LH-RH agonists/GnRH agonists for prostate cancer

Examples

Generic Name Brand Name
goserelin acetate Zoladex
leuprolide acetate Lupron
triptorelin pamoate Trelstar Depot

How It Works

Luteinizing hormone-releasing hormone (LH-RH) agonists and gonadotropin-releasing hormone (GnRH) agonists are hormone therapy drugs that lower the production of testosterone in a man's body. This drop in testosterone usually slows or stops the growth of prostate cancer for a period of time.

These drugs work by causing the pituitary gland to release the hormones that cause the testicles and adrenal glands to make testosterone. The pituitary gland then runs out of its hormones, and testosterone production drops.

These drugs are usually given by injection. They may be given once a month, once every 3 to 4 months, or once a year.

Why It Is Used

LH-RH and GnRH agonists are used to treat advanced prostate cancer. They are often used with other treatments, such as surgery or radiation therapy.

LH-RH and GnRH agonist therapy can also be used to relieve pain caused by metastatic prostate cancer.

How Well It Works

LH-RH agonist therapy improves a man's chances of living longer. One study of men with locally advanced prostate cancer found that treatment with LH-RH agonists and radiation therapy resulted in an improvement of overall survival rates.1

When combined with radiation therapy or surgery to remove the prostate, LH-RH therapy may improve survival in men who have locally advanced cancer. One study of treatment for locally advanced cancer found that 74% of men who received both external radiation and LH-RH therapy were disease-free after 5 years, compared with 40% for men who received radiation therapy alone.1

Treatment with LH-RH agonists may control severe pain caused by metastatic prostate cancer and may improve a man's quality of life. LH-RH agonists may be able to reduce bone fractures and spinal cord compression caused by metastatic disease if treatment is started as soon as cancer progression is evident.2

Side Effects

Side effects from LH-RH agonists and GnRH agonists may include:3

Because these drugs work on the pituitary gland to release its hormones, the testicles may temporarily produce extra testosterone, causing a temporary growth in the tumor. This is called a tumor flare. Tumor flare may be accompanied by bone pain, urinary blockage, or other symptoms of rapid cancer growth. This may indicate that the drug is working, and although the tumor may grow initially, it will shrink over time. Tumor flare can be prevented by taking a different hormone drug called an antiandrogen before or during treatment with the LH-RH agonist.

One study found that treating prostate cancer with drugs to block androgen may increase the risk for gum disease.4

See Drug Reference for a full list of side effects. (Drug Reference is not available in all systems.)

What To Think About

These medicines are less likely to cause larger breasts and heart problems than older hormone medications, such as diethylstilbestrol (DES).5

Complete the new medication information form (PDF)(What is a PDF document?) to help you understand this medication.

References

Citations

  1. Bolla M, et al. (2002). Long-term results with immediate androgen suppression and external irradiation in patients with locally advanced prostate cancer (an EORTC study): A phase III randomised trial. Lancet, 360(9327): 103–108.
  2. National Cancer Institute (2007): Prostate Cancer (PDQ): Treatment—Health Professional Version. Available online: http://www.nci.nih.gov/cancertopics/pdq/treatment/prostate/healthprofessional.
  3. Nelson JB (2007). Hormonal therapy for prostate cancer. In AJ Wein et al., eds., Campbell-Walsh Urology, 9th ed., vol. 3, pp. 3082–3100. Philadelphia: Saunders Elsevier.
  4. Famili P, et al. (2007). The effect of androgen deprivation therapy on periodontal disease in men with prostate cancer. Journal of Urology, 177(3): 921–924.
  5. Hellerstedt BA, Pienta KJ (2002). The current state of hormonal therapy for prostate cancer. CA—A Cancer Journal for Clinicians, 52(3): 154–179.

Last Updated: July 1, 2008

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