Inhaledsteroids in COPD? Not in Mybook!-Juniper publishers
JUNIPER PUBLISHERS-OPEN ACCESS INTERNATIONAL JOURNAL OF PULMONARY & RESPIRATORY SCIENCES
Perspective
Chronic Obstructive Pulmonary Disease COPD, is
currently the fourth leading cause of death in the world, but projected
to be the 3rd leading cause by 2020. More than 3 million people died of
COPD in 2012, accounting for 6% of all deaths worldwide. COPD represents
an important public health challenge that is both preventable and
treatable, if not curable [1]. Characteristically, bronchitis
andemphysema are both present in most patients. Smoking cessation is by
far the most effective intervention in COPD resulting in better health
status, less exacerbations and improved survival [2]. Physical exercise,
especially when in the shape of multidisciplinary rehabilitation also
has significant effects [3].
Inhaled bronchodilators improve air flow and hyper
inflation, reduce symptoms and exacerbation frequency and improve health
status and quality of life [4]. In patients with frequent exacerbations
inhaled steroids are advised, although the actual effects of these ICS
in COPD are still under debate [5]. They appear to be less effective
when added to adequate doses of two types of long acting bronchodilators
[6] and can be stopped without increased of exacerbations in many of
these patients [7]. Also, ICS were found to increase the risk of
pneumonia [8].
The evidence for the effects of ICS in COPD comes
from a number of large randomised trials. Typically, these trials have
included huge numbers of patients with a diagnosis of COPD, usually
based on spirometry findings that fit with such diagnosis. Attempts are
made to exclude patients with asthma. However, there are reasons to
believe that succesful exclusion of asthma is not always achieved as in
many of these studies out comes vary substantially between study
subjects, sometimes even to the extent that lung function appears to
have normalised altogether. These patients had better not been included
in the trial, by putting more effort into excluding these so-called
steroid responders using appropriate history-taking. Unfortunately, in
many trials this is not done adequately. “Current asthmatiçs” may be
excluded, or “patients with a history of asthma”, but what may very well
point at asthma is often over looked. “Childhood bronchitis”,
persistent airflow limitation in never-smokers, atopy, subjects with a
family history of asthma or atopy should better be excluded as well when
studying effects of ICS in COPD.
Some believe that steroids responders can be
identified, e.g. with measuring eosinophils in sputum. However, if this
is done in post-hoc analyses of the studies with contaminated cohorts
the problem is likely to persist [9].
Some believe that steroids responders can be
identified, e.g. with measuring eosinophils in sputum. However, if this
is done in post-hoc analyses of the studies with contaminated cohorts
the problem is likely to persist [9].
Another means is to reassess all these landmark
studies on ICS in COPD by eliminating real responders after 3-6 months
of treatment and studying the effects of ICS in the remaining
“non-responders”. One might argue that it would be unfair to study the
effects of anygiven drug in non-responders, but my point is, that many
of the early responders may not have had COPD in the first place, or
that the diagnosis should be discarded in patients with asthma-like
responses or even normalization of the lung function. The latter is
likelyto have been the case in a substantial number of patients, given
the wide range of responses seen in many of these trials.
I challenge the companies that have these data on file to share the outcomes of such additional analyses with us!
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