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The complexities of hypogonadism



The complexities of hypogonadism
Male hypogonadism is a clinical syndrome defined by low testosterone levels associated with sexual dysfunction, particularly diminished libido, mood disturbances, reduced lean body mass and increased adipose tissue mass.
A wide range of effective and well-tolerated treatment options exist. These include testosterone (T) gels and T patches. There is also a mucoadhesive sustained-release buccal tablet, but this is not available in Ireland. Intramuscular testosterone injections and subcutaneous depot implants (T pellets) are still the standard therapy.
Testosterone replacement therapy (TRT) can be individualised to enhance patient health and wellbeing. Screening and ongoing monitoring are necessary to ensure both the efficacy and safety of TRT, particularly prostate safety. Investigational agents, including selective androgen receptor modulators, may offer new pharmacodynamic and/or pharmacokinetic properties that enhance outcomes of TRT.
Male hypogonadism is defined as the failure of the testes to produce androgen, sperm or both. Although the disorder is exceedingly common, its exact prevalence is uncertain.
Testosterone production declines with advancing age; some 20 per cent of men older than 60 years and 30-40 per cent of men older than 80 years have serum testosterone levels that would be subnormal in their younger adult male counterparts.
This apparent physiologic decline in circulating androgen levels is compounded in frequency by permanent disorders of the hypothalamic-pituitary-gonadal axis. These include the transient deficiency states associated with acute stressful illnesses, such as surgery and myocardial infarction, and the more chronic deficiency states associated with wasting illnesses, such as cancer and acquired immunodeficiency syndrome (AIDS).
Pathophysiology
Circulating testosterone is largely protein-bound — the major protein is sex hormone-binding globulin (SHBG) — with only 2 per cent present as the biologically active or free fraction. Hepatic SHBG production rises with ageing and thyroid hormone excess and declines in hyperinsulinemic states (obesity and type II diabetes), so that free testosterone values may not always be concordant with total testosterone values.
The biologic effects of testosterone may be mediated directly by testosterone or by its metabolites 5a-dihydrotestosterone or estradiol. The single decapeptide gonadotropin-releasing hormone (GnRH) stimulates the release of follicle-stimulating hormone (FSH) and luteinising hormone (LH).
Pulsatile GnRH is required. Chronic exposure down regulates the GnRH receptor and causes impaired FSH and LH release, the mechanism whereby pharmacologic GnRH agonists result in chemical castration. Prolactin excess also results in impaired GnRH pulse generator function and hypo-gonadotropic hypogonadism.
Feedback inhibition of LH secretion is a sex steroid–mediated event, whereas FSH secretion has dual feedback regulation involving inhibition by sex steroids and the Sertoli cell product inhibin. Accordingly, a monotropic elevation of the FSH level (normal LH and testosterone levels) may result from deficient Sertoli cell–spermatogenic function.
Major causes of primary (hypergonadotropic) hypo-gonadism include: genetic (Klinefelter’s syndrome, XX males, XYY syndrome); congenital (anorchia, Noonan syndrome, cryptorchidism, myotonic dystrophy); toxins (alcohol, heavy metals, antineoplastics, radion); orchitis; trauma; infarction; and ageing.
Major causes of secondary (hypogonadotropic) hypogonadism include: pubertal delay; hypogonadotropism (Kallman’s syndrome); congenital or acquired; isolated or combined pituitary disease; space-occupying lesions of pituitary, hypothalamus; hyperprolactinaemia per se; infiltrative, infectious; suppression; sex steroids; gonadotropin-releasing hormone analogues; and (possibly) ageing.
Clinical features
Manifestations in adults are generally more subtle. Perhaps the minor contribution of adrenal androgens (or androgenic precursors) may substitute for testicular deficiency once the target tissues have been fully developed. Moreover, ingrained behaviour patterns may be resistant to androgenic hormone deficiency.
Certainly, prolactin excess, testosterone deficiency, or both in men may result in impaired libido and erectile dysfunction. The yield of finding hyperprolactinaemia or testosterone deficiency, or both, in patients presenting with these symptoms is generally considered to be low, usually less than 5 per cent.
A. More specific symptoms and signs
• Incomplete or delayed sexual development, eunuchoidism;
• Reduced sexual desire (libido) and activity;
• Decreased spontaneous erections;
• Breast discomfort, gynaecomastia;
• Loss of body (axillary and pubic) hair, reduced shaving;
• Very small (especially 51 per cent).
In genuinely hypogonadal men, testosterone administration can be expected to result in improvements in a variety of clinical areas. These include: increase in lean body mass; decreased fat mass; increased bone density (no fracture data available); improved mood and wellbeing; improved sexual function; better cognitive function; better muscle strength, physical function. Least predictable of these are the effects on sexual function, cognitive function and muscle strength.
Summary
Male hypogonadism is defined as the failure of the testes to produce androgen, sperm, or both. Although the disorder is exceedingly common, its exact prevalence is uncertain.
Signs and symptoms vary, according to age.
Diagnosis requires the determination of low testosterone levels. Normal ranges vary among laboratories. Measurement of free testosterone levels or bioavailable testosterone levels (performed adequately in select commercial laboratories) may provide additional information, in addition to serum follicle-stimulating hormone, luteinising hormone and prolactin levels. MRI scans of the brain and sella should be considered.
Androgen replacement therapy is used for the treatment of male hypogonadism. In addition to monitoring testosterone levels periodically, prostate screening by digital rectal examination and prostate-specific antigen determinations at periodic intervals when the patient is on therapy should be carried out.
Haemoglobin and haematocrit levels should also be checked periodically.