In a reaction to our paper Dr Martin Olmedo asks what factors may
explain the observed better control of illness in our self-management
group.
The self-management program in our study consisted of education,
skills training and written instructions for autonomous adaptation of
maintenance therapy with inhaled corticosteroids. As this intervention
consisted of more than one element, it is n...
In a reaction to our paper Dr Martin Olmedo asks what factors may
explain the observed better control of illness in our self-management
group.
The self-management program in our study consisted of education,
skills training and written instructions for autonomous adaptation of
maintenance therapy with inhaled corticosteroids. As this intervention
consisted of more than one element, it is not possible to clearly identify
what caused the effects. We can only speculate on that, but we have some
indications about factors that may have contributed to our findings. In a
cost-effectiveness analysis we observed that a larger proportion of
subjects took domestic house dust mite avoidance measures and there were
significantly more influenza vaccinations in the self-management group.[1]
In another secondary analysis we explored possible determinants of
resource use. Although we have reasons to believe that in this study some
relevant factors may have remained unrevealed, we concluded that subjects
that are more self-efficacious are likely to benefit most from self-
management of asthma.[2]
Our findings indicate that asthma patients may be more aware of their
own responsibilities in the management of their asthma. This may also
explain the observed better control of illness with less inhaled
corticosteroids.
We would like to stress that our study was not designed to identify
individual factors to improve asthma care. There are strong indications
that a combined approach is needed in order to improve outcomes of asthma
care.[3,4] Rearranging the organisation and delivery of asthma care into
a mode of cooperation, aiming at shared responsibilities is a more patient
centred approach. It may be the key to bridge the gap between efficacy and
effectiveness of asthma care. Our findings demonstrate that the typical
features of asthma self-management may provide the means for such mode of
cooperation. In our view the self-management program can only be
successful as a whole. It's success can best be explained by the
integrated patient-centred approach.
References
(1) Schermer TRJ, Thoonen BPA, van den Boom G, Akkermans RP, Grol RP,
Folgering HT et al. Randomized Controlled Economic Evaluation of Asthma
Self-Management in Primary Health Care. Am J Respir Crit Care Med
2002;155:1062–72.
(2) Thoonen BPA, Schermer TRJ, Fejzic Z, van Schayck CP. Determinants
of resource use in a cost-effective asthma self management program. Eur
Resp J 2002; Supplement 38:396s.
(3) Gibson PG, Coughlan J, Wilson AJ, Abramson M, Bauman A, Hensley
MJ, et al. Self-management education and regular practitioner review for
adults with asthma (Cochrane review). The Cochrane Library 2000;3.
(4) Thoonen BPA, van Weel C. Role of family physicians in
implementing asthma self-management programs. Disease Management and
Health Outcomes 2002;10:141-6.
The New Guidelines use evidence based methodology
extensively. This methodology has been developed by the Scottish
Intercollegiate Guidelines Network and is not only well respected
but has been widely applied to develop other guidelines. The
guidelines use levels of evidence, I quote “Level A is: At least one
meta analysis, systematic review, or RCT rated as 1++ and directly
applicab...
The New Guidelines use evidence based methodology
extensively. This methodology has been developed by the Scottish
Intercollegiate Guidelines Network and is not only well respected
but has been widely applied to develop other guidelines. The
guidelines use levels of evidence, I quote “Level A is: At least one
meta analysis, systematic review, or RCT rated as 1++ and directly
applicable to the target population or A body of evidence
consisting principally of studies rated as 1+ and directly applicable
to the target population and demonstrating overall consistency of
results.”
How have these principles been applied?
The section on Primary prophylaxis makes only one grade A
recommendation and this is on breast feeding. In the evidence the
authors site two main pieces of evidence which contradict each
other. The first is a systematic review and a meta-analysis
involving 8183 subjects followed for 4 years which apparently
revealed a significant protective effect of breast feeding against the
development of asthma. The second study contradicts this. The
second study is in 1246 patients and found that there was a
reduction in early life wheeze but an increase in asthma at six
years. If the question is does breast feeding protect against the
subsequent development of asthma then the answer on the given
evidence is clearly undecided and surely no evidence based
advice can be given, certainly not level A guidance. What advice
should I give to a worried mother to be if she asks me what she
can do to prevent her child developing asthma?
The section on secondary prophylaxis is also confusing. House
dust mite control measures are reviewed and no less than two
Cochrane reviews are quoted. Both reviews concluded that current
physical and chemical methods are ineffective. By the SIGN
methodology a clear recommendation could be made at grade A
level that house dust mite control measures can not be
recommended. The guidelines do not do this. The guidelines
instead use a tick box to suggest that the user can ignore the
evidence and use all the techniques for house dust mite
avoidance which have just been reviewed and shown to be
ineffective.
There are other confusing statements. There is a comment in the
section on dosing of inhaled short acting beta 2 agonists which
refers to
“>10-12 puffs per day as a marker of poorly controlled
asthma.”
Surely this is an understatement. The previous BTS
guidelines, the American Thoracic Society Guidelines and
Consensus international guidelines have used doses of greater
than 1 puff a day as a sign of poor asthma control. The inference
being that 1 or more puffs a day should lead to a stepping up of
treatment. Are the new guidelines suggesting that we step up only
when patients are using >10-12 puffs of beta 2 agonist a day?
Finally intravenous aminophylline is removed from the routine
management of acute severe asthma and replaced by
magnesium. Aminophylline will never do well in any evidence
based guidelines as the studies are old, usually underpowered
and poorly designed. The guidelines methodology permits a
“tick box”
to represent
“recommended best practice based on the clinical experience of the guideline development group”.
Why
could intravenous aminophylline not have received such a
commendation? It is hard to find a GP or consultant who can not
remember using aminophylline with good effect. Clearly this is
anecdote but is a good example of “recommended best practice
based on the clinical experience of” doctors who look after patients
with acute severe asthma. I feel very unhappy about this change
and will hesitate before recommending that our hospital adopt the
new management charts for acute severe asthma as set out in
Annex 2 of the guidelines.
I read with interest the article of Tate et al. indicating that
exhaled condensates are acidic in patients with CF and become more acidic
during exacerbations. The data show differences in mean values (with some
overlap) and the hypothesis that the airways are acidic in these patients
seems plausible. However I am concerned that the condensate measurements
cannot give a reliable estimate of airway...
I read with interest the article of Tate et al. indicating that
exhaled condensates are acidic in patients with CF and become more acidic
during exacerbations. The data show differences in mean values (with some
overlap) and the hypothesis that the airways are acidic in these patients
seems plausible. However I am concerned that the condensate measurements
cannot give a reliable estimate of airway pH. Several studies have shown
that NH4+ is the predominant solute and buffer in condensates and that
most of this is derived from NH3 generated in the mouth.[1,3]
Furthermore, NH4+ concentrations are significantly reduced in patients
with inflammatory lung disease.[2] Low pH in the condensates may
therefore reflect decreased concentrations of NH4+ in the condensate.
Condensate NH4+ concentrations are presumably determined by the efficiency
with which NH3 is exchanged in the mouth and the condenser, and not by NH3
generated in the lungs (condensate concentrations of NH4+are very low in
patients with tracheostomies). These alterations in exchange could be due
to low salivary NH4+ concentrations or alterations in respiratory flow
rates. Interpretation of condensate pH is not possible unless the
contribution of oral NH4+ is determined and objective evidence is provided
for increased concentrations of inorganic and/or organic acids in the
respiratory droplets. It remains to be shown that acidification of the
condensate in patients with inflammatory disease is due to acidification
of the airways (to a pH as low as 4.6) rather than decreased exchange of
NH3 outside the lungs. The latter mechanism would seem much less relevant
to the severity or course of CF lung disease.
References
(1) Effros R, Hoagland K, Bosbous M, Castillo D, Foss B, Dunning M,
Gare M, Lin W, Sun F. Dilution of respiratory solutes in exhaled
condensates. Am J Respir Crit Care Med 2002;165:663–669.
(2) Hunt J, Fang K, Malik R, Snyder A, Malhotra N, Platts-Mills TAE,
Gaston B. Endogenous airway acidification: implications for asthma
pathophysiology. Am J Respir Crit Care Med 2000;161:694–699
(3) Hunt J, Erwin E, Palmer L, Vaughan J, Malhotra N, Platts-Mills TAE,
Gaston B. Expression and activity of pH-regulatory glutaminase in the
human airway epithelium. Am J Respir Crit Care Med 2001;165:101–107.
We read with interest the case report “Respiratory bronchiolitis
associated
interstitial lung disease (RB-ILD): a case of an acute presentation”
published in
Thorax 2004; 59: 910–911. The case presented was of a young female, a
heavy
smoker, diagnosed as acute interstitial lung disease (ILD) based on
clinical
presentation, and respiratory bronchiolitis associated interstitial lung
disease (RBILD)
o...
We read with interest the case report “Respiratory bronchiolitis
associated
interstitial lung disease (RB-ILD): a case of an acute presentation”
published in
Thorax 2004; 59: 910–911. The case presented was of a young female, a
heavy
smoker, diagnosed as acute interstitial lung disease (ILD) based on
clinical
presentation, and respiratory bronchiolitis associated interstitial lung
disease (RBILD)
on transbronchial lung biopsy. However, we do not agree that the diagnosis
is
RB-ILD and we feel that the diagnosis appears more consistent with
desquamative
interstitial pneumonia (DIP).
DIP has been linked to RB-ILD and any discussion of R-BILD must also
include DIP. There is an overlap in clinical, radiological and
histopathological
appearances between the two entities, and RB-ILD and DIP can be considered
to be
two different spectrum of the same disease. [1,2] Both are common in
cigarette smokers
(95-100%), occur in the fourth-fifth decade, are steroid-responsive and
associated
with a good prognosis. [1] Poorly defined nodules and regions of ground-
glass
attenuation on CT are features common to both DIP and RB-ILD. [3]
Pathologically, the
features that distinguish DIP from RB-ILD are that DIP affects the lung
in a uniform
diffuse manner, and it lacks the bronchiolocentric distribution seen in RB
-ILD. In
both, there is abnormal accumulation of “pigmented” macrophages in the air
spaces;
in DIP there is an excess of these macrophages within the alveoli whereas
in RB-ILD
they are predominantly around the peribronchiolar airspaces. [2] Not
surprisingly, in
many instances an overlap in appearance is well recognized and in these
instances a
diagnosis of “smoking related ILD” has been suggested. [4]
In conclusion, we feel that the case presented is more consistent
with DIP and
not RB-ILD, as the histopathological examination showed predominance of
macrophages in the alveolar spaces. Surgical lung biopsy could have
suggested a
more definite diagnosis.
References
1. Ryu JH, Colby TV, Hartman TE, Vassallo R. Smoking related
interstitial lung
disease: a concise review. Eur Respir J 2001; 17: 122-132.
2. Travis WD, King TE jr, Bateman ED, Lynch DA, Capron F, Center D, et al. American Thoracic Society (ATS)/European Respiratory Society (ERS)
International Multidisciplinary Consensus Classification of the Idiopathic
Interstitial Pneumonias. Am J Respir Crit Care Med 2002; 165: 277–304.
3. Desai SR, Ryan SM, Colby TV. Smoking-related Interstitial Lung
Diseases:
Histopathological and Imaging Perspectives. Clinical Radiology 2003; 58:
259–268.
4. Moon J, du Bois RM, Colby TV, Hansell DM, Nicholson AG. Clinical
significance of respiratory bronchiolitis on open lung biopsy and its
relationship to smoking related interstitial lung disease. Thorax 1999;
54:
1009–1014.
We thank Dr Chanarin for his interest in the new Asthma Guideline.
We will answer the points made in the order in which he raises them.
1. The quoted studies on breast-feeding appear to be equivocal in
terms of the protective effect on asthma, but both show protection against
wheezing illness in the first years of life. The recommendation in the
guideline specifies such wheezing illne...
We thank Dr Chanarin for his interest in the new Asthma Guideline.
We will answer the points made in the order in which he raises them.
1. The quoted studies on breast-feeding appear to be equivocal in
terms of the protective effect on asthma, but both show protection against
wheezing illness in the first years of life. The recommendation in the
guideline specifies such wheezing illnesses rather than asthma and is
therefore justified. We do agree that this is a difficult area,
principally because of the problem of distinguishing asthma from the other
causes of childhood wheeze. We believe other pertinent data will be
available for the next revision of the guideline, and we will consider
whether the current recommendation should be changed or its grading
altered.
2. Dr Chanarin is wrong to accuse us of ignoring the conclusions of
the Cochrane reviews on house dust mite (HDM) avoidance. The second,
updated Cochrane report concludes that definitive evidence is still
lacking, that routine use of HDM control measures cannot be recommended,
and suggests possible benefit from “physical” methods as opposed to
“chemical”. Our paragraphs on the topic reproduce these views. Faced
with this conclusion, but knowing that patients and parents of asthmatic
children may well wish to take reasonable measures to reduce HDM exposure,
we simply listed methods which might be used by those who feel that they
wish to follow this course despite the uncertain benefits. We do not
recommend that HDM control is advocated routinely.
3. There has been little information available regarding the criteria
for moving between treatment steps (although we note with interest the
recent publication on monitoring sputum eosinophilia). The conventional
advice includes, among other things, the advice that treatment should
minimize bronchodilator requirements, and using a bronchodilator more than
once a day is often taken as indicating the need to step up. However,
this is not supported by any hard data. In the guideline, we do not
suggest 10-12 puffs a day as the correct threshold, and Dr Chanarin will
recognise that no such recommendation is made. This was simply quoted in
the text in relation to one paper which had addressed the issue of
assessing asthma control. In retrospect, we can see how this might be
taken in a different context and we will address it in the next revision.
4. Regarding intravenous Aminophylline, Dr Chanarin seems to take
the opposite stance to his position on HDM avoidance. Here he wants us to
ignore the available evidence. The papers on Aminophylline are not all
old (several of them are from the 1990s) and the Cochrane review judged
them to be of moderate quality rather than poor. We therefore have to
take note of these studies and it is difficult to recommend Aminophylline
in the face of the consistent absence of benefit which they show,
particularly when there are better alternatives. We too recognise the
power of personal experience on this issue, but feel that intravenous
Aminophylline has been justifiably down-graded.
In relation to introducing the new pieces of advice to his hospital,
we can only say to Dr Chanarin that this is simply a guideline, and we
fully understand that each doctor must take responsibility for his own
treatment strategies. However, we can assure him that these
recommendations were all given careful thought and, whilst some may prove
to be wrong, we would hope that they are not rejected without equally
careful consideration.
We thank Dr Chanarin again for the attention he has obviously given
to the document and for taking the time to feed back to us.
Dr BG Higgins
Co-Chairman
British Thoracic Society/SIGN Asthma Guideline Committee
Dr G Douglas
Co-Chairman
British Thoracic Society/SIGN Asthma Guideline Committee
We read with interest the recent paper by Ojoo et al. [1] showing
dissociation between exhaled breath condensate (EBC) pH and FENO in
patients with asthma and cystic fibrosis. We note that EBC pH was
measured without prior deaeration of the sample using argon gas, in common
with other studies [2,3]. An alternative method is to pass argon gas
through or over EBC samples in order to remove dissolved c...
We read with interest the recent paper by Ojoo et al. [1] showing
dissociation between exhaled breath condensate (EBC) pH and FENO in
patients with asthma and cystic fibrosis. We note that EBC pH was
measured without prior deaeration of the sample using argon gas, in common
with other studies [2,3]. An alternative method is to pass argon gas
through or over EBC samples in order to remove dissolved carbon dioxide [3,4,5]. Argon deaeration has been shown to be highly reproducible [4,5]. Both methods have demonstrated differences in pH between disease
and control samples [1,2,3,5], but their relative benefits have not
been established.
There is currently no consensus definition of the range of “normal”
airway pH. Defining this range is hindered by the lack of standardisation
regarding the use of argon e.g. in healthy controls, mean pH values in
studies without argon deaeration have ranged from 6.08 [1] to 7.46 [2],
and from 7.7 [4] to 8.3 [3] in studies using argon deaeration. We suggest
that standardization of EBC methodology with respect to the use of argon
is required. This will enable comparable data from different studies to be
obtained, so that the range of pH values in controls and disease can be
fully understood.
References
1. Ojoo JC, Mulrennan SA, Kastelik JA, Morice AH, Reddington.
Exhaled breath condensate pH and exhaled nitric oxide in allergic asthma
and cystic fibrosis. Thorax 2005;60:22-26.
2. Gessner C, Hammerschmidt S, Kuhn H, Seyfarth H-J, Sack U,
Engelmann L, Schauer J, Wirtz H. Exhaled breath condensate acidification
in acute lung injury. Respir Med 2003;97:1188-1194.
3. Niimi A, Nguyen LT, Usmani O, Mann B, Chung KF. Reduced pH and
chloride levels in exhaled breath condensate of patients with chronic
cough. Thorax 2004; 59: 608-612.
4. Vaughan J, Ngamtrakulpanit L, Pajewski TN, Turner R, Nguyen T-A,
Smith A, Urban P, Horn S, Gaston B, Hunt J. Exhaled breath condensate pH
is a robust and reproducible assay of airway acidity. Eur Respir J 2003;
22: 889-894.
5. Borrill ZL, Starkey C, Vestbo J, Singh D. Reproducibility of
exhaled breath condensate pH in chronic obstructive pulmonary disease.
Eur Respir J 2005; 25: 269-274.
This study of quality of life in children with asthma treated with
homeopathy is fatally flawed.[1] The Childhood Asthma Quality of Life
instrument used was validated in a study by French et al.[2] The children entered into White’s study had
scores consistent with those of normal children who don’t have asthma. For
a statistically significant improvement to occur in this score, the
treated group wo...
This study of quality of life in children with asthma treated with
homeopathy is fatally flawed.[1] The Childhood Asthma Quality of Life
instrument used was validated in a study by French et al.[2] The children entered into White’s study had
scores consistent with those of normal children who don’t have asthma. For
a statistically significant improvement to occur in this score, the
treated group would have to develop scores of around 100% ie better than
normal, non-asthmatic children. This is clearly highly unlikely. In
addition, a similar “ceiling effect” applies to the PEFR readings – again,
at entry they were 100.4% and 96.9% of expected for the verum and placebo
groups, respectively.
This is a very poor quality trial which does absolutely nothing to further
our understanding of the potential value of homeopathic treatment in
children with asthma. In fact, the press release from the journal has been
picked up by the media and used to support a headline of “Homeopathy of no
use in Asthma”.
Publishing this quality of research at best does not improve our necessary
evidence base, and, at worst, contributes to the denial of services which
may indeed be of value to patients. A close analysis of the study shows
that the treatment group had a trend to better outcomes than the placebo
group. If this were a pilot study, it would be indicating that there is
indeed a potential benefit to asthmatic children from homeopathy which
should be investigated with a proper trial of good methodological quality.
References
(1) A White, P Slade, C Hunt, A Hart, and E Ernst. Individualised homeopathy as an adjunct in the treatment of childhood asthma: a randomised placebo controlled trial. Thorax 2003; 58:317-321.
(2) French DJ, Christie MJ, Sowden AJ. The reproducibility of the childhood asthma questionnaires: measures of quality of life for children with asthma aged 4–16 years. Qual Life Res 1994;3:215–24.
I am a Respiratory Nurse Educator working daily with Maori Clients in
the Waikato, in regards to smoking cessation, and so it was with great
interest that I read the article 'Efficacy of bupropion in the indigenous
Maori population in New Zealand'. (Thorax 2005:60:120-123).
While it is encouraging to see the success rate in the study group,
it is very disappointing to see so many lost to fol...
I am a Respiratory Nurse Educator working daily with Maori Clients in
the Waikato, in regards to smoking cessation, and so it was with great
interest that I read the article 'Efficacy of bupropion in the indigenous
Maori population in New Zealand'. (Thorax 2005:60:120-123).
While it is encouraging to see the success rate in the study group,
it is very disappointing to see so many lost to follow-up: more than in my
own experience. This has meant that the twelve month figures are not
statistically significant. Long term smoking cessation is required to
effect health outcomes.
Paramount in this study was the valuable time given by Maori Nurses
working in the community, and I wonder if they were adequately reimbursed
for their efforts, or how the study impacted on their daily workloads
which are usually very demanding. Could this have contributed to the high
drop out rates perhaps?
The efficacy and clinical effectiveness of homeopathy engenders
considerable debate; it is therefore essential that clinical trials are
accurately interpreted and reported. The recent publication by White et al.[1] has highlighted this issue.
The study, assessing classical homeopathy
as an adjunctive treatment for childhood asthma concluded that, based on
the primary outcome (the active qua...
The efficacy and clinical effectiveness of homeopathy engenders
considerable debate; it is therefore essential that clinical trials are
accurately interpreted and reported. The recent publication by White et al.[1] has highlighted this issue.
The study, assessing classical homeopathy
as an adjunctive treatment for childhood asthma concluded that, based on
the primary outcome (the active quality of living subscale of the
Childhood Asthma Questionnaire) classical homeopathy was not superior to
placebo. We disagree with this conclusion. The scale used to assess the
primary outcome was inappropriate [it does not distinguish between
asthmatics and non-asthmatics [2] and is more suitable as a cross-sectional
measure rather than a longitudinal outcome; and the ability to identify
any therapeutic improvement was severely reduced due to ceiling/flooring
effects in both the primary and some secondary outcome data. For example,
baseline scores identified that the study population had good quality of
life, and that two of the three age groups studied had mild asthma.
Therefore, any therapeutic improvement would be hard to identify let alone
quantify.
Other design issues were apparent, e.g. no data was reported on
homeopathic exacerbations (an indicator of the healing response), and the
security of blinding was not assessed. Yet despite these limitations, some
encouraging therapeutic effects were apparent. For example, a clinically
relevant improvement in asthma severity (unadjusted scores) was seen in
two of the three groups and a favourable pattern in the days off
school/days attended was seen in the homeopathic treated children
(although no data was presented).
We suggest that a balanced and accurate conclusion to this data would
be that no definitive conclusions could be drawn but that further
investigation is needed. We therefore hope that the authors’ inaccurate
conclusions neither dampens future research, nor bias future systematic
reviews.[3]
References
(1) White A, Slade P, Hunt C, Hart A and Ernst E. Individualised
homeopathy as an adjunct in the treatment of childhood asthma ;a
randomised placebo controlled trial. Thorax 2003: 58:317-321.
(2) French DJ, Christie MJ, Snowden AJ. The reproducibility of the
childhood asthma questionnaires: measures of aulity of life fro children
with asthma aged 4-16 years. Quality of Life Research 1994;3:215-224.
(3) White, P, Lewith G, Berman B and Birch S. Reviews of acupuncture for
chronic neck pain : pitfalls in conduting systematic reviews. Rheumatology
2002;41:1224–1231.
It is indeed a pity that there was no comparison between continuous
aminophylline and continuous salbutamol. The authors did not make it very
clear why they did not choose this option. The conclusion that there is
some favourable outcome with aminophylline is therefore, in my opinion, too
strong for the data they present.
Another query is: Why did the authors use aminophylline, instead of
theofylline, wit...
It is indeed a pity that there was no comparison between continuous
aminophylline and continuous salbutamol. The authors did not make it very
clear why they did not choose this option. The conclusion that there is
some favourable outcome with aminophylline is therefore, in my opinion, too
strong for the data they present.
Another query is: Why did the authors use aminophylline, instead of
theofylline, with the risk of provoking an allergy to ethylenediamine?
Reference
(1) Hardy C, Schofield O, George CF: Allergy to aminophylline. Br Med J
(Clin Res Ed) 1983 Jun 25;286(6383):2051-2.
Dear Editor
In a reaction to our paper Dr Martin Olmedo asks what factors may explain the observed better control of illness in our self-management group.
The self-management program in our study consisted of education, skills training and written instructions for autonomous adaptation of maintenance therapy with inhaled corticosteroids. As this intervention consisted of more than one element, it is n...
Dear Editor
The New Guidelines use evidence based methodology extensively. This methodology has been developed by the Scottish Intercollegiate Guidelines Network and is not only well respected but has been widely applied to develop other guidelines. The guidelines use levels of evidence, I quote
“Level A is: At least one meta analysis, systematic review, or RCT rated as 1++ and directly applicab...
Dear Editor
I read with interest the article of Tate et al. indicating that exhaled condensates are acidic in patients with CF and become more acidic during exacerbations. The data show differences in mean values (with some overlap) and the hypothesis that the airways are acidic in these patients seems plausible. However I am concerned that the condensate measurements cannot give a reliable estimate of airway...
Dear Editor,
We read with interest the case report “Respiratory bronchiolitis associated interstitial lung disease (RB-ILD): a case of an acute presentation” published in Thorax 2004; 59: 910–911. The case presented was of a young female, a heavy smoker, diagnosed as acute interstitial lung disease (ILD) based on clinical presentation, and respiratory bronchiolitis associated interstitial lung disease (RBILD) o...
Dear Editor
We thank Dr Chanarin for his interest in the new Asthma Guideline. We will answer the points made in the order in which he raises them.
1. The quoted studies on breast-feeding appear to be equivocal in terms of the protective effect on asthma, but both show protection against wheezing illness in the first years of life. The recommendation in the guideline specifies such wheezing illne...
Dear Editor,
We read with interest the recent paper by Ojoo et al. [1] showing dissociation between exhaled breath condensate (EBC) pH and FENO in patients with asthma and cystic fibrosis. We note that EBC pH was measured without prior deaeration of the sample using argon gas, in common with other studies [2,3]. An alternative method is to pass argon gas through or over EBC samples in order to remove dissolved c...
Dear Editor
This study of quality of life in children with asthma treated with homeopathy is fatally flawed.[1] The Childhood Asthma Quality of Life instrument used was validated in a study by French et al.[2] The children entered into White’s study had scores consistent with those of normal children who don’t have asthma. For a statistically significant improvement to occur in this score, the treated group wo...
Dear Editor,
I am a Respiratory Nurse Educator working daily with Maori Clients in the Waikato, in regards to smoking cessation, and so it was with great interest that I read the article 'Efficacy of bupropion in the indigenous Maori population in New Zealand'. (Thorax 2005:60:120-123).
While it is encouraging to see the success rate in the study group, it is very disappointing to see so many lost to fol...
Dear Editor
The efficacy and clinical effectiveness of homeopathy engenders considerable debate; it is therefore essential that clinical trials are accurately interpreted and reported. The recent publication by White et al.[1] has highlighted this issue.
The study, assessing classical homeopathy as an adjunctive treatment for childhood asthma concluded that, based on the primary outcome (the active qua...
Dear Editor
It is indeed a pity that there was no comparison between continuous aminophylline and continuous salbutamol. The authors did not make it very clear why they did not choose this option. The conclusion that there is some favourable outcome with aminophylline is therefore, in my opinion, too strong for the data they present. Another query is: Why did the authors use aminophylline, instead of theofylline, wit...
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