Asthma drugs suppress children's growth say researchers

Corticosteroid drugs that are given by inhalers to children with asthma may suppress their growth, evidence suggests.

Two new systematic reviews published in The Cochrane Library focus on the effects of inhaled corticosteroid drugs (ICS) on growth rates.

The authors found children’s growth slowed in the first year of treatment, although the effects were minimized by using lower doses.

Inhaled corticosteroids are prescribed as first-line treatments for adults and children with persistent asthma.

They are the most effective drugs for controlling asthma and clearly reduce asthma deaths, hospital visits and the number and severity of exacerbations, and improve quality of life.

Yet, their potential effect on the growth of children is a source of worry for parents and doctors.

Worldwide, seven ICS drugs are currently available: beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone, mometasone and triamcinolone.

Ciclesonide, fluticasone and mometasone are newer and supposedly safer drugs.

The first systematic review focused on 25 trials involving 8,471 children up to 18 years old with mild to moderate persistent asthma.

These trials tested all available inhaled corticosteroids except triamcinolone and showed that, as a group, they suppressed growth rates when compared to placebos or non-steroidal drugs. 14 of the trials, involving 5,717 children, reported growth over a year.

The average growth rate, which was around 6-9 cm per year in control groups, was reduced by about 0.5 cm in treatment groups.

The researchers found that growth suppression varied across studies, and so they looked at the relationship between a variety of factors and their effects on growth. Some of the variation could be explained by the drugs used, although since this was an indirect comparison the authors say more evidence is needed.

“Conclusions about the superiority of one drug over another should be confirmed by further trials that directly compare the drugs,” said Zhang.

More long-term trials and trials comparing different doses are also needed, particularly in children with more severe asthma requiring higher doses of inhaled corticosteroids, the researchers conclude.

“Only 14% of the trials we looked at monitored growth in a systematic way for over a year. This is a matter of major concern given the importance of this topic,” said Francine Ducharme, one of the authors of both reviews and senior author of the second review, based at the Department of Paediatrics at the University of Montreal in Montreal, Canada.

“We recommend that the minimal effective dose be used in children with asthma until further data on doses becomes available. Growth should be carefully documented in all children treated with inhaled corticosteroids, as well in all future trials testing inhaled corticosteroids in children.”

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Air Quality Alert: High health risk for Canada's Northern Territories

Environment Canada has issued a high health risk warning for Yellowknife and surrounding area because of heavy smoke in the region due to forest fires. Currently 160 wildfires are burning across the region. 
 
This satellite image was collected by the Moderate Resolution Imaging Spectroradiometer (MODIS) aboard the Aqua satellite on July 20, 2014. Actively burning areas, detected by MODIS’s thermal bands, are outlined in red.

Fire danger in this area remains very high to extreme, with no discernible change in that forecast in the near future.

Source:: NASA/Goddard, Lynn Jenner with information from Canada's National Wildland Fire Situation site.

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What's third-hand smoke? Researchers say it's far more dangerous than we ever realized.

"The results indicate potentially severe, long-term consequences, particularly to children."

Have you ever walked out of a building and smelled smoke even after the smoker has moved on? Or maybe caught a whiff on someone's clothes long after their cigarette has been extinguished? That's what scientists have termed - third hand smoke, and its effects may have been greatly underestimated.

Research led by the University of York has highlighted the potential cancer risk in non-smokers – particularly young children – of tobacco smoke gases and particles deposited to surfaces and in household dust.

Until now, the risks of this kind of exposure have not been well studied or considered in public policy.

However, a new study published in the journal Environment International, has estimated for the first time the potential cancer risk by age group through non-dietary ingestion and skin exposure to third hand smoke. The results indicate potentially severe, long-term consequences, particularly to children.

The research was carried out by York’s Wolfson Atmospheric Chemistry Laboratories, the National Centre for Atmospheric Science, and the Chromatography and Environmental Applications research group at the Universitat Rovira i Virgili, Spain.

The study demonstrates for the first time the widespread presence of tobacco related carcinogens in house dust, even in ‘smoke-free’ environments.

Scientists collected dust samples from private homes occupied by both smokers and non-smokers. Using observations of house dust composition, they estimated the cancer risk by applying the most recent official toxicology information.

They found that for children aged one to six years old, the cancer risks exceeded the limit recommended by the US Environmental Protection Agency (EPA) in three quarters of smokers’ homes and two thirds of non-smokers’ homes. The maximum risk predicted from the third hand smoke levels in a smoker occupied home equated to one extra cancer case per one thousand population exposed.

Lead investigator, Dr Jacqueline Hamilton, from York’s Wolfson Atmospheric Chemistry Laboratories, said: “The risks of tobacco exposure do not end when a cigarette is extinguished. Non-smokers, especially children, are also at risk through contact with surfaces and dust contaminated with residual smoke gases and particles, the so-called third hand smoke. This risk should not be overlooked and its impact should be included in future educational programs and tobacco-related public health policies.”

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Gene discovered that could stop the spread of a common type of lung cancer

Scientists at the Salk Institute have identified a gene responsible for stopping the movement of cancer from the lungs to other parts of the body, indicating a new way to fight one of the world’s deadliest cancers.

By identifying the cause of this metastasis—which often happens quickly in lung cancer and results in a bleak survival rate—scientists are able to explain why some tumors are more prone to spreading than others. The newly discovered pathway, detailed in Molecular Cell, may also help researchers understand and treat the spread of melanoma and cervical cancers.

“Lung cancer, even when it’s discovered early, is often able to metastasize almost immediately and take hold throughout the body,” says Reuben J. Shaw, professor of molecular and cell biology and a Howard Hughes Medical Institute. “The reason behind why some tumors do that and others don’t has not been very well understood. Now, through this work, we are beginning to understand why some subsets of lung cancer are so invasive.”

Lung cancer, which also affects nonsmokers, is the leading cause of cancer-related deaths in the country (estimated to be nearly 160,000 this year). The United States spends more than $12 billion on lung cancer treatments, according to the National Cancer Institute. Nevertheless, the survival rate for lung cancer is dismal: 80 percent of patients die within five years of diagnosis largely due to the disease’s aggressive tendency to spread throughout the body.

Deviously, cancer can switch on and off their "molecular anchors" protruding from the cell membrane , preparing the cell for migration. This allows cancer cells to begin the processes to move through the bloodstream and take up residence in new organs.

In addition to different cancers being able to manipulate these anchors, it was also known that about a fifth of lung cancer cases are missing an anti-cancer gene called LKB1 (also known as STK11). Cancers missing LKB1 are often aggressive, rapidly spreading through the body. However, no one knew how LKB1 and focal adhesions were connected.

Now, the Salk team has found the connection and a new target for therapy: a little-known gene called DIXDC1. The researchers discovered that DIXDC1 receives instructions from LKB1 to go to focal adhesions and change their size and number.

When DIXDC1 is “turned on,” half a dozen or so focal adhesions grow large and sticky, anchoring cells to their spot. When DIXDC1 is blocked or inactivated, focal adhesions become small and numerous, resulting in hundreds of small “hands” that pull the cell forward in response to extracellular cues. That increased tendency to be mobile aids in the escape from, for example, the lungs and allows tumor cells to survive travel through the bloodstream and dock at organs throughout the body.

“The communication between LKB1 and DIXDC1 is responsible for a ‘stay-put’ signal in cells,” says first author and Ph.D. graduate student Jonathan Goodwin. “DIXDC1, which no one knew much about, turns out to be inhibited in cancer and metastasis.”

Tumors, Shaw and collaborators found in the new research, have two ways to turn off this “stay-put” signal. One is by inhibiting DIXDC1 directly. The other way is by deleting LKB1, which then never sends the signal to DIXDC1 to move to the focal adhesions to anchor the cell. Given this, the scientists wondered if reactivating DIXDC1 could halt a cancer’s metastasis. The team took metastatic cells, which had low levels of DIXDC1, and overexpressed the gene. The addition of DIXDC1 did indeed blunt the ability of these cells to be metastatic in vitro and in vivo.

“It was very, very surprising that this gene would be so powerful,” says Goodwin. “At the start of this study, we had no idea DIXDC1 would be involved in metastasis. There are dozens of proteins that LKB1 affects; for a single one to control so much of this phenotype was not expected.”

Right now, there is no specific treatment for cancers harboring LKB1 or DIXDC1 alterations, but those with a deletion of either gene would likely see results from cancer drugs that target the focal adhesions, says Shaw.

“The good news is that this finding predicts that patients missing either gene should be sensitive to new therapies targeting focal adhesion enzymes, which are currently being tested in early-stage clinical trials,” says Shaw, who is also a member of the Moores Cancer Center and an adjunct professor at the University of California, San Diego.

“By identifying this unexpected connection between DIXDC1 and LKB1 in certain tumors, we have expanded the potential patient population that may be good candidates for these therapies,” adds Goodwin.

Source: Press Release

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