Showing posts with label androgen deprivation therapy. Show all posts
Showing posts with label androgen deprivation therapy. Show all posts

Monday, July 30, 2012

Bone Health and Prostate Cancer: What Every Man on Androgen Deprivation Therapy Should Know


One of the most significant risks facing men on androgen deprivation therapy (ADT) for prostate cancer is osteoporosis.  Representing a critical decrease in the density of bones, osteoporosis is usually associated with menopause in women.  However, men with prostate cancer, particularly those on androgen deprivation therapy, are also at risk for this condition.  So why do we care about osteoporosis?  By making bones less dense, osteoporosis also makes them more prone to fracture.  These fractures can be devastating, decreasing the ability to move around and, even worse, substantially increasing the risk of death.  In fact one study demonstrated that people with osteoporosis related fractures had a risk of death two times that of similarly aged people without fractures.  In addition, another study showed that fractures decreased the life expectancy of men with prostate cancer by more than 3 years. As a result, men with prostate cancer who receive ADT should make bone health a top priority.  In this post, I will discuss the steps all men undergoing ADT need to take to prevent osteoporosis.  In addition, I will describe the treatment options for those men found to already have low bone density.

ADT and Osteoporosis:  What is the Connection?

When most people think about bones, they imagine sturdy, stable structures that really don’t change much from day to day.  In reality, however, this perception could not be further from the truth.  Every bone in the body represents a constant battle between two opposing classes of cells.  Osteoblasts, the bone builders, work frantically to strengthen bones by incorporating calcium into them.  Osteoclasts, in contrast, remove calcium from bones and, in so doing, weaken them.  While most of the time, these two cells are in a stalemate called “dynamic equilibrium”, occasionally one cell type wins.  For example, when there is not enough calcium circulating in the body, osteoclasts free calcium from bones into the bloodstream.  In this situation, bones are weakened.  When this situation continues for a prolonged period of time and bones are weakened beyond a critical point, osteoporosis occurs.

So what does ADT have to do with osteoporosis and the battle between osteoblasts and osteoclasts?  These competing cells are regulated by various hormones in the body.  Two of these very important hormones are estrogen and testosterone.  Estrogen works to deactivate osteoclasts .  As a result, the hormone works to increase the strength of bones.  During menopause, estrogen levels are decreased, allowing osteoclasts to function more effectively and to weaken bones.  This leads to osteoporosis associated with menopause in women.  Testosterone also functions to strengthen bones through its impact on the osteoclasts and osteoblasts.  This male hormone activates osteoblasts, stimulating them to strengthen bones by incorporating more calcium.  In addition, in men, some testosterone gets converted to estrogen, leading to deactivation of osteoclasts and secondary strengthening of bones as well.  For men with prostate cancer, the administration of ADT leads to the decrease of testosterone (and subsequently estrogen) in the body.  While this decrease in testosterone is great in battling prostate cancer, it can be devastating to bone health. 
Through its decrease of testosterone and estrogen, ADT secondarily shifts the balance of power to osteoclasts and leads to osteoporosis and its associated risks for many men undergoing this treatment for prostate cancer.  Studies have demonstrated that ADT decreases bone density in men by 1-5% per year.  As a result, one study demonstrated that 80% of men on ADT develop osteoporosis after 10 years of treatment.  As a result, men on ADT have been found to be 13-30% more likely to develop a fracture as compared to their counterparts with prostate cancer not treated with ADT. 

Starting ADT?  Get Your Bone Density Checked

Given this propensity for ADT to decrease the density of bones, it is important for men starting this hormonal therapy to evaluate their risk of osteoporosis at the outset of treatment.  This task is accomplished through a bone density scan. Also known as a DEXA scan, this simple x ray test can easily and non invasively determine the density of bones over the span of 10-30 minutes.  It is no more painful than a chest x ray and its only risk is the low level of ionizing radiation that you absorb during the test.

The bone density scan is reported as a series of scores.  The first score, called the T score, determines the overall bone density as compared to the maximal potential bone density.  A T score of greater (more positive) than -1 is considered normal.  Men with T scores ranging from -1 to -2.5 are considered to have low bone density or osteopenia.  T scores of less than -2.5 indicate osteoporosis.  The second score, called the Z score, compares the measured bone density to that of other people with the same age and gender.  This score helps to differentiate a pathologically low bone density from a low bone density that is “normal” for a particular age and gender.  Using these scores, a physician can determine whether a man about to start ADT has low bone density and who, in turn, is at higher risk for fractures.  As such, the scores help determine who needs pre-emptive treatment for osteoporosis or osteopenia and what kind of treatment would best suit them.

Treatments to Maximize Bone Density in Men Starting ADT

Once bone density and strength is determined via a DEXA scan, a man starting ADT can begin protecting his bones with various treatment options.  While some treatment options should be undertaken by all men starting ADT, others should be reserved for those with documented osteoporosis. All men undergoing ADT, for example, should undergo lifestyle modifications to maximize their bone health.  Simple steps such as exercising more, stopping smoking, and limiting caffeine and alcohol can significantly prevent the onset and progression of osteoporosis.  In addition, most men starting ADT should begin supplementation with Calcium and Vitamin D.  These supplements serve as the building blocks with which the osteoblast cells build up bones. The usual dosage is 1500 milligrams of calcium and 800 units of Vitamin D per day in divided doses.  Certain medical conditions (such as kidney stones) prevent men from taking these supplements at full or even decreased doses.  As a result, all men contemplating taking these supplements should first seek guidance from a physician. 

While such treatments are applicable to all men undergoing ADT, some therapies are reserved only for men with confirmed osteoporosis.  One such treatment involves a class of drugs called bisphosphonates.  Available in oral or intravenous forms, bisphosphonates improve bone density and fight against osteoporosis by blocking the bone destroying activity of osteoclast cells.  Numerous studies have evaluated this class of drugs in men with prostate cancer undergoing ADT.  These studies have demonstrated that while bisphosphonates do prevent loss of bone density over time (some studies demonstrate that these drugs can even increase bone density), they have yet to demonstrate that these drugs can prevent fractures in these men.  However, a decrease in fracture risk has been demonstrated in postmenopausal women taking bisphosphonates.  While this class of drugs can, indeed, be helpful in protecting the bones of men on ADT, they are not without risks.  Oral bisphosphonates, like Alendronate (Fosamax), often produce upset stomachs as well as other gastrointestinal side effects.  As a result, many patients often do not stick with the therapy.  In fact, one study of postmenopausal women demonstrated that less than 60% actually continued the once monthly oral therapy long term. 

Intravenous bisphosphonates, like Zolendronic Acid (Zometa) and Pamidronate (Aredia), are usually better tolerated.  Some patients do experience flu like symptoms during the first intravenous infusion but this reaction is usually mild.  A much more serious potential side effect is kidney toxicity, sometimes leading to kidney failure requiring dialysis.  As a result, men undergoing treatment with these drugs need to have their kidney function closely monitored with periodic blood tests.  Another very serious, although thankfully rare, side effect of these IV drugs is osteonecrosis or destruction of the jaw bone.  Because of this potential side effect, all men starting these drugs should have dental work completed prior to the start of therapy, maintain good oral hygiene, and get periodic dental checkups.

As I mentioned previously, the female hormone, estrogen, potently blocks the bone destroying activities of osteoclast cells, making bones stronger.  Not surprisingly then, estrogen has been tried in the treatment of osteoporosis.  While, indeed, successful in increasing bone density, estrogen unfortunately comes with the associated risks of heart attack as well as blood clots.  Because healthy bones are of no use to people dead from heart disease, estrogen is not routinely used to treat osteoporosis in men on ADT.  Instead, a related class of drugs called selective estrogen receptor modulators (SERM) have been successfully used to fight osteoporosis while avoiding the heart risks. Including drugs such as Raloxifene and Toremifine, SERMs have been demonstrated to significantly increase the bone density of men on ADT.  A  recent study of 1389 men on ADT also demonstrated that Toremifine reduced vertebral (spine) fractures by 53%.

Another new method of tackling osteoporosis in men on ADT for prostate cancer is the creation of antibodies against a compound called RANKL.  In the body, RANKL binds to osteoclast cells, activating them and prolonging their survival.  As you may remember from earlier in this post, osteoclasts resorb bone, making it less dense and promoting osteoporosis.  Drugs that serve as antibodies against RANKL, in turn de-activate it.  As a result, its ability to activate osteoclasts is diminished, preventing bone resorption and subsequent osteoporosis.  One such drug called Denosumab(Xgeva) was recently studies in 1468 men with nonmetastatic prostate cancer who were undergoing ADT.  The study reported that Denosumab, given as an injection once every 6 months, significantly improved bone density throughout the body and decreased the risk of fracture by 62% over a 3 year period.  This success was even more impressive given that the drug was extremely well tolerated with minimal adverse side effects.

Take Home Message

Osteoporosis is a serious problem facing men with prostate cancer treated with ADT.  All men starting ADT should undergo bone density testing to determine how strong and dense their bones are.  Depending on the results, men should undergo one of the various treatments to increase or maintain bone density.  At the very least, barring any contraindications, all men undergoing ADT should take Calcium and Vitamin D in addition to making some lifestyle modifications.  In addition, those men diagnosed with osteoporosis prior to or during ADT should begin one of the many excellent treatment options available. Of course, all men considering treatment for this and any other medical conditions should carefully discuss the options with their physician prior to embarking on any treatment plan.  Through such measures, men undergoing ADT for prostate cancer can enjoy good bone health and prevent the dreaded fractures associated with osteoporosis. 

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This blog is not a medical practice and cannot provide specific medical advice. This information should never be used to replace or discount the medical advice you receive from your physician


Sunday, April 8, 2012

Hot Flashes and Prostate Cancer: Treating One of the Most Dreaded Side Effects of Androgen Deprivation Therapy


One of the earliest and most bothersome side effects of androgen deprivation therapy for prostate cancer is the hot flash.  Very similar to those experienced by women during menopause, hot flashes can be debilitating for men receiving medications such as Lupron.  Many are too embarrassed by hot flashes to even mention them to their physician.  Others don’t discuss them because they feel that these hot flashes cannot be treated or prevented.  In reality, this could not be further from the truth.  In this post, I will describe hot flashes and discuss what causes them.  In addition, I will review the most common medications employed to prevent and treat hot flashes experienced by men undergoing androgen deprivation therapy for prostate cancer.

What Is a Hot Flash?

A hot flash is a sudden overwhelming sensation of warmth usually experienced in the face, neck, upper chest and back.  This feeling is often accompanied by redness or blotching of the skin as well as heavy sweating.  This constellation of symptoms can occur to varying degrees, with some being so severe that they require a change of clothing or a shower.  Other associated symptoms can include nausea, rapid heartbeat, anxiety, and even trouble breathing.  Hot flashes can last from less than 5 minutes to over 30 minutes.  They can also occur with varying frequency, from once in a few days to several times per hour.

Why Does Androgen Deprivation Therapy Cause Hot Flashes?

Men undergoing androgen deprivation therapy (ADT) with medicines such as Lupron to treat their prostate cancer often get hot flashes.  In fact, studies have demonstrated that 60-80% of men undergoing ADT experience hot flashes at some point during treatment.  For most men, this first occurs within the first few months of treatment .  Interestingly, nearly a third of men who experience hot flashes during ADT for prostate cancer state that these symptoms are the most debilitating side effects of the treatment.  Nearly half of men experiencing hot flashes report a significant decrease in their quality of life.

Recent research has helped determine why men undergoing ADT actually experience hot flashes.  As you may remember from my previous post,  ADT fights prostate cancer by removing its food, testosterone, from the blood stream.  It turns out that testosterone, like other sex hormones, is an important regulator of the “thermostat” of the human body.  This “thermostat” is actually located in a part of the brain called the hypothalamus.  By causing a rapid drop of testosterone in the bloodstream, ADT confuses the “thermostat.”  Without its usual input from testosterone, the “thermostat” believes that the body is too hot.  As a result, the “thermostat” tries to cool the body off by making the blood vessels near the skin dilate, which allows for the release of heat on the skin surface.  This, in turn, leads to the characteristic blotching of the skin, feeling of warmth, and perspiration. 


How Do You Treat Hot Flashes?

1.     Hormonal Treatments:  As you would imagine, if a lack of hormones is the cause of hot flashes, replacing these hormones can help to treat these bothersome symptoms.  Certainly, we cannot simply replace the testosterone removed by ADT as this would defeat the purpose of the treatment: starving the prostate cancer.  However, studies have shown that other hormones, aside from testosterone, can also be used to regulate the “thermostat” and, thus, prevent hot flashes.  The first of these hormones to be tested was the female hormone, estrogen.  While estrogen did, indeed, reduce the incidence of hot flashes, it also increased the incidence of life threatening blood clots and painful breast tenderness.  As a result, estrogen has not been used as a mainstream treatment for hot flashes.  Other hormones, however, have been demonstrated to improve hot flashes while avoiding the risks of estrogen.  Two of the most popular treatments for hot flashes are derived from just such a hormone: progesterone.


A.     Megestrol Acetate – A study of 66 men undergoing ADT for prostate cancer were given either Megestrol Acetate (20 milligrams twice a day) or a placebo(sugar pill) for 4 weeks.  The study found that 79% of men receiving Megestrol Acetate reported a 50% decrease in hot flashes as opposed to only 12% of men receiving placebo pills.  The time to achieve the maximal effect of the drug was 2-3 weeks and the most common side effects were weight gain, fluid retention, and headaches.

B.     Medroxyprogesterone Acetate – A study of over 100 men undergoing ADT for prostate cancer were given Medroxyprogesterone Acetate (20 milligrams daily) for 4 weeks.  The study reported that 84% of men demonstrated a greater than 50% improvement in hot flashes while 37% enjoyed a complete resolution of hot flash symptoms.  Side effects of the medication included intestinal upset, water retention, and increased blood pressure.
    
2.     Non-Hormonal Treatments:  As more research has been carried out about hot flashes, studies have found that hormones are not the only substances in the body that control the “thermostat.”  These discoveries have provided more treatment options for men with prostate cancer suffering from hot flashes from ADT.

A.     Venlafaxine – Also known as Effexor, this drug is part of a class of antidepressant drugs known as serotonin norepinephrine reuptake inhibitors (SNRI).  The utility of this drug for treating hot flashes was discovered when postmenopausal women taking Venlafaxine for depression were found to have fewer and less intense hot flashes.  Subsequent studies confirmed the benefit of this drug in treating hot flashes in men treated with ADT.  One small study of 16 men demonstrated that taking 25 milligrams of Venlafaxine daily for 4 weeks decreased hot flashes by 50% in 63% of men.  A larger study of 97 men taking 75 milligrams of Venlafaxine daily confirmed the benefit, demonstrating a 47% decrease in hot flashes.  Of note, however, this same study demonstrated that medroxyprogesterone was more effective, reducing hot flashes by 84%.  The most common side effects of the drug are gastrointestinal in nature, including dry mouth, nausea, and decreased appetite.

B.     Gabapentin – The mechanism by which Gabapentin, a drug used to alleviate nerve pain, relieves hot flashes is unknown.  Nonetheless, a study of 350 women with hot flashes demonstrated a 46% decrease in hot flashes for women taking 900 milligrams of the drug daily versus a 15% decrease for those women taking a placebo drug.  To my knowledge, no specific study has looked at the benefits of Gabapentin for treating hot flashes in men on ADT.


3.     Alternative Therapies:  Small studies have also demonstrated that hot flashes can also be treated without taking medications at all. 

A.      Acupuncture – A very small study of 7 men with prostate cancer evaluated the effects of acupuncture on hot flashes.  The men in the study underwent 30 minutes of acupuncture treatment twice a week for 2 weeks and then once a week for 10 weeks.  The study reported that the men enjoyed a 50% reduction in hot flashes at 3 months following the final treatment.
B.      Electroacupuncture – A study of 15 postmenopausal women undergoing electroacupuncture demonstrated at least a 50% decrease in hot flashes in 73% of women as late as 6 months following the final treatment.


Take Home Message

Hot flashes are very common side effects of androgen deprivation therapy for men fighting advanced prostate cancer.  While most men reluctantly accept these debilitating symptoms and their subsequent impact on quality of life, they should not.  Numerous medications and alternative therapies are available to significantly decrease hot flashes.  While these treatments have their own side effects, they are often worth trying for men with severe hot flashes.  Of course, the various medications and treatments I have discussed in this post may not be for everyone.  Certain people have medical conditions that preclude the use of some or all of these medications.  As always, never start any medicine without first discussing it with your doctor. 


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This blog is not a medical practice and cannot provide specific medical advice. This information should never be used to replace or discount the medical advice you receive from your physician

Thursday, November 17, 2011

Androgen Deprivation Therapy For Prostate Cancer: Understanding How It Works

Approximately one third of men with prostate cancer will eventually need androgen deprivation therapy.  While this treatment was first used for advanced, metastatic prostate cancer, androgen deprivation therapy is increasingly used for other indications as well.  Many patients undergoing radiation therapy for aggressive prostate cancer are treated concurrently with androgen deprivation therapy to maximize treatment outcomes.  Men with PSA recurrence after prostatectomy are also placed on this therapy.  Despite the frequency with which androgen deprivation therapy is used, many men undergoing the treatment don’t know how it works. In this post, I will introduce androgen deprivation therapy.  Specifically, I will focus on the first line androgen deprivation therapy and how it works.

The Food of Prostate Cancer

One of the most important discoveries related to prostate cancer was that androgens serve as the fuel or food of prostate cells and prostate cancer cells.  Androgens are basically male hormones.  They are the compounds, circulating in the bloodstream, which give men their masculine features.  The most famous androgen, testosterone, is mainly produced in the testes.  Other, less potent androgens are also produced in the adrenal glands.  Once produced, testosterone and the adrenal androgens are secreted into the bloodstream and travel to the prostate.

Testosterone binds to a target on prostate cells called the androgen receptor.  By binding the androgen receptor, testosterone initiates a cascade of events that stimulates further growth and multiplication of the prostate cells.  The same occurs with prostate cancer cells which, fueled by testosterone, multiply and spread to distant sites in the body. 

Starving the Beast

The understanding that prostate cancer feeds on testosterone was perhaps the fundamental discovery in the battle against the disease.  With this understanding, the next obvious step was to try to prevent prostate cancer cells from obtaining their fuel.  The most direct way of ridding the body of testosterone is to get rid of the source: the testicles.  As a result, the first form of androgen deprivation therapy was simple surgical castration.  By surgically removing the testicles, doctors were able to dramatically and rapidly decrease the level of circulating testosterone and, in turn, significantly slow down the growth of advanced prostate cancer.  Of course, surgical castration has its downsides.  Most men are psychologically impacted by having their testicles removed and would rather avoid surgery.  As a result, the search began for a chemical means to decrease the amount of testosterone in the body.

Chemical Castration

A turning point in the treatment of prostate cancer came with the discovery that the  production of testosterone in the testicles is not constant or automatic  Rather, it is regulated.  Studies demonstrated that the presence of testosterone or estrogen (the female equivalent of testosterone) in the bloodstream have a negative effect on the production of testosterone by the testicles.  In other words, the body regulates the amount of sex hormones in the blood stream by a process of negative feedback: large amounts of circulating sex hormones actually inhibit the testicles from producing more testosterone.  Negative feedback is a useful regulatory tool that the body uses to make sure that too much of given compound is not produced or present at a given time.

The discovery of negative feedback led to the use of an estrogen-like compound called DES in treating advanced prostate cancer.  Scientists reasoned that the presence of this ingested estrogen analog in the bloodstream could provide the negative feedback to the testicles needed to stop testosterone production.  As a result, they reasoned, prostate cancer would be starved of its vital fuel.  Turns out, they were right.  The use of DES worked incredibly well in reducing the growth and extent of prostate cancer.  However, it was soon discovered that men treated with DES suffered from heart attacks and other blood clots.  As a result, DES was no longer offered for men with advanced prostate cancer.

The real breakthrough in androgen deprivation therapy came in the late 1970s when the actual mechanism behind the negative feedback regulation of  testosterone production was revealed.  At that time, it was demonstrated that the negative feedback which regulates testosterone production by the testicles is actually carried out by hormones produced in the brain.  A part of the brain called the hypothalamus produces a compound called gonadotropin releasing hormone(GNRH) which stimulates another part of the brain called the pituitary gland to produce a hormone called leutinizing hormone(LH).  LH travels from the brain through the blood stream and into the testicles to stimulate the production of testosterone. High levels of testosterone and/or estrogen circulate through the bloodstream to the brain to provide the negative feedback.  This negative feedback allowed DES (a compound very similar to estrogen) to successfully decrease testosterone production and limit the growth of prostate cancer.

Stemming from this discovery was the further understanding that the hypothalamus usually emits GNRH in spurts rather than in a continuous fashion.  As long as this hormone is released in this fashion, the pituitary gland will continue to produce LH.  In turn, the LH will then stimulate testosterone production by the testicles.  However, researchers found that if the GNRH is secreted continuously it would actually decrease LHRH by the pituitary which would then decrease the production of testosterone by the testicles.  With this discovery, modern androgen deprivation was born in the form of GNRH agonists like Leuprolide and Goserilin.  These monumental drugs, used in mainstream androgen deprivation protocols today, work by maintaining a steady, continuous flow of GNRH which serves to shut down production of LH by the pituitary and, subsequently, stops the production of testosterone by the testicles.

Several years later, this discovery of the pathway and regulation mechanisms of testosterone production led to the development of another class of drugs used in androgen deprivation.  Rather than relying on GNRH analogs that shut down the production of LHRH in the pituitary, researchers developed a compound that inactivates GNRH altogether.  These GNRH antagonists, like Abarelix and Degarelix, have some important advantages over GNRH agonist drugs.  However, due to cost issues and some important side effects, these drugs have not reached the same level of mainstream use as GNRH agonists except for certain specific indications.  I will further explore this issue in a future post.

Take Home Message

Modern androgen deprivation therapy has evolved greatly over time.  From surgical castration to GNRH agonists and antagonists, the treatment of advanced prostate cancer has become more and more refined as discoveries have shed greater light on how the food of prostate cancer is created and regulated.  Understanding this background can help men undergoing androgen deprivation therapy have a better grasp of the rationale behind the often complex twists and turns experienced during their battle against advanced prostate cancer.  In future posts, I will build upon this background to explain some limitations and pitfalls of androgen deprivation therapy as well as to describe what happens when such first-line therapy fails.


This blog is not a medical practice and cannot provide specific medical advice. This information should never be used to replace or discount the medical advice you receive from your physician