH levels are usually elevated, with normal LH levels. Testosterone levels may be normal with reduced or absent spermatogenesis. Most boys will undergo pubertal development without the addition of testosterone. Testicular irradiation (usually for leukemia) is associated with low testosterone levels. Boys who have undergone testicular irradiation should be followed closely as they enter puberty. Estrogen is necessary for breast development and for the growth spurt that occurs at puberty. In prepubertal females who undergo HSCT, the recovery of ovarian function may be more likely than in post-pu-bertal patients, 36 ,but approximately 70 will have hypogonadotropic hypogonadism and require estrogen replacement therapy 34 . Failure of progression through puberty is often an indication for the need for estrogen replacement. Patients without breast development who have increased FSH...


Osteopenia may result from HPA abnormality (GH deficiency, hypothyroidism, hypogonadism or hyper-prolactinemia) in association with the direct effects of glucocorticoid therapy, methotrexate, inactivity and dietary changes. Osteopenia may present with fractures or may be asymptomatic. Among 141 survivors of childhood leukemia in one study, 30 (21 ) had abnormally low bone mineral density (BMD 1.645 SD below the mean of normal population). Risk factors for bone mineral decrements included male gender, Caucasian race and cranial irradiation. BMD was inversely correlated with the cumulative dose of cranial irradiation or antimetabolites 20 .

Steroidogenic Cells

It is expressed in a variety of tissues, including the adrenal cortex, testis (Sertoli cells), ovary (granulosa and theca cells), the placenta, and the pituitary and hypothalamus. During development, SF-1 is expressed in the urogenital ridge as early as embryonic day 9 in mice, and its role in the differentiation of steroidogenic tissues is demonstrated by the absence of adrenal glands and gonads in mice with a null mutation of the SF-1 gene (48,49). In humans, mutations in SF-1 are associated with hypogonadism and hypoadrenalism (47). Among the targets of SF-1 are the genes that encode the steroidogenic cytochrome P450 enzymes (47).

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