Dear Doctor: I'm a middle-aged woman on blood pressure medication, but recently heard that one type of this medication could raise the risk of pancreatic cancer. What type is that, and if it's mine, should I change?

Dear Reader: It's scary to think that a medication to improve your health could also cause disease. So let's take a closer look at the recent data from the Women's Health Initiative on the possible link between blood pressure medications and pancreatic cancer.

In the study, 145,551 postmenopausal women, ages 50 to 79, were asked about their use of anti-hypertensive medications. The women were followed on average for about 13.8 years, and 841 cases of pancreatic cancer were noted in that time. Women who had ever used calcium channel blockers (CCBs) for high blood pressure had a 33 percent increased risk of the cancer compared to those who had never used the drugs. Those who had used the drugs for three years or more had a 48 percent increased risk of pancreatic cancer compared to those who never used them.

Calcium channel blockers have been around for many years, with most of those used in the past being the short-acting variety. The authors found that women who had ever used the short-acting type had a 66 percent increased risk of pancreatic cancer, and those who had used them for three or more years had a 107 percent increased risk -- both as compared to women who had never used the drugs.

Keep in mind that most CCBs given today are the extended-release variety. When the authors looked at the extended-release CCBs, they found no association with pancreatic cancer. Nor did they find an association with any other medication for high blood pressure. At the time of this writing, the full article about the findings was not yet available, so it is difficult to know if confounding factors were involved, but the authors did say that they adjusted for obesity, diabetes, smoking and age.

The traditional short-acting CCBs are verapamil, diltiazem and nifedipine. As for why they might increase the risk of pancreatic cancer, chronic inflammation may play a role. The authors theorized that CCBs may block the release of a receptor needed to counter inflammation. In fact, in the 489 pancreatic cancer patients in whom levels of the receptor were measured, CCBs reduced the level of the receptor, thereby theoretically increasing the rate of pancreatic cancer.

While the preliminary data are concerning, they're not wholly definitive. If you're taking the short-acting verapamil, diltiazem or nifedipine, I would consider switching to an extended-release form of this medication. Although long-acting CCBs have not been associated with risk, you could also consider changing to an entirely different class of medication, such as an ACE inhibitor, an angiotensin receptor blocker, an alpha blocker, a diuretic or a beta blocker. Your doctor is the best person to decide which is the most appropriate choice.

And please note: The data was taken from postmenopausal women, so it may not be applicable to women who have not gone through menopause or to men.

(Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095. Owing to the volume of mail, personal replies cannot be provided.)

Dear Doctor: I read that scientists are close to being able to "turn off" inflammation. What does that mean? And isn't that dangerous, since inflammation is a natural part of the immune system?

Dear Reader: The body's inflammation reaction is a double-edged sword. Most of the time we're grateful for the array of specialized white blood cells that rally to our defense. First to the scene of injury, illness and infection, they're specialists in detecting bacteria, viruses and other harmful organisms. They not only emit chemicals that destroy harmful invaders, they also cart away debris and rally the rest of the immune system to mount a robust response.

That's all great when things are working properly. But sometimes the body's inflammation response goes haywire. The same white blood cells that race to the rescue can be triggered by a case of mistaken identity and attack the body's own tissues. That's what's happening in autoimmune diseases like lupus, Crohn's disease or rheumatoid arthritis.

Certain conditions, like obesity, can rev up the inflammation process as well. That's because fat cells produce a class of small proteins known as cytokines, which are the same biochemicals that our white blood cells produce when they're on the attack. Those cytokines act as a 911 call to a host of other immune system cells, and thus encourage a state of ongoing inflammation. In addition to the autoimmune disorders we mentioned earlier, chronic inflammation has been linked to heart disease and certain cancers. And studies suggest that inflammation may have a hand in some diseases of the central nervous system as well.

All of which brings us back to the recent research that (we suspect) prompted your question. Among the cells that get involved in that initial immune response are white blood cells known as macrophages, which circulate throughout the tissues of the body. Now, a team of scientists from the United States, Ireland and the United Kingdom has identified a metabolic process that's able to get macrophages to stand down.

It turns out that a molecule known as itaconate, which is derived from glucose, acts as an "off" switch for macrophages. In a study published recently in the journal Nature, the researchers reported that the macrophages themselves can be instructed to make itaconate from glucose molecules. The presence of itaconate blocks the cascade of biochemical processes that add up to inflammation.

Specifically, a derivative of itaconate that can move in and out of the walls of our cells can actually decrease the production of cytokines, those small signaling proteins we were talking about earlier. The ability to control how macrophages produce and disperse cytokines would mean that certain types of inflammation could be controlled, or even stopped. The fact that it appears cytokines play a role in pain adds another intriguing layer of possibility to this discovery.

But before we celebrate the end of random inflammation, it's important to understand that at this point, the research has focused on mouse and human cells. The leap between the petri dish and the release of a targeted medication to control inflammation is a huge one.

(Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095. Owing to the volume of mail, personal replies cannot be provided.)

Dear Doctor: About 15 years ago, while giving blood, I was advised of an irregularity, which my doctor confirmed after an EKG, known as premature ventricular contractions. He told me not to worry, and I've not had any problems. Now I'm 79 and still in good health, but my current doctor had me wear a heart monitor and has now referred me to a cardiologist. Should I be concerned?

Dear Reader: Premature ventricular contractions (PVCs) are very common. In healthy people without any evidence of heart disease, 50-54 percent will be found to have some degree of PVCs when monitored for 24 hours. Here are the basics: Electrical impulses normally begin in the atria of the heart before they make their way down to the ventricles. This leads to the atria contracting first, followed by the ventricles. However, PVCs are ventricular contractions that bypass the atrial beat, leading to an extra heartbeat.

PVCs are more common in men than in women, increase in frequency with age and are more common in African-Americans. Lastly, they are more common in people with structural heart disease, especially those with congestive heart failure and those who have had heart attacks.

Most PVCs are not felt. It sounds as if you weren't having symptoms from the PVCs, but rather that they were simply noted on examination by your doctor. When patients feel PVCs, they often describe a sensation of a pause or a skipped beat. People also sometimes feel that the heart is beating hard or fast or that they have a strong pulsation in the neck. Sometimes PVCs can cause lightheadedness and anxiety. Very frequent PVCs have been associated with heart failure.

Sometimes, concerns about PVCs are related to their frequency, especially if they were sporadic and then become more numerous. Increased frequency of PVCs has been associated with an increase in mortality. This was illustrated in a 2006 study of 15,070 patients ages 45 to 64 who had no history of heart disease and who had a two-minute electrocardiogram performed. Those with one or more PVCs on the electrocardiogram had twice the likelihood of dying of coronary heart disease.

Similarly, a 2007 study of 45,402 veterans showed that 3.8 percent of the veterans studied had PVCs on a routine electrocardiogram -- and that the PVCs were associated with a nearly twofold increase in mortality. Note that routine electrocardiograms only last for 10 seconds, so detecting a PVC on an electrocardiogram suggests a very high frequency over a 24-hour period.

Studies over a 24-hour period have also shown that more frequent PVCs -- recorded in this way -- are also linked to an increased risk of heart failure and heart-related deaths, but the risk is greater when a PVC is seen on a routine electrocardiogram.

The heart monitor that your doctor recommended should pick up the number of PVCs over a 24-hour period. If the PVCs are frequent, the cardiologist may want to do other studies, like an echocardiogram, to determine whether there is any structural damage to the heart.

Treatment of PVCs for people with symptoms include calcium channel blockers and beta blockers. If these don't help control symptoms or if there is structural heart disease, anti-arrhythmic medication or electrical destruction of the area of heart that is causing PVCs may be necessary.

I would have some degree of concern regarding PVCs, but the results of the 24-hour monitor and your visit to the cardiologist will provide more information.

(Send your questions to askthedoctors@mednet.ucla.edu, or write: Ask the Doctors, c/o Media Relations, UCLA Health, 924 Westwood Blvd., Suite 350, Los Angeles, CA, 90095. Owing to the volume of mail, personal replies cannot be provided.)