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For years, doctors considered BPH to be a simple disease. The prostate was enlarged, it obstructed the bladder. The obstructing tissue was removed, and the patient got better. This simplistic approach to the disease was possible in an era when there was only one form of treatment for BPH—surgery.

However, as medical therapy has become a reality, it’s now clear that BPH is a complicated disease, involving hormones and other factors, appearing in various kinds of cells, taking many shapes, and affecting every man differentiy. In some men, BPH manifests itself mainly in glandular epithelial cells; under the microscope, their prostate tissue looks like a sponge. In other men, BPH tissue consists mainly of smooth-muscle and stromal cells, with very few glands. In some men, prostate enlargement presents itself in big lateral lobes; other men produce a middle lobe that can seal off the bladder neck like a cork in a botde. Finally, in addition to all these considerations, the response of the bladder is crucial: If the bladder’s in fairly good shape and is able to respond to the obstruction, a man is likely to respond well to any kind of drug treatment. But if the bladder muscle is stretched out and is no longer able to contract forcefully, it might be that no drug can improve urinary flow—no matter how well it relieves the obstruction.

In the not-too-distant past, when the only option was surgery, treatment was simple. By producing a “surgical strike,” and eliminating the critical tissue that was causing the obstruction, results were good—despite the causative factors, the makeup of tissue, type and degree of obstruction, configuration of the prostate, or even the bladder’s response. By removing the obstructing tissue, the bladder outiet was opened so wide that often even the weakest bladder was able to empty.

Contrast that with the current approaches to medical management of BPH: Treating patients with hormonal therapy to shrink the prostate can only be expected to work in cases when a hormonal factor plays a big role in the disease, and when the glandular tissue is primarily responsible for the obstruction.

Conversely, using smooth-muscle relaxants can only be expected to work well in men with mostly smooth-muscle tissue in their prostate, and a predominantly dynamic form of obstruction. Also, because drugs provide only modest relief of obstruction, neither approach can be expected to be very effective in men with a weak bladder muscle.

Why Diuretics Don’t Help

Diuretics work by altering the way the body metabolizes sodium; the kidneys absorb less water, so more of it leaves the body in the form of urine. For most people, diuretics mean more frequent urination and a more forceful stream. But they can be disastrous for a man with BPH. Imagine a clogged pipe. Turning on the faucet full-blast isn’t going to make the obstruction go away. Instead, the water’s just going to back up, or overflow (and, in the case of BPH, distend the bladder). The only way to get rid of the clog is to dissolve it with chemicals, or to extract it from the pipe.

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You’ll receive fluids intravenously (through your veins) the day of surgery, but you should be able to eat normal meals the next day. You’ll probably be given a stool softener or mild laxative to keep you from straining and to make the first bowel movement after surgery easier. A Foley catheter, inserted in the penis (and anchored by a tiny balloon in the bladder) during surgery, will remain in place until the bleeding has stopped. In addition to removing urine from your body, the catheter also keeps the bladder irrigated to help prevent infection or a blood clot from developing. Another catheter is inserted during surgery; this one is called a suprapubic tube because it’s placed directly in the bladder and exits through the lower abdomen. It will be taken out between three and five days after surgery. Your incision probably will have staples, not stitches, and these will be removed one week after the operation—probably on your return visit to the doctor’s office. When you get home, take it easy but don’t just sit around the house—gradually resume your usual exercise and activity. You should feel fully recovered within four to six weeks.

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Your doctor may want you to undergo further evaluation, which may include something called a “nocturnal penile tumescence test.” This is to see whether you have erections during your sleep (see above). If your doctor suspects a problem with penile blood flow, you may need to undergo pulsed Doppler evaluation. This test uses high-resolution ultrasound to evaluate the arteries’ blood supply to the penis. Another test involves the injection of smooth muscle relaxants through a small needle directly into the penis; the idea here is to see whether an erection can be produced. If this shot doesn’t cause an erection, this is a good hint that there’s a vascular problem—trouble with arterial blood flow Sometimes during this test a man develops an erection but gradually loses it; this usually signifies that there’s a problem with the veins—they’re not shutting off the blood supply, so the blood is escaping from the penis, and thus the erection is failing.

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Several years ago, an estrogen-related drug called estramustine phosphate (EMCYT) generated some enthusiasm among doctors in Europe for its ability to diminish testosterone and to kill some cancer cells. (This drug is related to the chemical weapon mustard gas used in World War I.) But more recent studies have shown that, although it uses different mechanisms to achieve its effects, it doesn’t prolong survival any longer than DES. And it can have side effects including nausea.

Therefore, we believe that among oral estrogens, DES is the way to go. It’s relatively inexpensive (far cheaper than some LHRH analogs, for instance) and it accomplishes the same goal as surgery—reducing testosterone to the castrate range.

Now, what’s the right dosage? How much DES do you need to take? This has been a source of great controversy in the medical community. Decades ago, doctors gave high-powered doses of DES—ten to twenty milligrams a day— thinking that this would not only eliminate testosterone, it might also kill cancer cells. This didn’t happen; testosterone was lowered, but that was it. Then, studies by the Veterans Administration showed that lower doses could achieve the same results. But even five milligrams a day proved to be too much. One study found that, over time, men on five milligrams of DES a day died— from heart disease caused by the estrogen, not from prostate cancer! Then doctors tried three milligrams, and then one milligram a day. And one milligram of DES a day proved sufficient to suppress testosterone without endangering the heart. A large study in Europe found that men on one milligram of DES a day showed no signs of irreversible damage to the cardiovascular system.

Other studies have proved that there is no statistical difference between the lifespans of men who were castrated and those who took one milligram of DES a day. (Some doctors argue that it takes three milligrams of DES a day to lower testosterone to the castrate range. This is true. However, if there’s no difference in the length of survival, and the heart-related side effects are fewer with one milligram than with three milligrams, what’s to be gained by taking the higher dose?)

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Radical prostatectomy may be considered in the small subset of men who initially had cancer confined to the prostate, if the local recurrence of cancer appears to be well- to moderately well-differentiated (a Gleason score of 7 or lower) and still confined within the prostate, and if the PSA level is less than 10. But even in these, the best possible candidates for prostate surgery after radiation treatment, the complications are much higher than for men who have surgery first. The risk of incontinence is as high as 25 percent, and other injuries—to delicate rectal tissue made even more fragile by radiation, for example—also are much more common.

Recently cryotherapy—freezing the prostate—has been considered as a “Plan B” for radiation with a rising PSA. But at the writing of this book, there is only preliminary information available on how often this affects the tumor, and on the complications that might accompany cryotherapy after the prostate has been irradiated.

The bottom line, for most patients who have a progressive increase in PSA after radiation therapy, is that it’s unlikely that any form of additional treatment will cure the cancer. One option is that these patients begin hormone therapy in an attempt to shrink the tumor (for a discussion of hormone therapy. Another is that they be followed closely with watchful waiting, and that they receive additional treatment only if or when they have symptoms of metastatic disease.

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