Clinical Hypogonadism and Androgen Replacement Therapy: An Overview

Dana A. Ohl; Susanne A. Quallich


Urol Nurs. 2006;26(4):253-259,269. 

In This Article

Clinical Presentation

Establishing the presence of hypogonadism on the basis of clinical symptoms alone is difficult, except in the most profound of cases. There is no consensus as to what laboratory level of testosterone defines a clinically significant deficiency. Significant intra-individual variations in testosterone levels may be attributed to time of day, medications, stress, illness, or recent surgery. An individual may suffer from an overall decline in endocrine function that acts synergistically to produce symptoms of hypogonadism, but it remains unclear what the contribution of testosterone is in the presentation of these symptoms. The loss of muscle mass and bone density, for instance, can be attributed to a decline in physical activity as the incidence of mobility- limiting co-morbidities rises.

There are several accepted elements that compose ADAM. An individual may demonstrate some or all of these components:

  • Changes in mood (fatigue, depression, anger).

  • Decreased body hair (feminization).

  • Decreased bone mineral density and possible resulting osteoporosis.

  • Decreased lean body mass and muscle strength.

  • Decreased libido and erectile quality.

  • Increased visceral fat.

  • Oligospermia or azoospermia.

The diagnosis of hypogonadism can be facilitated through the use of screening questionnaires such as the ADAM questionnaire (see Figure 1). This survey exhibits a statistical sensitivity of 88%, but a specificity of only 60% (Morley et al., 2000). This means that the ADAM questionnaire will rarely miss diagnosing individuals who actually have hypogonadism, but will also incorrectly identify many non-hypogonadal individuals as having the condition. This is due to the fact that many positive responses in the questionnaire may be indicative of other conditions, such as depression. Its use as a screening tool nonetheless aids in prompting a more detailed discussion of symptoms.

Figure 1.

ADAM Questionnaire

Physical examination in hypogonadism is commonly unremarkable, though there may be evidence of decreased hair distribution, truncal fat distribution, testicles that may be of a softer consistency, or gynecomastia. There is no consensus as to what degree these signs should be present or how severe they must be in order to diagnose ADAM.

There are some conditions in which a male is at increased risk for developing hypogonadism. Diabetic men are at increased risk for the condition, with the prevalence varying between 30% and 55% depending on age (Dhindsa et al., 2004). This is further complicated by obesity, which further increases the risk for both hypogonadism and diabetes due to the aromatization of testosterone to estradiol.

Patients who present with sexual dysfunction complaints should raise the suspicion of hypogonadism. This is not limited to those men who complain of erectile difficulties or the elderly male. Presentation could include complaints of decreased spontaneous erections, poor quality erections, and low libido. This may be the only aspect in which some men fit the ADAM criteria, and it is impossible to predict the testosterone required by an individual to maintain sexual function. It is likely that as men age, the hormonal component to sexual function begins to have an increasing role. Hypogonadal patients who have failed a trial of phosphodiesterase-5 (PDE5) in hibitors may respond to these medications if their testosterone levels are returned to normal (Aversa, Isidors, Spera, Lenzi, & Fabbri, 2003), which may enable them to avoid more invasive treatments. However, it is important to remember that men who are hypogonadal can have adequate erectile function. Likewise, restoration of testosterone to normal levels does not alone necessarily restore erectile function in men with concomitant hypogonadism and erectile dysfunction.

Given the widespread influence and maintenance functions that testosterone has, it has been proposed that clinicians begin screening for low or low normal testosterone routinely in their aging patients. There are multiple drawbacks to this approach, with one of the most obvious being the lack of controlled data to indicate what lower limit of the normal range should be used for beginning treatment. Similarly, there is no long-term randomized data that establishes appropriate endpoints or goal for androgen replacement. There is also the question of which laboratory assay(s) would provide the most clinically relevant information.


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