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Hormones are produced by the glands in the body and circulated through the bloodstream. Most prostate cancer cells thrive on male hormones (androgens) such as testosterone for their growth. The vast majority (90%-95%) of these androgens come from the testicles while the rest are from the adrenal glands.
The goal of hormone therapy is to keep cancer cells from getting the male hormones they need to grow. Hormonal therapy has long played an important role in managing prostate cancer. It can control localized tumors as well as those that have spread to other areas of the body.
When prostate cancer begins spreading to other areas of the body, the treatment protocol may shift to hormonal therapy. This involves reducing the testosterone that nourishes the prostate gland. Depleting the testosterone may help reduce symptoms while preventing further growth.
Hormonal therapy causes the cancer to shrink in 85%-90% of patients with an advanced stage of the cancer, but it does not cure it. Treatment duration varies from person to person and may not effect all prostate cancer cells. The types of cells that don’t respond to this type of therapy are are called “hormone-independent” or “androgen-insensitive” cells.
Usually, surgery or medication are used to reduce or eliminate male hormones such as testosterone.
Surgery. Testosterone levels can be reduced by removing the testes during what is called a bilateral orchiectomy. This involves surgically opening the scrotum in order to free the blood vessels and nerves. Then the testicles are removed from surrounding tissue.
Medication. The second option that is commonly utilized is chemical castration. This procedure involves using medications to disrupt the body’s normal production or use of testosterone. Types of medication may include:
- Luteinizing Hormone-Releasing Hormone Agonists (LHRH). This is the most common way used to suppress the production of male hormones. These types of drugs, such as TRELSTAR, shut down certain signals from the brain that cause the testes to produce testosterone.
- Estrogens: Estrogen therapy works by blocking the secretion of LHRH. As a result, the pituitary is not stimulated and therefore other organs, such as the testes, do not produce testosterone.
- Anti-androgens: Anti-androgens work to block androgen receptors in cells and thereby disrupt androgen type of actions which include cell proliferation.
- LHRH antagonist: Unlike LHRH agonists that work to prevent the actual production of LHRH, antagonists work to prevent the already produced LHRH from binding to or working on it's receptor cells.
Like other therapies, hormonal therapy is a treatment, not a cure. Hormone therapy, however, can both relieve the symptoms of the disease and keep it from progressing. Discuss with your doctor which treatment options may be right for you.
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Indications and Usage
TRELSTAR® Depot and TRELSTAR® LA are indicated in
the palliative treatment of advanced prostate cancer. TRELSTAR Depot and TRELSTAR
LA offer an alternative treatment for prostate cancer when orchiectomy or estrogen
administration are either not indicated or unacceptable to the patient.
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Safety Information
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After your first injection of TRELSTAR, you might feel a temporary increase in your
cancer symptoms, such as pain in your bones. This is because the amount of testosterone
in your bloodstream actually goes up for a short period after the injection. If
your symptoms increase later than the first week or two following an injection,
tell your doctor. The most common side effects that patients taking TRELSTAR have
are actually the effect of lowering testosterone levels. The most common effect
of lowering testosterone is hot flushes or flashes. These are like the hot flashes
women have around the time of menopause. Other side effects include bone pain, impotence
(sexual side effect), headache, leg pain, and swelling in the legs. Women who are
or may become pregnant and those who are allergic to this type of drug should not
take TRELSTAR. For more information on these and other side effects, please talk
to your doctor.
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