ESTROGEN SKIN PATCHES can prevent osteoporosis when used as prostate cancer treatment


Men using female oestrogen hormone replacement therapy (HRT) patches as treatment for advanced prostate cancer suffer fewer side-effects such as osteoporosis than with current treatments.

The male sex hormone, testosterone, causes the growth of the prostate gland and other sex organs in men. Even as men pass through the age of puberty, testosterone continues to contribute to the growth of the organ. Testosterone will fuel the growth of any prostatic cell: the chemical cannot discriminate between the receptors of healthy tissue and cancerous tissue. Prostate cancer hormone therapy removes the chemical (testosterone) that “feeds” cells and can stop or slow the growth and spread of prostate tumors.

Owing to cardiovascular and thromboembolic toxicities, oral estrogens were abandoned as treatments for prostate carcinoma; however, it is now recognized much of this toxicity can be avoided by parenteral (intramuscular or transdermal) estrogen administration. Ockrim and coauthors highlight the cost and protective andropause advantages of estrogen therapy, advocating a re-evaluation of this promising, but forgotten therapy. Nature Clinical Practice Oncology (2006) 3, 552-563doi:10.1038/ncponc0602 11 November 2006 | Accepted 14 June 2006

Estrogen is the female sex hormone and cannot feed the prostatic tissue, but the hypothalamus will mistake estrogen for testosterone and stop GnRH production. This halts testosterone production and a drop in testosterone levels ensues. In most therapies which halt testosterone, a major side effect is osteoporosis or bone loss. Osteoporosis is a debilitating condition where bone-producing cells (osteoblasts) fail to keep up with bone-removing cells (osteoclasts). These normally function together in equilibrium, maintaining the skeleton in optimum condition. Approximately 10% of bone mass is removed and replaced each year, but current prostate cancer treatments using LHRH agonists (Lupron & Zoladex) tamper with this equilibrium, leading to bone weakening and susceptibility to fracture.

Estrogens have historically been used in the treatment of prostate cancer. For many years, a synthetic estrogen, diethylstilbestrol or DES, has been a mainstay in therapeutic regimens, primarily directed against late-stage disease. While DES-based therapy does cause regression of many prostate cancers, this treatment protocol often causes many untoward effects, including those on the cardiovascular system. New evidence shows that estrogen delivered via skin patches is effective as DES without many of the side effects.

For the first time, a team led by Mr Paul Abel and Professor El-Nasir Lalani, consultants at Hammersmith Hospitals NHS Trust and Imperial College London, has shown that estrogen patches prevent bone loss. In the Journal of Urology* they report that estrogen skin patches can increase bone density in patients with advanced cancer. The team found using these patches, commonly used to relieve menopausal symptoms in women, increased bone density by an average of more than 3% after a year on the 20 men treated. This in addition to the fact that the tumors were also regressing.

"The considerable promise of parenteral oestrogen in advanced prostate cancer has already been reported by our team, but the additional benefit of preventing bone loss is extremely exciting news," comments Mr Abel. "Osteoporosis was once seen as a women’s disease, but has become an increasingly important consideration in prostate cancer as patients survive with the disease for longer periods of time."

The study followed 20 men with late stage prostate cancer who were given oestrogen hormone replacement therapy skin patches. After an initial pre-treatment measurement of bone mineral density in the spine and femur using X-ray (DXA scanning) techniques, the patients returned after six months and a year for check-ups. In addition to controlling the cancer, patients showed an average increase in bone density of over 3%, with almost all gaining some benefit.

"Patients on conventional prostate cancer treatment can lose up to 10% of bone mass as a side-effect in the first year of treatment alone. As long as treatment continues, so does bone loss, with a corresponding increasing risk of bone fracture with time," explains Mr Abel. "Although other side-effects such as gynaecomastia (breast growth) are more common with oestrogen treatment, this represents much less of a co-morbid risk than osteoporosis."

"Using the patch system to deliver oestrogen has other advantages - it is far easier to alter the treatment if needed, simply by taking off or replacing the patch. The realization of this treatment as an established therapy will mean that we can offer patients a genuine choice of therapies customized for their disease state and lifestyle. This can only be a good thing."

In yet another study, Jonathan Q. Purnell, M.D., assistant professor of medicine (endocrinology, diabetes and clinical nutrition) in the OHSU School of Medicine, together with Beer and colleagues examined the effects of transdermal estrogen cholesterol and other lipids that have been associated with heart disease. The study was presented on June 7, 2004, at the American Society for Clinical Oncology annual meeting in New Orleans, La.

Eighteen androgen independent prostate cancer patients aged 49 to 92 participated in the study. They were treated with six 7.6 milligram (45.6 milligrams total) patches every seven days for eight weeks. Blood cholesterol and lipid levels were measured before and eight weeks after beginning transdermal estrogen therapy. Whole body composition and body fat also were measured.

"Transdermal estrogen increased protective cholesterols, decreased those associated with heart disease, and did not produce adverse effects seen with oral formulations of estrogen," Beer said.

One study looked at men who had been on estrogen therapy for prostate cancer and had died either from cancer or other causes and the authors conclude that estrogen therapy may prolong survival by slowing the rate of tumor growth rather than by inhibiting the metastatic progression of prostate cancer or destroying selective populations of tumor cells.

*Journal of Urology. 172(6):2203- 2207 December 2004.

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