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A gene variant that plays a role in inflammation seems to protect the lungs of children with asthma as well as adults who smoke.

Researchers also found that adult smokers with this variant of the MMP12 gene had a lower risk of developing chronic obstructive pulmonary disease (COPD), a progressive condition often brought on by smoking.

“The gene seems to be protective of the lungs in both asthma and COPD,” said Dr. Norman Edelman, chief medical officer of the American Lung Association.

Any new gene identified raises the hope that it will provide ways to prevent or treat the disease to which it is allied and this is no exception.

“Levels of the MMP12 gene may impact the quality of life for those individuals with asthma and COPD, and may allow us to come up with potential therapeutic approaches,” added Jeffrey Cirillo, professor of microbial and molecular pathogenesis at Texas A&M Health Science Center College of Medicine in College Station. “By understanding more about this specific gene we can find ways to induce or oppress that protein expression in the lungs.”

“The real question is not why people who smoke get COPD. We kind of know the answer to that. The question is why do people who don’t smoke get COPD,” added Edelman. “If we understood that, we could find ways to reverse it and protect people.”

The MMP12 gene has been implicated in the development of emphysema in mice that are exposed to smoke, suggesting that the gene may also be important in the onset of emphysema in humans. The gene is also linked with other genes involved in asthma.

This information, combined with the fact that factors that can cause the onset of asthma in children are also involved with how well your lungs function in adulthood spurred investigators to undertake this study.

Dr. Juan C. Celedon, an associate professor of medicine at Brigham and Women’s Hospital and Harvard Medical School in Boston and his colleagues looked at seven different groups of people, in all comprising 8,300 children and adults.

A variant of MMP12 was associated with better lung function in children with asthma.

In adults, the variant led to better lung function in adult smokers and reduced the risk of COPD in former or current smokers.

The findings, published online Dec. 16 in the New England Journal of Medicine, also shed new light on the connections between asthma and COPD.

“This suggests that there are some genes that may influence both asthma and COPD, so that for a subgroup of people there may be common determinants,” said study senior author Celedon.

“There is certainly overlapping in that how you get asthma and how you get COPD is related and probably very closely related,” Cirillo said. “That’s exciting because it suggests that if we can decrease or increase expression of genes that are common to both, we could potentially affect both. It’s nice to have one treatment.”

All of which makes sense, Edelman said. “This gene is involved in the inflammatory process, and asthma is a disease of inflammation and COPD is a disease of inflammation,” he noted. “The results are different and the pathways are different but you’re still talking about inflammation of the lung. It’s not terribly surprising that it appears to be protective in both circumstances.”

Canadian researchers are reporting that children with asthma are more likely to develop severe cases of H1N1 flu than seasonal flu.

“Asthma has been identified as a significant risk factor for admission with pandemic H1N1 influenza, present in 21 percent to 30 percent in the larger samples,” wrote Dr. Upton Allen and fellow researchers from the Hospital for Sick Children in Toronto.

Their study was published online Nov. 19 in the Canadian Medical Association Journal.

The finding stemmed from a comparison of medical data on 58 children admitted to the Toronto hospital with H1N1 flu, sometimes called swine flu, from May 8 to July 22 this year and data on 200 children who were admitted for seasonal flu from 2004 to 2009.

Of the children treated for H1N1 flu, 22 percent had asthma, but just 6 percent of those treated for seasonal flu had asthma, the study found. Also, almost half of the children admitted to the intensive care unit to be treated for H1N1 flu had asthma.

The researchers described the prevalence of asthma as “the most striking difference” between the two groups of children, but they found other differences as well. Children with H1N1 flu were older. But children with both kinds of flu spent about the same amount of time in the hospital: four days.

None of the children with H1N1 flu died; one child with seasonal flu died, the study reported.

New research may provide the foundation for future medical treatment of memory deficits associated with Down syndrome.

The research was conducted in mice that were genetically engineered to have a condition similar to Down syndrome, a genetic disorder. It is still not clear if humans would benefit from the findings.

Still, the researchers found that mice with the syndrome-like condition could use their brains more effectively when the signaling of norepinephrine, a neurotransmitter that helps nerve cells communicate, was boosted.

“If you intervene early enough, you will be able to help kids with Down syndrome to collect and modulate information,” Dr. Ahmad Salehi, the study’s primary author, said in a news release from Stanford University Medical Center. “Theoretically, that could lead to an improvement in cognitive functions in these kids.” Salehi, a research health science specialist at the Veterans Affairs Palo Alto Health Care System, in California, was a senior scientist at Stanford when the study was conducted.

The study found that the mice did better on cognitive tests such as nest-building — in fact, as well as normal mice — after getting drugs that boosted norepinephrine levels.

“We were very surprised to see that, wow, it worked so fast,” Salehi said. The results were published in Science Translational Medicine.

The study results give “a ray of hope and optimism for the Down syndrome community for the future,” Dr. Melanie Manning, director of the Center for Down Syndrome at Lucile Packard Children’s Hospital, said in the news release.

People’s genetic makeup has been shown to affect how they respond to asthma medications, but a new study finds that many people respond well to a particular combination treatment regardless of their genes.

However, the study did find a difference in response among blacks.

The drug combo in question combines the long-acting beta-agonist salmeterol (Serevent) and moderate doses of an inhaled corticosteroid. The genes in question relate to a receptor in the body that is crucial to the effectiveness of asthma bronchodilators.

Some research has suggested that a variation in these genes can affect how people respond to the drugs. The researchers tested that theory in 87 people who had two types of the genetic variation — B16 Arg/Arg or B16 Gly/Gly.

They found that lung function did not differ overall in the groups, although there was some difference in blacks. The results are reported online Nov. 19 in The Lancet.

“These findings provide reassurance that, in the general population, patients should continue to be treated with long-acting beta-agonists plus moderate-dose inhaled corticosteroids irrespective of B16 genotype,” the researchers wrote.

However, there are still questions to be answered, particularly involving blacks’ response to salmeterol, they said.

Recent reports show that the rate of preterm deliveries continues to climb in the United States. Now, a new study suggests one reason why: Many women are confused about what constitutes a full-term birth in the first place.

About one-quarter of new mothers surveyed in the study considered a baby born at 34 to 36 weeks of gestation to be full term, while slightly more than half of women considered 37 to 38 weeks full term.

Though technically speaking, preterm births are babies born prior to 37 weeks, 39 to 40 weeks is optimal, according to the researchers.

Many women interviewed were also unaware that babies born even a little bit premature are at a higher risk of serious health problems compared to babies born at term, the new survey shows.

Misconceptions about what constitutes full gestation and how soon it’s safe to schedule an elective induction or cesarean delivery are contributing to increasing numbers of premature births in the United States, said lead study author Dr. Robert L. Goldenberg, professor of obstetrics and director of research at Drexel University College of Medicine in Philadelphia.

“Clearly, the preterm birth rate is going up, as are early deliveries that are at term but are 37 and 38 weeks,” Goldenberg said. “The data is becoming more and more clear that the outcomes of births at those earlier gestational ages are not as good as babies that are born at 39 or 40 weeks.”

The study, which included 650 first-time mothers ages 21 to 45 from around the nation who had health insurance, is in the December issue of Obstetrics & Gynecology.

When asked, “What is the earliest point in pregnancy that it is safe to deliver the baby, should there not be other medical complications requiring early delivery?”, more than half chose 34 to 36 weeks, 41 percent chose 37 to 38 weeks and less than 8 percent chose 39 to 40 weeks.

However, experts warn that any delivery short of 39 weeks puts a baby at higher risk of respiratory distress, sepsis (blood infection) and needing to be placed in the neonatal intensive care unit, according to background information in the study. Only one-quarter of new moms realized 39 to 40 weeks was safest.

Premature births are a growing problem in the United States. In fact, the percentage of babies born preterm rose by more than 20 percent from 1990 to 2006, according to a report released in November by the U.S. National Center for Health Statistics.

Technically, the World Health Organization and other major medical organizations define preterm births as babies born before 37 weeks. But that definition was developed some 50 years ago and is outdated, said Dr. Alan Fleischman, medical director for the March of Dimes.

More recently, studies have shown that babies born even a bit too early — at 37 or 38 weeks — have a greater chance of chronic respiratory disease and learning disorders than children born at 39 weeks or later.

Babies born between 34 and 37 weeks are six times more likely to die during their first week or life and three times more likely to die during their first year than babies born at 39 or 40 weeks, Fleishman added.

“Everybody knows a baby who has been born a bit early who has done pretty well,” Fleischman said. “But what we’ve learned is that, going backwards, there is increasing mortality and morbidity for every week prior to 39 weeks of gestation.”

Many experts now refer to babies born between 34 and 36 weeks as “late preterm,” while babies born at 37 and 38 weeks are “early term.”

The American College of Obstetricians and Gynecologists and the March of Dimes recommend against elective inductions or C-sections prior to 39 weeks.

In many situations, there is probably some medical reason for choosing to deliver early — perhaps the mother has slightly elevated blood pressure, for example, Goldenberg said.

“I call them semi-electives,” Goldenberg said. “I believe over the last 15 or 20 years, the practice is evolving to deliver those babies earlier and earlier when there is no evidence of benefits.”

TV shows and news reports about very premature babies that survive may also be fueling misconceptions, Goldenberg said. Some women are left with the impression that if babies born before 30 weeks can survive, infants that are just a little bit premature should have no problems.

“Because the shows don’t emphasize the bad outcomes at those ages, it’s led not only women but doctors to conclude that by the time you get up to 34, 35 or 36 weeks, everything is fine,” Goldenberg said. “But the recent research is showing it’s not fine.”

The last few weeks of gestation are critical to fetal development. All of the organs continue to mature in preparation for moving from the womb to the outside world, Fleischman explained. Between 35 and 40 weeks, the fetal brain grows by about 50 percent.

Educating expectant mothers and their physicians about the risk of preterm births may help women to make more informed decisions about when to schedule elective inductions and C-sections, Goldenberg said. That includes setting up hospital policies that discourage elective deliveries prior to 39 weeks and enforcing it through peer review to help curb the practice.

Women who get migraine headaches with aura should stop smoking and using birth control pills because they may increase their risk of stroke, researchers say.

For people who suffer migraine headaches with aura — visual disturbances before or during the migraine — the risk for ischemic stroke is doubled, they found. Being female, under 45, smoking and using oral contraceptives that contain estrogen added to the risk.

Ischemic stroke is caused by a blockage in a blood vessel. The connection between migraine and stroke was already suspected. What was unknown was the extent of risk and who is most at risk, the researchers said.

Migraine headaches affect up to 20 percent of the population. Women are up to four times more likely than men to get migraines, and as many as one third also experience an aura before or during a migraine.

“Migraine with aura is associated with a twofold increased risk for ischemic stroke compared to people without migraine, while migraine without aura does not appear to change the risk,” said lead researcher Dr. Markus Schurks, from the division of preventive medicine at Brigham and Women’s Hospital in Boston.

“But, considering the low absolute risk, there is no reason to panic, but modifiable risk factors such as smoking and oral contraceptive use should be considered,” he said.

The report is published in the Oct. 27 online edition of the British Medical Journal.

For the study, Schurks and colleagues analyzed nine studies concerning the association between migraine, with and without aura, and cardiovascular disease.

“The risk appears to be highest among women with migraine with aura who smoke and use oral contraceptives,” Schurks said.

In contrast, migraine alone does not appear to alter the risk for heart attack and death from cardiovascular disease, he added.

“In the scheme of things, aura is just one among many potential risk factors for stroke, so it is important to put this in context,” said Dr. Elizabeth Loder, chief of the division of headache and pain at Brigham and Women’s Hospital and author of an accompanying journal editorial.

“The risk of stroke for most people with migraine is low — stroke is an uncommon event — and so a doubling of that low baseline risk is not cause for alarm,” she said. “Although it’s not a reason for panic, having aura is a reason to pay extra attention to other stroke risk factors that can be modified. These include high blood pressure, high cholesterol, smoking and use of estrogen-containing contraceptives.”

Other experts agreed.

Dr. Vincent Martin, an associate professor of medicine at the University of Cincinnati, said that “we have always known that the risk of stroke increased in patients with migraine, but this clarifies the situation in terms of which groups of migrainers are at more risk.”

“If you are a female and you’ve got migraine with aura, you really need to be careful about managing your risk factors for stroke, because your risk for stroke is increased,” he said. Smoking and birth control pills just aren’t a good idea, he added.

Scientists have identified two genetic mutations that help account for the presence of recurring yeast infections in certain women.

Although the researchers focused their work on small and very specific populations with extreme conditions, the findings provide new insights into one of the most common and annoying maladies to afflict women.

“This discovery is important as a starting point for further work,” said Dr. Bart Jan Kullberg, co-author of one of two papers appearing in the Oct. 29 issue of the New England Journal of Medicine.

“It is the first proof in the area of fungal infections that subtle genetic differences exist that explain why some [apparently healthy] persons do get certain ailments, and even suffer from recurrent episodes, whereas others never acquire these infections,” said Kullberg, a professor of medicine at Radboud University in Nijmegan, the Netherlands.

Although the people studied here had extreme conditions, “you could potentially move to other mutations in the [same] gene or in this pathway to give more subtle phenotypes that we might see in everyday medicine,” said Dr. Anthony Gregg, director of maternal and fetal medicine and medical director of genetics at the University of South Carolina in Columbia.

Ultimately, researchers hope to use the findings to develop better treatments for these conditions, which become serious in some people.

“Once we understand the pathway, what we can potentially offer is therapies that take advantage of augmenting the normal pathways or utilizing redundant pathways that are working just fine but are not normally turned on to such a high degree,” Gregg said.

At this point, however, the reports really have no relevance to patients, cautioned Dr. Steven Goldstein, a professor of obstetrics and gynecology at New York University Langone Medical Center in New York City.

Yeast infections, which are typically caused by Candida albicans, arise from imbalances in the body’s internal flora, especially in the vaginal tract, although it can affect the nail beds, mouth and bloodstream.

“The vagina is a finely tuned ecosystem with almost a dozen bacteria and yeast forms, and as long as they’re in harmony, it’s comfortable,” Goldstein explained. “But if you take antibiotics, for instance, and eliminate some of the normal bacteria, then the yeast that live there all the time have a field day.”

A healthy body is able to detect the first signs of a yeast infection and dispatch immune cells to take care of the problem, but not when one of the mutations is present, explained Narendra Kumar, an assistant professor of pharmaceutical sciences at Texas A&M Health Science Center Irma Lerma Rangel College of Pharmacy in Kingsville.

“It’s like a burglary in your house,” Kumar said. “First, the alarm goes off, and here the mutation alarm does not go off properly so you don’t have the police force coming to your house. That’s how it gets colonized.”

Kullberg’s study looked at one woman and her three sisters who had recurring vaginal yeast infections.

“We discovered that her immune cells did not react normally on encounter with Candida,” Kullberg explained. “Neither she nor her sisters had any other recurrent or severe infections, which underscores that this mutation is very specific, and just affects the susceptibility to mucosal Candida infections, not to Candida bloodstream infections or to other microorganisms. This is an otherwise perfectly healthy young lady.”

The mutation was found in the dectin-1 gene.

The second study looked at 36 members of an extended Iranian family, several of whom had a predisposition to yeast infections. Three died during adolescence, two after invasive fungal infections of the brain.

This time, the mutation was found in the CARD9 gene, also involved in the immune system.

“Both studies are talking about the same sort of immunological pathways that are triggered in Candida type of infections,” Gregg said.

These findings are noteworthy, said Jeffrey Sands, a professor of biological sciences at Lehigh University in Bethlehem, Pa. “We’ve been co-evolving with fungi for millions of years, and we have these mechanisms for detecting fungal infections, maybe not wiping them out but preventing them from becoming really serious in most cases,” Sands said. “The fact that we can now identify individual genes in which there’s a mutation, that’s certainly a major advance.”