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Experts predict that one out of every two men will eventually develop lower urinary tract symptoms that require medical treatment during their lifetime. Given these numbers, finding the best treatment for the cause of these symptoms— benign prostate hyperplasia (BPH)—is an important goal.

Prostate resection, an operation in which part of the prostate is removed, has been the standard therapy for benign prostate hyperplasia for decades. In recent years, treatments based on removing prostate tissue using heat have been developed. These include microwave therapy, ultrasound, and needle ablation.

A recent study in the” Journal of Urology” compared the success of prostate resection and transurethral needle ablation in 121 men with benign prostate hyperplasia. The men were randomly assigned to receive one of the procedures, and their progress was followed for six months. In addition to several measures of symptoms, the researchers evaluated objective measures of free urinary flow and pressure flow. The study took place at seven centers around the United States.

Measured after treatment and again six months later, both procedures produced significant improvements in symptoms, quality-of-life, and free urine and pressure flow. Resection, however, produced significantly more improvement in urine flow than ablation. There were no other differences between the two groups at six months after treatment.

The researchers also wanted to know if objective measures of urinary flow can predict how well patients will respond to treatment. These measures, however, did not predict response either right after treatment or at the six-month follow-up. The researchers concluded that these tests do not help doctors decide which treatment is best for each individual patient.

Even though there was no difference in how much patient symptoms improved, resection did decrease urinary obstruction more than ablation. On the other hand, the degree of obstruction did not predict how well patients would respond to treatment. The researchers concluded that more research is needed in this area before conclusions about the “best” treatment can be made.

Until recently, there was little data about risk factors for acute urinary retention (AUR). Men with enlarged prostates seem to get it more, but that’s about all that was certain about this problem. Now, a new study published in the “Journal of Urology” sheds light on who’s most at risk for this painful condition.

Over 6,000 men from a long-term health study completed questionnaires about AUR and lower urinary tract symptoms. These men also filled out general health questionnaires every other year.

Overall, four to five men per 1,000 had acute urinary retention episodes each year during this two-year study. Chances of AUR increased with age, severity of urinary symptoms, and diagnosis of benign prostatic hyperplasia (BPH). Men with BPH who also had high symptom scores were nine times more likely to have an AUR episode than men without severe symptoms or benign prostatic hyperplasia.

About two-thirds of the men with AUR episodes had either high symptom scores or BPH, but about 20 percent of episodes occurred in “low-risk” men with no urinary problems or benign prostatic hyperplasia.

The urinary tract symptoms that made up the scale are:

Sensation of incomplete bladder emptying,
Having to void again after less than two hours,
Stopping and starting several times during voiding,
Difficulty postponing voiding,
Weak urinary stream,
Having to push or strain to begin voiding, and
Typically got up three times/night or more to void during the past month.

Having one of these symptoms more than 25 percent of the time doubled or tripled the risk for acute urinary retention, as did worsening of symptoms over a two-year period. Symptoms of urinary irritation or obstruction (incomplete emptying, urinary frequency, weak urine stream) particularly increased risk for AUR. Men taking calcium blockers, beta-blockers, or antiarrhythmic drugs were also at increased risk.

This research confirms that lower urinary tract symptoms are an important risk factor for AUR, whether measured by severity or increased frequency — a fact that has been inconclusively studied in the past. The study also confirms that acute urinary retention risk increases with age and presence of benign prostatic hyperplasia.

Results from a Phase I human study of a new treatment option for benign prostatic hyerplasia (BPH) helps men overcome problems associated with an enlarged prostate gland without the need for surgery.

BPH accounts for a variety of urinary difficulties in men over the age of 50. These symptoms typically include a need to pass urine more frequently (especially at night), an urgent need to urinate, weak or interrupted urine flow, a feeling that the bladder is not completely empty, and a delay or hesitation at the onset of urination. It is estimated that 50 percent of men over age 50 suffer from BPH.

Produced by Celsion Corporation, this exciting new therapy uses two mechanisms to overcome the problem of an enlarged prostate. First, a microwave balloon catheter system shrinks the prostate through the delivery of microwave heating. Second, simultaneous expansion of the balloon catheter compresses the walls of the urethra, enlarging the urinary opening.

Since the system is designed to relieve obstruction, it concomitantly relieves uncomfortable urinary symptoms. The procedure can be performed on a one-time, outpatient basis.

The results of the Phase I trial, conducted by researchers at the Montefiore Medical Center in New York, are reportedly encouraging. Principal investigator Dr. Arnold Melman stated that “(The) preliminary results suggest that the system, when fully tested and approved, could provide immediate symptomatic relief.” He added, “If Phase II studies are successful, I believe Celsion’s system should encourage a greater number of men with BPH to seek treatment, particularly those who suffer from milder forms of the condition.”

The company is in the midst of seeking approval from the U.S. Food and Drug Administration (FDA) for multi-site Phase II clinical studies. The studies are required to determine the safety and effectiveness of the system in benign prostatic hyperplasia patients. Pending FDA approval, Celsion plans to start Phase II studies in the summer of 1999. If the results obtained are positive, the company will then apply for premarket approval from the FDA to market the system in the United States.

Several studies in the past year have reported racial variations in the incidence of benign prostatic hyperplasia (BPH). Some have suggested that African-American men are more likely to get this condition than white Americans. Others report no differences. A new study looked at different definitions of race and BPH to try to sort it all out.

Researchers from the Harvard Medical School and Brigham and Women’s Hospital, both in Boston, examined data from the Health Professionals Follow-Up Study, a long-term study of more than 50,000 male healthcare professionals. The men were aged 40 to 70 when the study began in 1986, and have completed questionnaires and physical examinations every other year since.

Of the 31,775 men in this study, 3345 were defined as having benign prostatic hyperplasia, based on symptom reports, surgery for the condition, or diagnosis from a rectal exam.

After accounting for age, alcohol intake, smoking, weight, and other factors that affect BPH, the researchers found that black and Asian men were no more or less likely to develop benign prostatic hyperplasia than white men. They were, however, less likely to have surgery for it. The researchers also measured a number of hormones related to prostate symptoms, and again found no racial differences.

When Caucasians were split into groups, those of southern European origin were slightly more likely to have a variety of prostate problems, including BPH, than other white men, and those of Scandinavian origin were slightly less likely.

In the February issue of the Journal of Urology, the researchers explain that they used three different ways of classifying race and ethnicity to analyze the data, and the results were similar each time. They also used different combinations of benign prostatic hyperplasia symptoms, and again the results were the same.

The men in this study were well-educated professionals, the researchers point out, so they may not represent the general population of American men in health behaviors — diet, lifestyle and other factors that influence BPH. On the other hand, none of the factors measured in the study, including diet, obesity, lifestyle, vasectomy, blood pressure, or heart disease, accounted for the racial differences.

The researchers conclude that the “common contention” that black men are at higher risk, and Asian men at lower risk, than whites was not supported. They recommend further study of differences among different Caucasian groups.

If you are an older adult with recurring episodes of cough, wheezing, chest tightness, or difficulty breathing, you may have asthma. Are you surprised? There is a common misconception among health-care providers and the general public that older people are not at risk for asthma. Most people figure that it is a disease that only affects children or young adults. Actually, statistics reveal that six to 10 percent of older adults may suffer from asthma. It is a cause for serious concern in the elderly, because patterns of the disease are usually more severe and complete symptom remission is rare.

Asthma is a disease of the lung’s airways. With asthma, the airways are inflamed and react easily to certain triggers, such as viruses, smoke, or pollen. When the inflamed airways react, they become narrow and make breathing difficult.

According to the National Heart, Lung, and Blood Institute, the older adult with asthma typically experiences a more complicated course of events. Asthma severity usually ranges from moderate to severe in older adults, and age-related changes in lung structure and function tend to exacerbate asthma symptoms. This makes wheezing and acute attacks more common. Respiratory problems caused by other illnesses can also contribute to or worsen asthma. The older adult may also face medication-related difficulties. Once again, age-related physical changes make the older adult more susceptible to side effects of asthma medications. In addition, drugs used to treat a pre-existing ailment may aggravate asthma symptoms.

Asthma in the elderly is often difficult to diagnose because it can be confused with or hidden by other diseases, such as bronchitis, emphysema, or various cardiac conditions. Following a careful examination that includes a medical history, physical examination, and laboratory testing, asthma can usually be differentiated from other coexisting illnesses.

Despite these difficulties, the goals of diagnosis and treating remain the same for the older asthmatic. Education, monitoring, controlling asthma triggers, and providing appropriate drug therapy are all high priorities. Compared to younger patients, however, many older patients need to be monitored more closely.

If you have respiratory symptoms that will not go away, please consult your doctor. There are many programs in place to provide assistance and follow-up to asthma sufferers. Even though you may face greater challenges, your asthma can be managed.

A recent study concludes that viral infections may cause asthma attacks in a significant proportion of asthma patients. Researchers at the Baylor College of Medicine studied 122 asthmatics treated for acute symptoms of asthma at hospital emergency departments and 29 asthmatic adults treated at a pulmonary clinic to collect data. The study found that 55% of asthma attacks treated at emergency department were linked to respiratory tract viral infections, while 44% of attacks in asthmatic pulmonary clinic patients were associated with similar infections. Authors say the findings suggest that more effort should be placed on preventing respiratory tract viral infections among asthma patients.

Questions and Answers:

1. How can a person be sure that their asthma symptoms are caused by exposure to something at work? Are there specific tests?

There are three types of work-related asthma. The first type is related to an allergy to something in the workplace. In that case, patients note that the asthma clears up whenever they’re not at work or they’re on vacation. The second type is where there is pre-existing asthma; irritants at the work site will constantly aggravate the existing asthma, so that they always have a lot of minor attacks at work because there may be several things that bother them. The third type is irritant-induced asthma or reactive airways dysfunction syndrome (RADS), reactive airways dysfunction syndrome, which is due to a high level of exposure. In these cases, patients become immediately ill and require medical care, and they would have asthma subsequent to that.

The most common are the first two types. Testing for these would require seeing a specialist, who may do a variety of tests involving specific challenges. For instance, a doctor might do what is called a natural challenge, in which a peak flow meter is used to measure asthma attacks. A peak flow meter is routinely used by family doctors to monitor asthma. By blowing into a cylinder, the meter shows high or low numbers which represent a reliable, objective measurement of the severity of asthma. This device can easily be used at home or in the workplace. Patients can take measurements themselves using a peak flow meter for about two weeks at home, and then go back to work and do the same, to document for the physician if there are differences: this way you can tell if they are really having more asthma at work than at home. By keeping a diary of peak flow measurements, patterns can emerge: asthma may be better or worse at certain times of the day, which may also help in tracking irritants that may be exacerbating the asthma.

2. Are asthma symptoms very different in asthma with latency and asthma without latency?

Basically, asthma is asthma; symptoms are the same whether it is with or without latency. Only the initiation of attacks will be different. Asthma with latency, which is the allergy-related asthma, requires a long exposure of several months or years during which time a person develops an allergy or sensitivity to a chemical in the workplace. This is the type that gets better when the patient is away from work, on the weekends or on vacation. The other type of asthma, without latency, is the high-dose, sudden-onset asthma, which can be put down to a single exposure at one moment in time.

3. Can you explain briefly why you don’t have to be allergic to a substance to have an asthma attack?

Asthma without latency is due to an irritant. The irritant is of such high magnitude that it actually produces injury to the airways of the lung, similar to a respiratory infection or the type of injury induced by an allergic response that causes inflammation of the lungs. This inflammation persists for reasons that aren’t clear, but it is due to this persistent inflammation that they suffer from asthma.

4. Why is taking appropriate asthma medication to keep you on the job site not a good idea?

If you have the type of asthma that is irritant-induced (RADS) or if it is aggravated by some substances at work like cigarette smoke or welding fumes, medication in many cases will allow you to tolerate these exposures and be able to work. In contrast, if you are allergic to something specific, every time you’re exposed to it, your asthma worsens, and continues to increase in severity. There have been a few reports of allergic-type asthma or asthma with latency where the exposure has led to the death of a person. Once you are allergic or sensitized, it is recommended that you have no further exposure to the substance, because it can produce significant worsening and may have serious consequences. In these cases we recommend the person not return to work if the exposure can’t be avoided. This is in contrast to the irritant-type asthma, where the aggravation, even if it is acute and precipitates attacks, doesn’t severely injure the airways. Generally, this type of asthma is not specific to the workplace. In these people, medication seems to improve response to irritants and they can usually stay on the job.

For asthmatics in general, avoiding irritants is probably a good idea, as is getting appropriate medication.

A myriad of factors are implicated in causing asthma in the workplace: the nature of the job being done, the location of the work site, the degree of exposure to irritants, and what kind of materials — vapours, fumes, as well as dusts — are being inhaled, among others. Various ways of defining asthma caused by work site conditions have been proposed but a newer classification system suggests two primary types of occupational asthma, asthma with latency and asthma without latency. Asthma with latency is precipitated by prolonged exposure (the latency period) to a substance present on the work site, which eventually causes allergic sensitization. This sensitization process eventually changes the way the respiratory and immune systems react, causing asthma symptoms. Asthma without latency occurs after only a single contact with an irritant substance that produces a sudden reaction that affects the airways without an allergic component necessarily being present. This leads to a condition called reactive airways dysfunction syndrome (RADS), which keeps the airways hyperresponsive.

To date, over 200 substances have been linked to occupational asthma with a latency period. Depending on the level of exposure, these triggers lead to asthma by precipitating immune responses characterized by IgE antibodies — the same function that sets off an allergic reaction to ragweed in many people.

Sudden onset of asthma (no latency period) can take place within minutes or hours of exposure, precipitate RADS, and can continue to cause asthma symptoms for years. In most cases, this kind of onset is due to an industrial accident, or ventilation of the workplace being compromised. Documented cases of such asthma attacks were triggered by uranium hexafluoride gas, spray paint with ammonia, fumigants, metal coating remover and smoke inhalation.

By-products of industrial manufacturing are heavily implicated in causing asthma symptoms. Allergic sensitization (associated with a latency period) is commonly caused by such materials as baking products and cotton dust. How much exposure is involved plays a large role in inducing symptoms of asthma, particularly in very dusty types of work. Polyurethane processing and foundry work are notable causes of asthma; millers and bakers exposed to grain dust have an asthma prevalence of up to 40%. If more hazardous activities are added to the list — pouring chemicals, blasting, sawing — the rate goes up even more.

Where the job site is located will affect asthma rates. For instance, western red cedar causes asthma in the western U.S., where it is native, and in Japan, where dock workers are exposed to it while unloading the ships that import the wood. An epidemic of asthma was caused in Barcelona, Spain, when a shipment of soybeans was unloaded in weather conditions that allowed dust from the beans to spread, demonstrating how climate conditions also affect the rate of asthma.

What can be done to reduce the risk factors for asthma in the workplace? Obviously, the ideal solution is to stay away from the kinds of employment that trigger asthma. As this is not always possible, employers should consider adopting strategies such as ensuring proper ventilation, providing personal protective devices (masks), rotating jobs to cut down on the amount of time a worker spends in a particular environment, and enforcing safety measures that eliminate the risk of an accident, such as a chemical spill.

While symptoms may clear up once a worker is no longer exposed to the irritant, many people find that the asthma persists and leads to the chronic airflow problems (hyperresponsiveness) typical of RADS. Further, the longer the exposure, the more chronic the asthma. Once asthma is diagnosed as being occupational in nature, it is not enough to merely open more windows or take a few more puffs on a bronchodilator. A serious discussion regarding options needs to take place between patient and doctor — away from the workplace.

Questions and Answers:

1. What causes a sensitivity to a particular allergen or irritant?

There is a genetic predisposition in some individuals to become immunologically sensitized to different aeroallergens, like cat or house dust mite. The exact mechanism responsible for this genetic predisposition is unknown. It may have to do with the genetic predisposition to have inflammation of the lungs to begin with, which would make it easier for people to become sensitized and induce an immune response against things that they inhale. But this is an active area of research: while we know that the genetic predisposition is there and that it has a strong influence, we don’t know how it is linked to the sensitization process.

2. Briefly, would you explain why asthma and allergies are two distinct disorders, when they are so closely linked?

Asthma is related to inflammation in the airways of the lungs, while allergies result in inflammation of the eyes, skin or nose. Where the inflammation occurs determines whether it’s asthma or something else. Also, many people have both allergies and asthma, and the allergies can enhance the risk of having asthma. On the other hand, you can have allergies and not have a manifestation in the lungs. And you can also have asthma without having allergies. For example, for some kinds of asthma in the workplace, you can become sensitized to a chemical without a history of allergies whatsoever. Yet with repeated exposure to a chemical, you can develop this immunological response or sensitization anyway.

Asthma is such a complex — and confusing — topic because there are many different types of it: with or without allergies, as a result of airway damage from high-level exposure to a chemical, or even as a result of damage done by severe bronchitis.

3. Do pollutants cause allergies? That is, can they be allergens in the same way that house dust mite is an allergen?

This is very unlikely. The gases, the air pollutants like sulphur dioxide and ozone, can in and of themselves cause airway inflammation. But we’re not aware of anyone becoming truly allergic to any of these materials. These material are irritants, and they are much more likely to potentiate asthma in someone who already has a predisposition. For instance, many people think that they’re allergic to cigarette smoke, because every time they get exposed, they get their asthma. But for almost everyone, this is due to the irritant effect of the smoke and not to an allergy. People who have asthma are more sensitive to these irritants — sometimes exquisitely so, but it is not allergy.

4. In your paper you mention that asthma is much more prevalent among blacks than whites. Are your observations on the prevalence of cockroach allergen in the inner city relevant to this statistic?

We don’t really understand all of the epidemiology. Core inner-city people are more likely to have problems with cockroach allergy, and when you go up the social ladder between blacks and whites, the two groups do seem to have different patterns of sensitization. However, accounting for this is also complex and probably depends on factors such as location. Presumably, some years ago here in the northeastern U.S. when heating became much more expensive, people started living in more crowded conditions and had more carpeting and bedding, which increased the population of house dust mites and sensitization to them, which in turn increased the risk of asthma — which came to be seen as an inner city problem.

In a city like Atlanta, Georgia, the environment is very different from the northeast; it’s very wet and humid. The observation made about Atlanta is an interesting one, but as to why sensitization to cockroach is more prevalent there as opposed to house dust mite is still an open question.

Editorial:

This study makes it clear that the environment is a very important factor in asthma, and that different problems occur in different regions and population groups. It’s a very complicated area, in which there are no simple answers. One major aspect that we tried to present in the paper was that while the environment can be a cause of asthma, it can also be a trigger for it, independent of a causative factor. For instance, air pollution doesn’t cause asthma, as best we can tell, but you rarely get exacerbations of asthma outdoors unless you’re exercising — the air pollution worsens the existing asthma. The message here is that the environment is important both in causing and potentiating asthma.

These days, asthma and its causes are fairly well understood. Inflamed lungs, reversible airway obstruction, and hyperresponsiveness of airways are all typical symptoms of asthma. These can be triggered by a growing list of risk factors, especially from air pollutants and airborne allergens. Even so, in spite of a better grasp of the disease and improved therapy, asthma mortality is climbing. Researchers do not yet have clear answers to some important questions, including why death rates have been going up for the last 10 years, and why the incidence is higher among blacks than whites.

The environment generates countless allergens and irritants, but sorting out which ones have an impact on asthma has important implications for treatment, especially as avoidance is one therapeutic option. The authors of this paper scrutinize environmentally induced asthma from three perspectives: by examining the role of air pollutants such as sulphur dioxide, nitrogen dioxide, and airborne acids; by looking at ways of controlling airborne allergens such as cat dander and dust mite; and by exploring the possibility that interactions between air pollutants and allergens may be responsible for additional detrimental effects on respiratory health.

Air Pollution

Controlled studies show that asthmatics are particularly sensitive to sulphur dioxide. Ordinary people can inhale as much as 5.0 parts per million of sulphur dioxide and experience only slight reductions in airway function. For asthmatics, as little as five minutes of sustained exposure to sulphur dioxide at concentrations of 1.0 parts per million or less produces pronounced bronchoconstriction. Elevated levels of ozone have also been linked to increased visits to the emergency room to treat acute asthma attacks but, interestingly, normal subjects appear to be as susceptible to ozone as asthmatics. However, more studies need to be done, as few to date have compared healthy and asthmatic subjects using the same criteria.

Airborne Allergens

While we know that certain allergens can provoke an acute asthma attack (the average encounter of an asthmatic with a cat will demonstrate this effect), the role of airborne or aeroallergens and chronic asthma can’t be quantified with such assurance. However, there is increasing evidence that chronic asthma and aeroallergens are connected.

Indoor allergens are basic to asthma almost everywhere: house dust mites, mice, cockroaches and pets are common triggers. The usual advice from specialists is to remove — as much as possible — the allergen from the home environment. Studies have demonstrated that this is a very effective method if strictly controlled. For dust mites, all bedding and mattresses should be encased in impermeable covers, bedding should be washed in very hot water (over 130F), and humidity levels kept well in hand. For cat allergen, removing the animal from a household is the best solution. The allergen is produced by the salivary and sweat glands of the cat (which it then carefully washes all over its coat). Cat hairs spreading throughout the household can keep the allergen in the air for months. But as many people are reluctant to give up a cherished pet, weekly washing of the animal and rigourous cleaning and removal of allergen reservoirs such as carpets can be helpful.

Outdoor allergens depend on geography. In Europe, olive trees create seasonal allergies the same way that ragweed does in North America. In Australia, researchers compared samples of dust mite and mould spore aeroallergens in both coastal and inland cities. They found that on the damper coast, house dust mites were much more numerous, and increased the relative risk for asthma by 21 times that for the inland city. Other findings from the U.S. also show that there is a striking relationship between elevated levels of house dust mite aeroallergen and increased prevalence of asthma. This adds further credence to the theory that the level of exposure to an allergen is a determining factor in inducing asthma.

Another factor needs to be added to the mix: socioeconomic class. Researchers are increasingly recognizing that a combination of location and social class has an impact on asthma. For instance, inner city children in Atlanta, Georgia, are generally sensitive to cockroach allergens, and not to cats; however, it was precisely the other way around for their suburban counterparts. Moreover, the major allergen for the inner city poor is not house dust mite, as is common in affluent households, but cockroach. Measures to exterminate cockroaches are available, but for this population, moving to an non-infested building may be difficult.

Sometimes, it is social change that can alter asthma statistics. For instance, asthma is not very common in the Third World, but one population in New Guinea saw their asthma prevalence rise from a scant 0.1% in 1960 to 7% by 1990. In those years, the house dust mite count went up dramatically, probably due to the introduction of cloth bedding.

The Interaction Factor

Do environmental pollutants combine with airborne allergens to exacerbate asthma? While the jury is still out on this question, at least one study has shown a relationship between these two factors. Researchers asked asthmatics who were sensitive to seasonal allergies to breathe in 0.12 parts per million of ozone for one hour; they were then tested for any change in airway function. Although the ozone in itself did not seem to have an effect, the sensitivity of the patients to the inhaled allergen increased significantly, showing that a detrimental interaction was indeed at work.

Such studies highlight new areas to be probed, including analyzing the effect on airways of mixtures of pollutants and allergens in different permutations. As the authors point out, the relationship of asthma to the environment is intricate and will be difficult to clarify. However, the more information about this relationship that becomes available, the better equipped clinicians will be to offer therapeutic solutions.