Figure 48.1. Evaluation of male hypogonadism.

    In addition to assessing the etiology of the hypogonadism, it is also important to assess the end-organ effects of the patient’s hypogonadism. These assessments may include a semen analysis to assess sperm counts, hematocrit to assess for anemia, and bone mass density (BMD) scan to assess for osteopenia/osteoporosis.

Primary Hypogonadism

Primary hypogonadism may be congenital or acquired (table 48.2). The most common congenital etiology is Klinefelter syndrome, which has been described to occur in 1 in 800 live births. In patients with Klinefelter mosaicism, the hypogonadism may not be recognized until later in life. Therefore, all patients with primary hypogonadism should have a karyotype.

    Acquired etiologies for primary hypogonadism include infectious etiologies such as mumps, chemotherapy, or radiation therapy to the pelvic area.

Secondary Hypogonadism

Secondary hypogonadism may also be congenital or acquired. Congenital etiologies include idiopathic hypogonadotropic hypogonadism, with or without anosmia. Acquired etiologies include hemochromatosis, hyperprolactinemia, opiate use, and pituitary or hypothalamic tumors.

    All patients with secondary hypogonadism require a transferrin saturation to assess for hemochromatosis and a prolactin level to assess for hyperprolactinemia. All patients under the age of 60 with secondary hypogonadism require imaging of their pituitary gland to exclude a pituitary neoplasm.

Treatment

    Treatment depends on the patient’s goals. Testosterone replacement therapy is prescribed in men without immediate desire for fertility. Various formulations are available including intramuscular injections, transdermal patches, transdermal gels, buccal tablets, and axillary solution. Older oral formulations are no longer available in the United States because of the significant hepatotoxicity associated with them.

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