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There have been many advances in treatment for HIV infection and in our understanding of how the virus works over the past fifteen years, but unfortunately no cure is anticipated in the near future. Since 1985, drugs have been available to prolong the interval that a person with HIV infection can live without developing AIDS and its related illnesses. These medications have also been shown to delay death from AIDS.

In the past two years, newer medications, called protease inhibitors, have offered additional hope for people infected with HIV to live longer and healthier lives. The protease inhibitors (in combination with the older medications) are being tested to see if treatment early in the course of the infection will prevent the virus from gaining a foothold in the body after exposure. In the future these medications may offer an opportunity to treat newly exposed persons and prevent them from becoming infected. This strategy has been employed in persons who were exposed to infection in a health care setting, and it may also be an option for people exposed in other ways.

All of these medications are very expensive and have side effects. Their cost poses a serious problem for many people, although several of the manufacturers in the United States have instituted programs to offer these medications at lower cost to those who need them and cannot afford them. Unfortunately, in developing areas of the world, where poverty is a way of life for many and the number of HIV-infected people is escalating rapidly, there is no hope that these medications will be available to the masses infected with HIV. Therefore the enthusiasm generated by the development of such new medications must be tempered by the realization that the majority of people in the world infected with HIV will not be able to use them because of their cost. In addition, studies are continuing to determine if resistance to these newer medications will diminish their effectiveness over time, as it has with some of the older medications.

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Many people are surprised to learn that most of those who are infected with hepatitis B do not manifest any symptoms. In fact, only about one-third of those who show evidence of past infection with hepatitis B on blood testing recall ever having had the disease. Older people and those in poor health generally have a higher risk of becoming sicker with infection.

Symptoms, if they do occur, usually arise within one to four months after infection, most often within about two months. Symptoms can occur sooner (if a person was exposed to a large amount of virus at infection) or later (if a person received immune globulin soon after being infected). (Immune globulin, described in more detail shortly, is an injection that provides some protection against acquiring the infection after someone has been exposed.)

Before they become sick with the more classic symptoms of hepatitis, about 15-20 percent of those infected develop joint aches and a flat to slightly raised rash that may itch. This occurs as the body is developing an immune response to the infection and is a result of the large quantity of antibody produced. An infected person may next develop jaundice (yellowing of the skin), abdominal pain, nausea and vomiting, lightening of the color of the stools to a so-called clay color, and darkening of the urine to a brownish color.

These symptoms, which can be severe, usually last about one to two months. A small percentage of infected people go on to develop what is called fulminant hepatitis, with severe liver damage that can lead to death. About 1 percent of people who develop symptoms of acute hepatitis progress to liver failure, and about 75 percent of them die from this severe illness. Remember, however, that most people do not show any symptoms that they have even been infected.

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Which medication is chosen depends on the woman and her situation. She and her health care provider should discuss the treatment options, including a thorough discussion of the risks and benefits of each choice. Women who are pregnant are usually treated with lower dosages than nonpregnant women.

All medications have potential side effects. Topical creams generally have fewer side effects than oral medications. Metronidazole pills, for example, should not be taken with alcohol, since the combination can cause severe nausea and vomiting. If a woman will be consuming alcohol during her treatment, then topical treatment with either metronidazole gel or clindamycin cream is the preferred course. Metronidazole pills can also cause stomach upset and a metallic taste in the mouth. Clindamycin pills rarely cause a severe form of diarrhea called pseudomembranous colitis. In addition, clindamycin cream may weaken condoms and diaphragms made of latex.

Even with treatment of BV and the relief of symptoms, recurrences can occur, and treatment with an alternative medication is usually recommended if this happens. Women who have had BV once tend to have recurrences, and relapses way to help answer this question.

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We’ve said that it’s impossible to predict the course of prostate cancer. This dilemma is at the heart of the treatment debate. However, some research has shown that the volume of a prostate tumor has a lot to do with its behavior. Scientists who studied 100 radical prostatectomy specimens (tissue removed in surgery) found that the volume of cancer corresponded with the extent (or lack) of cell differentiation, with capsular penetration (cancer that has reached beyond the prostate wall), invasion of the seminal vesicles, and metastases to distant tissue. These researchers showed that tumors less than 1 cubic centimeter (just smaller than a half-inch) rarely metastasize, and that most tumors less than 3.5 cubic centimeters stay inside the prostate. But as a tumor gets bigger, they found, it tends to get more aggressive—and when prostate cancer is bigger than 5 cubic centimeters, its chances of being curable dwindle.

This is how prostate cancer spreads: First, of course, it grows inside the prostate. Most—about 72 percent of cancers—begin in the peripheral zone, 20 percent start in the transition zone, and 8 percent originate in the central zone. (For a look at the prostate’s zones, see figure 1.8.) It reaches, and then penetrates, the prostate wall (also called the capsule). Then it continues to creep, reaching into the seminal vesicles, bladder, urethra and pelvic sidewalls. It also can expand in leaps, by metastases—invading the lymph system (channels that run throughout the body) or hitching a ride to far-off sites via the bloodstream to bone. When doctors speak of “distant metastases” of prostate cancer, they generally mean it has reached the lymph nodes, bone—the spine, ribs, or pelvic bones—or the lungs.

As prostate tumors grow, they become more heterogeneous, or poorly differentiated. Prostate cancer generally is a slow grower; in its early stages, it can take longer than four years for a tumor to double in size. Before a tumor even gets big enough for a doctor to feel—about one cubic centimeter in volume— it has to double at least thirty times. But after this, it only takes about ten more doublings for prostate cancer to become fatal—when it reaches 1 kilogram in volume.

Once again, to hammer home a point, this time of silent early growth is the ideal time to detect and strike prostate cancer.

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The prostate is a complicated organ. In part, it is a storehouse for a series of tiny, spongy glands; the minilobes that make up these glands form fifteen to thirty secretory ducts, which empty their contents into the urethra. Buried in its fibromuscular tissue are alveoli, cul-de-sacs lined with a forest of tall, column-shaped secretory cells that drain into the urethra via a system of branching ducts and tubes.

The ingredients of the prostate’s secretions, in a clear, mildly acidic fluid, are many and varied: They include citric acid, acid phosphatase, spermine, potassium, calcium and zinc. The prostate is regulated by sex hormones called androgens, which come from the testes. Foremost among these is testosterone, produced in the testes but controlled by a hormone from the pituitary gland, called luteinizing hormone. Testosterone, released from the testes, circulates in the blood. It enters cells in the prostate by diffusion, like water through a tea bag, and soon is transformed into another chemical called dihy-drotestosterone (DHT). DHT hooks up chemically with a specific protein, moves to the cellular seat of power—the nucleus—and quickly becomes a powerful force in the transmission of genetic information from prostate cells.

Some components of prostatic secretions may serve to protect the urinary tract and reproductive system from harmful substances in the body that may enter the urethra (see “What Is Semen?“). Perhaps most significant among these is prostate-specific antigen (PSA), an enzyme detectable by a blood test. In recent years, the PSA test has become a crucial addition to medicine’s arsenal for detecting, and thus treating, prostate cancer and BPH.

For all we know about prostatic secretions, their exact role in sexual function is still an enigma. And, problems in the prostate, unlike those in most bodily systems, don’t manifest themselves with symptoms easily traceable to prostate function. Urinary trouble generally is the first sign that something’s not right in the prostate.

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