Hypogonadism Can Result From Defects at Several Levels

Male hypogonadism may result from defects in spermato-genesis, steroidogenesis, or both. It may be a primary defect in the testes or secondary to hypothalamic-pituitary dysfunction, and determining whether the onset of gonadal failure occurred before or after puberty is important in establishing the cause. However, several factors must be considered. First, normal spermatogenesis almost never occurs with defective steroidogenesis, but normal steroidogenesis can be present with defective spermatogenesis. Second, primary testicular failure removes feedback inhibition from the hypothalamic-pituitary axis, resulting in elevated plasma gonadotropins. In contrast, hypothalamic and/or pituitary failure is almost always accompanied by decreased gonadotropin and steroid levels and reduced testicular size. Third, gonadal failure before puberty results in the absence of secondary sex characteristics, creating a distinctive clinical presentation called eunuchoidism. In contrast, men with a postpubertal testicular failure retain masculine features but exhibit low sperm counts or a reduced ability to produce functional sperm.

To establish the cause(s) of reproductive dysfunction, physical examination and medical history, semen analysis, hormone determinations, hormone stimulation tests, and genetic analysis are performed. Physical examination should establish whether eunuchoidal features (i.e., infantile appearance of external genitalia and poor or absent development of secondary sex characteristics) are present. In men with adult-onset reproductive dysfunction, physical examination can uncover problems such as cryptorchidism (nondescendent testes), testicular injury, varicocele (an abnormality of the spermatic vasculature), testicular tumors, prostatic inflammation, or gynecomastia. Medical and family history help determine delayed puberty, anosmia (an inability to smell, often associated with GnRH dysfunction), previous fertility, changes in sexual performance, ejacula-tory disturbances, or impotence (an inability to achieve or maintain erection).

One step in the evaluation of fertility is semen analysis. Semen are analyzed on specimens collected after 3 to 5 days of sexual abstinence, as the number of sperm ejaculated remains low for a couple of days after ejaculation. Initial examination includes determination of viscosity, liquefaction, and semen volume. The sperm are then counted and the percentage of sperm showing forward motility is scored. The spermatozoa are evaluated morphologically, with attention to abnormal head configuration and defective tails. Chemical analysis can provide information on the secretory activity of the accessory glands, which is considered abnormal if semen volume is too low or sperm motility is impaired. Fructose and prostaglandin levels are determined to assess the function of the seminal vesicles and levels of zinc, magnesium, and acid phosphatase to evaluate the prostate. Terms used in evaluating fertility include aspermia (no semen), hypospermia and hyperspermia (too small or too large semen volume), azoospermia (no spermatozoa), and oligozoospermia (reduced number of spermatozoa).

Serum testosterone, estradiol, LH, and FSH analyses are performed using radioimmunoassays. Free and total testosterone levels should be measured; because of the pulsatile nature of LH release, several consecutive blood samples are needed. Dynamic hormone stimulation tests are most valuable for establishing the site of abnormality. A failure to increase LH release upon treatment with clomiphene, an


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  • maarit alho
    What is meant by hyperspermia genesis?
    7 years ago

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