According to lung disease experts at Johns Hopkins, there is a great need for caution by physicians in prescribing inhaled corticosteroids for patients with COPD (chronic obstructive pulmonary disease). This finding was revealed after it was found out that anti-inflammatory medications increase the risk of pneumonia by a full third.

It is presently estimated that more than 11 million Americans, most of them former or current smokers, are suffering from COPD that is characterized by the fatal and lung-diminishing conditions of emphysema and chronic bronchitis.

From News-Medical.Net:

Senior study investigator and critical care specialist Eddy Fan, M.D., says the results of the analysis should not alarm patients or cause them to stop taking their medications but should spur physicians to screen and monitor their patients to find the lowest possible steroid dose that works, especially in the elderly, people with immune system problems, and people who have had multiple bouts of pneumonia and for whom repeat bacterial infection might be a life-threatening complication.

“Inhaled corticosteroids are not of equal benefit to all, and what we are seeing is that the treatment may be more harmful and pose a greater risk of harm to some,” says Fan, an instructor at the Johns Hopkins University School of Medicine.

“Physicians really need to strongly evaluate a patient’s individual characteristics before prescribing these steroid medications, and patients, in turn, should weigh the risks and benefits of taking the drugs, despite their proven record in providing symptomatic relief,” he says.

According to pulmonologist M. Brad Drummond, M.D., M.H.S., who led the study, “catching this bacterial infection can seriously disrupt quality of life, making it harder for COPD patients to breathe and possibly leading to hospitalization.”

Fan says that COPD is expected to become the third leading cause of death in the United States by 2020, behind heart ailments and cancer and ahead of stroke.

During the study, it was advised that physicians need to exercise a higher sense of caution than what is observed by them nowadays so that inhaled corticosteroids do not pose any danger to health of their patients. For this, patients and their families need to be made aware of the pros and cons of inhaled corticosteroid trearment.

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Scientists from the Imperial College, London have claimed that they are just one the verge of finding an amicable solution to one of the most common and fatal diseases in the UK - smokers lung - in relation to difficulties in treating it with a steroid treatment. In this regard, clinical trials of a potential therapy have already begun.

Chronic Obstructive Pulmonary Disease (COPD) – chronic bronchitis and emphysema, or ‘smoker’s lung’ - is responsible for affecting approximately 6 percent of UK’s population.

From News-Medical.Net:

Steroids would normally be effective at treating inflammatory diseases such as COPD. However, COPD patients do not respond to steroid therapy. This is a major clinical problem due to the prevalence of the disease and the fact that it gets progressively worse.

Inflammation is caused by cells producing certain chemical signals. They do this by ‘switching on’ specific genes. Switching these genes off – and stopping inflammation – requires an enzyme called Histone Deacetylase 2 (HDAC2).

Professor Peter Barnes and his colleagues discovered that steroids act as a ‘molecular bridge’ to recruit HDAC2 to the appropriate genes where it can act to switch them off.

The London researchers found that in COPD, levels of HDAC2 are very low compared to normal cells, so that the steroids have no effect in switching off the activated inflammatory genes.

They then found that in lung cells in vitro, and in rats, low doses of a cheap and widely available drug raised the levels of HDAC2 and broke the steroid resistance.

The first stages of clinical trials to test low doses of this drug, theophylline, in COPD patients are now underway. If successful, this may lead to a change in the treatment of COPD and other severe inflammatory diseases that do not respond well to steroid therapy.

Professor Peter Barnes and his colleagues found that steroids act a ‘molecular bridge’ in the recruitment of HDAC2 to the concerned genes where it can possibly act to switch them off. It was further found that low doses of theophylline can raise the levels of HDAC2 and break the resistance of steroids.

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Scientists from the Imperial College, London have found the reason why lungs of smokers are resistant to steroid treatment along with finding a solution to this resistance.

Chronic Obstructive Pulmonary Disease (COPD) - ‘smoker’s lung’, or chronic bronchitis and emphysema - presently affects 6 percent population of the United Kingdom and is considered to be the fourth most common death cause in the land of the Queen.

It is seen that steroids are normally very effective in the treatment of inflammatory ailments such as COPD but some COPD patients do not respond as per expectations to steroid therapy.

From News-Medical.Net:

Professor Peter Barnes and his colleagues discovered that steroids act as a ‘molecular bridge’ to recruit HDAC2 to the appropriate genes where it can act to switch them off.

The London researchers found that in COPD, levels of HDAC2 are very low compared to normal cells, so that the steroids have no effect in switching off the activated inflammatory genes.

They then found that in lung cells in vitro, and in rats, low doses of a cheap and widely available drug raised the levels of HDAC2 and broke the steroid resistance.

The first stages of clinical trials to test low doses of this drug, theophylline, in COPD patients are now underway. If successful, this may lead to a change in the treatment of COPD and other severe inflammatory diseases that do not respond well to steroid therapy.

Professor Peter Barnes commented, ‘COPD kills tens of thousands of people in the UK every year and currently we can only treat the symptoms, not the underlying problem of inflammation of the lungs. Our work has finally provided an explanation for steroid resistance in COPD, and has allowed us to identify ways to combat this.

Professor Peter Barnes and his colleagues found out that steroid are effective in playing an active role for acting as a molecular bridge in the recruitment of Histone Deacetylase 2 (HDAC2), an enzyme, to the relevant genes where it can switch them off.

They also discovered that levels of HDAC2 were very low compared to normal cells in the COPD patients. This means that the steroids are no longer potent enough to have any effect in switching off the activated inflammatory genes. In this direction, a new steroid has been found that can raise the levels of HDAC2 and break the resistance of steroids.

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Tags: chronic bronchitis, chronic obstructive pulmonary disease, COPD, emphysema, smoker’s lung, steroid therapy, steroid treatment, steroids

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