LHRH agonists shut down production of LH and FSH. Here’s how they work: LHRH is a small protein, built of ten blocks of amino acid. A synthetic substance called an LHRH-analog, or agonist, made by changing one of the ten blocks, works by inhibiting LH (the hormone that tells the pituitary gland to make testosterone). The hypothalamus acts like a lighthouse, sending out LHRH in signal pulses—like Morse code in flashes of light—to the pituitary gland. LHRH agonists work by providing prolonged signals—by turning on the light and keeping it on, instead of just sending flashes. So these drugs trick the pituitary; because the pituitary receives no flashes, or pulses, it thinks no signal is being sent—and it doesn’t make LH.
These drugs don’t work right away. In fact, for about a week after a man begins taking an LHRH agonist, his testosterone level kicks into overdrive. This is called a “flare,” and it happens because the constant LHRH signal initially stimulates LH production. But by about ten days, testosterone falls into the castrate range. For the first few weeks, doctors often prescribe another drug, such as flutamide, to block this surge.
The most commonly prescribed LHRH agonists are leuprolide (Lupron) and goserelin (Zoladex). In large studies, researchers have found that these LHRH agonists are equivalent to treatment with DES or surgical castration in their ability to lengthen the time until the cancer progresses, and to prolong survival. These drugs are given in monthly injections.
The chief advantages of LHRH agonists are that they avoid the need for surgery, and that they don’t cause breast swelling as often as treatment with estrogen. Also, they don’t have the risk of cardiovascular complications that can accompany estrogen treatment.
Side Effects. Like surgical castration, however, LHRH agonist treatment does cause hot flashes, loss of sex drive, and impotence. Other disadvantages include the need to get monthly shots, and the tremendous expense—LHRH agonists cost hundreds of dollars a month.
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