Todd M. Tartavoulle, MN, RN; Demetrius J. Porche, DNS, PhD

Disclosures

Journal for Nurse Practitioners. 2012;8(10):778-786. 

In This Article

Clinical Presentation and Diagnosis

Evaluation of Symptoms

A comprehensive history and physical exam should be performed to determine the cause and extent of low T levels and hypogonadism. During the physical exam, the amount and distribution of body hair (beard growth, axillary hair, and pubic hair), along with the presence of a male pattern escutcheon, should be noted, as well as inquiry regarding a decrease in body hair or beard growth. The length and width of the testes should be measured with a Prader orchidometer or calipers, and the scrotum examined for the presence of any masses (spermatoceles, hydroceles, or varicoceles).[13]

Signs and symptoms of low T are indicative of hypogonadism diagnosis. Clinical practice guidelines from the Endocrine Society and the American Association of Clinical Endocrinologists (AACE) suggest measuring testosterone levels of men with any of the signs and symptoms of low T (Table 2). Complaints of low libido, erectile dysfunction, depressed mood, difficulties with concentration and memory, decreased BMD, decreased vitality, and decreased muscle mass and increased body fat should be noted.[1]

The Androgen Deficiency in Aging Males (ADAM) screening questionnaire may be helpful in identifying men over 40 with a high probability of having low T and for evaluating the therapeutic response to TRT. The ADAM questionnaire assists the practitioner in initiating a conversation and should never be used in isolation to diagnose clinical hypogonadism.[14] It is important for practitioners to use ADAM and assess for the comorbidities associated with low T levels.[1]

Diagnosis

The Endocrine Society's diagnostic criteria for hypogonadism can be made with the consistent signs and symptoms of hypogonadism and low T levels. Initially, serum total testosterone levels are assessed. The serum total testosterone sample should be collected in the morning when the levels of circulating testosterone peak.[13] The society proposes that the normative ranges for total and free testosterone levels vary; however, the lower limit of normal, acceptable total testosterone range is approximately 280 to 300 nanograms per deciliter (ng/dL). AACE proposes 200 ng/dL as the lower normal limit of total testosterone levels.[1]

Serum total testosterone circulates in 3 forms: free testosterone, SHBG-bound testosterone, and albumin-bound testosterone. SHBG levels are presumably normal in young, healthy, and lean men, therefore, the serum total testosterone level is reliable. Because many conditions may cause an increase or decrease in SHBG, total testosterone levels can be misleading and may not be an accurate indicator of hypogonadism.[1] The Endocrine Society suggest measuring free or bioavailable testosterone levels as an accurate and reliable assay in men in whom the total testosterone levels are near the lower normal range and in whom SHBG alterations are suspected.[13] Table 3 lists conditions that impact SHBG.

Practitioners should not rely on total testosterone concentrations for diagnosing hypogonadism in obese or elderly men. A free testosterone level should be obtained in all men who are not healthy, lean, and young. The lower limit of normal free testosterone is 50 picograms per milliliter (pg/ml) measured by equilibrium dialysis, according to the Endocrine Society.[1]

If low T has been established, further laboratory testing will determine whether the male has primary or secondary hypogonadism by measuring serum LH and FSH. In primary hypogonadism, serum LH and FSH are elevated, whereas these hormones are decreased to normal in secondary hypogonadism. Decreased to normal levels of LH and FSH with low T suggest secondary hypogonadism, in which there are defects in the hypothalamus or pituitary.[15] Figure 2 presents a clinical presentation and diagnostic algorithm.

Figure 2.

Low T: Clinical Presentation and Diagnostic Algorithm

The cause of primary hypogonadism is testicular failure. Congenital causes of primary hypogonadism are Klinefelter syndrome, anorchia (bilateral), cryptorchidism, myotonic dystrophy, enzymatic defects in testosterone synthesis, Leydig cell aplasia, and Noonan syndrome. Acquired casuses of primary hypogonadism are chemotherapy or radiation therapy, testicular infection (mumps, echovirus, flavivirus), and high doses of certain drugs, such as cimetidine, spironolactone, aldactone, ketoconazole, flutamide, and cyproterone.[13]

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