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I read with interest the paper by Alfageme and colleagues (1) who
investigated the efficacy of anti-pneumococcal vaccination in patients
with COPD. To have new data in an area which has suffered from a surfeit
of meta-analysis and even analysis of the meta-analysis is good and their
results are quite clear. Although they do not specifically comment I
presume that their primary end point was accum...
I read with interest the paper by Alfageme and colleagues (1) who
investigated the efficacy of anti-pneumococcal vaccination in patients
with COPD. To have new data in an area which has suffered from a surfeit
of meta-analysis and even analysis of the meta-analysis is good and their
results are quite clear. Although they do not specifically comment I
presume that their primary end point was accumulative proportion of
patients without pneumonia during the follow up period. There is no
significant effect. Unfortunately, this clear result is then muddied by
data dredging. Small subgroups of patients, those under 65 and those with
severe COPD are extracted from the data and unsurprisingly are found to be
significantly improved. The reliability of this reanalysis is at best
dubious and probably should be reserved for building hypotheses to be
tested in subsequent studies.
Where then does this leave the costly vaccination programme
recommended by NICE? It should be urgently reconsidered, particularly as
the reanalysis produced by Alfageme and colleagues suggest that the
patients targeted by this programme, those over 65 years of age, may
actually be harmed with 14% greater incidence of pneumonia in the active
treatment group. Whilst statistically insignificant how can the national
guidelines, which are supposed to be evidence based, fly in the face of
such new evidence?
PROFESSOR ALYN H MORICE
Professor of Respiratory Medicine
Head of Division of Academic Medicine
References
1. Alfageme I, Vazquez R, Reyes N, et al. Clinical efficacy of anti-
pneumococcal vaccination in patients with COPD. Thorax 2006;61:189-195.
We appreciate the comments made by Prof. Quanjer concerning our
manuscript (1) and fully agree with his comments. In his letter to the
editor Prof. Quanjer gives valuable background information to the reasons
why pulmonary function tests are relatively insensitive to track pulmonary
changes in the longitudinal follow up of cystic fibrosis (CF) lung disease
(2). We agree with his arguments that this is...
We appreciate the comments made by Prof. Quanjer concerning our
manuscript (1) and fully agree with his comments. In his letter to the
editor Prof. Quanjer gives valuable background information to the reasons
why pulmonary function tests are relatively insensitive to track pulmonary
changes in the longitudinal follow up of cystic fibrosis (CF) lung disease
(2). We agree with his arguments that this is in part related to the use
of cross-sectional reference equations which do not adequately describe
longitudinal lung growth of individuals. For the clinical management of
our patients we routinely track for each patient the longitudinal pattern
of the lung function expressed in percent predicted. The patterns of the
individual curves are most often highly variable. This in part related to
the arguments given by Prof. Quanjer and in part this is disease related.
Unfortunately, these two important influences can not be untangled.
The data acquired in the cohort study were collected not as part of a
prospective study but as routine follow up of the patients (1). Hence, no
healthy control group was included in this study. We agree that ideally in
clinical intervention studies a healthy control group should be included.
Clearly such approach is likely to reduce the noise related to the use of
lung function parameters. However, we think that the use of such a control
group will only partially solve the problems discussed by Prof. Quanjer. A
good example of such a study is the Pulmozyme Early Intervention Study of
two years duration (3). In this study only children of ten years or
younger were included. Lung function behavior was heretic for both the
intervention as for the placebo group and could not be fitted into a
statistical model. Whether the inclusion of a third healthy control group
would have resolved these statistical problems is questionable.
The arguments given by Prof. Quanjer underline the difficulty of
using lung function as the key parameter to monitor lung disease in CF and
strengthens our view that computed tomography (CT) is a more suitable
tool to monitor the progression of lung disease of CF patients. The most
important structural changes observed on CT in the CF cohort were
bronchiectasis and mucus plugging both of which are not present in the
healthy population independent of age.
Sincerely,
Pim A de Jong MD PhD
Harm AWM Tiddens MD PhD
References
1. de Jong PA, Lindblad A, Rubin L, Hop WC, de Jongste JC, Brink M, et al.
Progression of lung disease on computed tomography and pulmonary function
tests in children and adults with cystic fibrosis. Thorax 2006;61(1):80-5.
2. Brody AS, Tiddens HA, Castile RG, Coxson HO, de Jong PA, Goldin J, et
al. Computed tomography in the evaluation of cystic fibrosis lung disease.
Am J Respir Crit Care Med 2005;172(10):1246-52.
3. Quan JM, Tiddens HA, Sy JP, McKenzie SG, Montgomery MD, Robinson PJ, et
al. A two-year randomized, placebo-controlled trial of dornase alfa in
young patients with cystic fibrosis with mild lung function abnormalities.
J Pediatr 2001;139(6):813-20.
We would like to comment to the limitations of the Christopher-study
(JAMA 2006;295) mentioned by Dr. Bari. He states that “the limitations of
this study include the use of two different kinds of CT scanner (multi-
detector and single-detector) with potentially different pick up rates”.
The other limitation stated is: “the prevalence of PE of 23.2% in the
‘clinically unlikely PE and abnormal D-dimer’...
We would like to comment to the limitations of the Christopher-study
(JAMA 2006;295) mentioned by Dr. Bari. He states that “the limitations of
this study include the use of two different kinds of CT scanner (multi-
detector and single-detector) with potentially different pick up rates”.
The other limitation stated is: “the prevalence of PE of 23.2% in the
‘clinically unlikely PE and abnormal D-dimer’ group shows that a clinical
scoring system alone is inadequate”.
It is commonly suggested that multi-detector row CT is more likely to
detect subsegmental PE in comparison to single-detector row CT. However,
whether subsegmental PE is clinically relevant and needs to be treated
with anticoagulants is uncertain(Eyer, Am J Roentgenol 2005;184, Goodman,
Radiology 2005;234). Because we used multi-detector row CT, there’s a
potential for overdiagnosis of subsegmental PE that are not clinically
important. The limitation of our study was that patients did not undergo
confirmatory pulmonary angiography and thus, our study design did not
permit assessing the rate of false-positive CT-scans. Because only 10% of
patients underwent single-detector row CT, a meaningful comparison of both
techniques was not possible. However, as we have mentioned in the
discussion section, the prevalence of PE in our study (20%) compares well
with the prevalence of PE in a previous study (24%, van Strijen, Ann Int
Med 2003;138) that used solely single-detector row CT and does not support
a concern that multi-detector row CT leads to a high number of
overdiagnosis of subsegmental PE.
Concerning the other limitation mentioned by Bari, we think that a
clinical scoring system is not designed to adequately diagnose PE, but to
categorize patients into groups with low and high risks of PE. The
clinical scoring system we used, showed that patients categorized as ‘PE
unlikely’ can be safely left untreated if the D-dimer test is normal. In
this way, we were able to prevent performing a CT-scan to exclude PE in
32% of our study population.
We congratulate Elkington and Friedland on their excellent review
which gives an overview of matrix metalloproteinases (MMPs) in various
destructive pulmonary diseases.[1] MMPs and neutrophil elastase do indeed
play instrumental roles in the development of ARDS and lung injury
following cardiopulmonary bypass (CPB), however, the mechanisms presented
may be too simplified.[2]
We congratulate Elkington and Friedland on their excellent review
which gives an overview of matrix metalloproteinases (MMPs) in various
destructive pulmonary diseases.[1] MMPs and neutrophil elastase do indeed
play instrumental roles in the development of ARDS and lung injury
following cardiopulmonary bypass (CPB), however, the mechanisms presented
may be too simplified.[2]
Apart from the artificial circuits, CPB intrinsically encompasses
many other factors such as global cardiopulmonary ischaemia-reperfusion,
hypothermia, heparin-protamine dosage, interrupted lung ventilation and
pulmonary artery perfusion, and non-pulsatile flow.[3] It is presumed
that each of these factors may play an individual role in the inflammatory
cascade and ARDS phenomena associated with cardiac operations. Moreover,
their combined effects could even be synergistic in influencing the
clinical outcome. Classically, CPB causes pulmonary neutrophil activation
and sequestration, which subsequently result in the release of
inflammatory mediators including neutrophil elastase, MMPs, and superoxide
species. These mediators are responsible for direct pneumocyte and
basement membrane injury.[2]
More recently, studies have shown the
important role of ischaemia and reperfusion during CPB in the development
of lung necrosis, apoptosis and pulmonary dysfunction.[4] MMPs and
neutrophil elastase contribute at least in part to the process of lung
apoptosis, nevertheless, pulmonary ischaemia and reperfusion are
responsible for increased levels of Fas-ligand, inflammatory cytokines,
metabolic and oxidant stresses following CPB, which are the main
activators of the extrinsic and intrinsic apoptotic pathways
respectively.[4] Pulmonary dysfunction following CPB is a complex problem
that has so far eluded our complete understanding, and further research is
warranted. “The important thing is not to stop questioning.” Albert
Einstein (1879-1955)
Kindest regards,
Dr. Calvin S.H. Ng, MBBS(Hons) MRCS
Prof. Song Wan, MD PhD FRCS
Prof. Malcolm J. Underwood, MD FRCS
Prof. Anthony P.C. Yim, MA DM FRCS
2) Ng CS, Wan S, Yim AP, Arifi AA. Pulmonary dysfunction after cardiac
surgery. Chest 2002;121:1269-77.
3) Wan S, Yim APC, Ng CSH, Arifi AA. Systematic Organ Protection in
Coronary Artery Surgery with or without Cardiopulmonary Bypass. J Card
Surg 2002;17:529-35.
4) Ng CS, Wan S, Yim AP. Pulmonary ischaemia-reperfusion injury: role of
apoptosis. Eur Respir J 2005;25:356-63.
We read with great interest the article published in Thorax by
Dickinson et al (February 2006)(1) investigating the response of FEF50
following EVH (Eucapnic voluntary hyperventilation) or exercise challenges
in elite athletes as an adjunct to FEV1.0. We were however, slightly
confused as to the research design selected by the researchers. It appears
from the stated methods that the researchers used...
We read with great interest the article published in Thorax by
Dickinson et al (February 2006)(1) investigating the response of FEF50
following EVH (Eucapnic voluntary hyperventilation) or exercise challenges
in elite athletes as an adjunct to FEV1.0. We were however, slightly
confused as to the research design selected by the researchers. It appears
from the stated methods that the researchers used either an EVH challenge
or an exercise challenge for EIB diagnosis in their elite athletes. If
this is indeed the case then the underlying assumption is, that the
exercise challenge test selected by the authors is not different in its
impact upon pulmonary function than the EVH challenge test. As the authors
do not present this data in their paper then it is impossible for us to
know if the data from different challenge tests can be pooled to provide a
single sample. Indeed in a recent publication from the same authors (2)
their contention is that EVH and exercise tests do not give identical
results and that they should not be used synonymously.
In addition, we were concerned about the authors selection of the ATS
(3) guidelines as the basis for their use of 85% of maximal heart rate as
an exercise intensity for the exercise challenge test. The ATS guidelines
clearly indicate that cold dry air should be used during an exercise test
and that the test should “produce 4-6 minutes of exercise at near maximal
targets”(3). On the basis the subjects being tested were ‘current or
potential Olympic competitive standard’ we would have recommended using an
exercise challenge that stressed the elite athletes closer to their
maximal capabilities (4). It is well documented (5) that elite endurance
athletes can exhibit adaptations to their physiology that allow them to
exercise at higher intensities for longer durations and so it is possible
that these Olympic caliber athletes were not ventilating at a sufficient
level to exhibit symptoms of EIB during the exercise challenge(6). It has
been shown previously, in young asthmatic patients, that exercise load is
of paramount importance when exercise challenge testing for EIB (due to
the level of ventilation) (7). The difference between 85% and 95%
predicted maximal heart rate had a 60% difference in terms of EIB
diagnosis (7).
Therefore, as suggested in our communication to the editor of BJSM
and the authors of the current paper (8), the levels of ventilation
reached during each test would be extremely useful in comparing exercise
and EVH challenge tests. This would allow a further examination of the
data presented by the authors and the removal of the different tests as
extraneous variables when discussing the negative and positive diagnosis
of EIB based upon pulmonary function.
References
1 Dickinson, J.W., Whyte, G.P., McConnell, A.K., Nevill, A.M. and
Harries, M.G. Mid-expiratory flow versus FEV1 measurements in the
diagnosis of exercise induced asthma in elite athletes. Thorax 2006; 61: 111-114.
2 Dickinson, J.W., Whyte, G.P., McConnell, A.K., Harries, M.G. and
Rundell, K.W.
Screening elite winter athletes for exercise induced asthma: a comparison
of three challenge methods. Commentary. British Journal of Sports
Medicine., February 2006; 40: 179 - 182.
3 American Thoracic Society. Guidelines for Methacholine and
Exercise Challenge Testing – 1999.American Journal of Respiratory and
Critical Care Medicine 2000; 161: 309-329.
4 Mickleborough TD, Murray RL, Ionescu AA, Lindley MR. Fish oil
supplementation reduces severity of exercise-induced bronchoconstriction
in elite athletes. American Journal of Respiratory and Critical Care
Medicine 2003; 168: 1181-1189.
5 Jones, A.M. and Carter, H. The effect of endurance training on
parameters of aerobic fitness. Sports Medicine. 2000 June, Vol 29 Issue
(6) 373-386.
6 Anderson SD, Holzer K. Exercise-induced asthma: is it the right
diagnosis in elite athletes? J Allergy Clin Immunol 2000; 106: 419-428.
7 Carlsen, K.H., Engh, G. and Mork, M. Respiratory Medicine. 2000
Aug, Vol 94, Issue(8):pages750-5.
8 Lindley, M.R. and Mickleborough, T.D. Exercise challenge testing of
elite winter athletes for exercise-induced asthma. British Journal of
Sports Medicine. Published on 13 February 2006.
http://bjsm.bmjjournals.com/cgi/eletters/40/2/179.
The editorial by Cullinan suggests that the relationship between
allergy, birth order and family size may not be completely explained by
the hygiene hypothesis.[1] A role for infection in protecting against
allergy has been under consideration for some years, although a credible
mechanism has not been identified. It has been suggested that reduced
exposure to infection in childhood shifted the balanc...
The editorial by Cullinan suggests that the relationship between
allergy, birth order and family size may not be completely explained by
the hygiene hypothesis.[1] A role for infection in protecting against
allergy has been under consideration for some years, although a credible
mechanism has not been identified. It has been suggested that reduced
exposure to infection in childhood shifted the balance between Th1 and Th2
cells in the adult immune system in favour of allergy associated Th2
cells.[2] This hypothesis failed to take account of the similarities in
epidemiology of Th1 type I diabetes and Th2 mediated allergic disease, and
while the role of infection was not challenged, the idea of Th2 dominated
adult immune system was rejected.3 Cullinan suggests that the effect of
birth order may be explained by differences in the intra uterine
environment or by some alternative, non-infective aetiology. If future
explanations are to have credibility, they require to take account of all
the available evidence. It is difficult to explain the higher prevalence
of Th1 and Th2 mediated disease in western societies and the more direct
evidence that exposure to a variety of infections is protective on the
basis of a non-infective cause.[2, 4-5]
The control of any immune response involves mechanisms which may
amplify or dampen the response. It seems likely that the presence of an
immune response to one infection may non-specifically down regulate other
immune responses, including allergic and autoimmune responses. The
mechanism of down regulation remains to be identified but a unifying
explanation which does not include infection seems implausible.
References
1. P Cullinan P. Childhood allergies, birth order and family size.
Thorax 2006; 61: 3-5.
2. Martinez F, Holt P. Role of microbial burdan in the aetiology of
allergy and asthma. Lancet 1999;354(Suppl 2):12-15.
3. Simpson C, Anderson W, Helms P, Taylor M, Watson L, Prescott G, et
al. Coincidence of immune-mediated diseases driven by Th1 and Th2 subsets
suggests a common aetiology. Clinical and experimental allergy
2002;2002:37-42.
4. Lynch N, Hagel I, Perez M, prisco MD, R RL, Alvarez N. Effect of
antihelminitic treatment on the allergic reactivity of children in a
tropical slum. Journal of Allergy and Clinical Immunology. 1993;92:404-
11.
5. Shirakawa T, Enomoto T, Shimazu S, JM. JH. The inverse association
between tuberculin responses and atopic disorder. Science 1997;275:77-9.
Imperatori et al. make a detailed comparison of lung cancer patients,
management and survival in two hospitals, one in England and one in Italy,
in an attempt to throw some light on the differences in published
survival between these nations[1]. In collecting similar data we have found
between 5 and 10% of the patients in our geographical catchment area have
not attended our hospital either as in-patie...
Imperatori et al. make a detailed comparison of lung cancer patients,
management and survival in two hospitals, one in England and one in Italy,
in an attempt to throw some light on the differences in published
survival between these nations[1]. In collecting similar data we have found
between 5 and 10% of the patients in our geographical catchment area have
not attended our hospital either as in-patients or as out-patients. These
patients were identified by our local cancer registry which uses
additional non-hospital sources to case find[2]. It is possible that
patients not referred or referred elsewhere are materially different from
those who are referred and that patterns of referral differ between the
two centres. Are the authors aware of any such patients in either centre
and could their inclusion alter the results?
References
1. Imperatori A, Harrison R, Leitch D, Rovera F, Lepore G, Dionigi G,
et al. Lung cancer in Teesside (UK) and Varese (Italy): a comparison of
management and survival. Thorax 2006(61):232-239.
2. Fitzpatrick D, Gavin A, Middleton R, Catney D. Cancer in Northern
Ireland 1993-2001. A Comprehensive report. Belfast: Northern Ireland
Cancer Registry.Queens University Belfast, 2004.
The correction by Zollner diverts the main issue we raised from
incorrectly citing our study as supporting the decrease/leveling off of
asthma and allergies in Germany when our study showed an increase, to a
reference order error [1]. Also, in Zollner's reply our data were again
misinterpreted, as we showed clearly for example that symptoms of asthma,
rhinitis, and rhino-conjunctivitis increased sig...
The correction by Zollner diverts the main issue we raised from
incorrectly citing our study as supporting the decrease/leveling off of
asthma and allergies in Germany when our study showed an increase, to a
reference order error [1]. Also, in Zollner's reply our data were again
misinterpreted, as we showed clearly for example that symptoms of asthma,
rhinitis, and rhino-conjunctivitis increased significantly among girls in
both age groups, while diagnosis of asthma and hey fever either did not
show the same trend or increased to a lesser extent (Tables 2,3) [2],
arguing against implicating a change in diagnostic behavior as a plausible
explanation for our findings [1,2]. We regret this continuing selective
approach to dealing with data unsupportive of the main claim of the
original article debated [3].
References
1- Maziak W, Keil U, Zollner I. Asthma and allergies in Germany.
Thorax 2006;61: 274.
2- Maziak W, Behrens T, Brasky TM, et al. Are asthma and allergies in
children and adolescents increasing? Results from ISAAC phase I and phase
III surveys in Münster, Germany. Allergy 2003;58:572–9.
3- Zollner IK, Weiland SK, Piechotowski I, et al. No increase in the
prevalence of asthma, allergies, and atopic sensitisation among children
in Germany: 1992–2001. Thorax 2005;60:545–8.
I was very interested to read of your research on the effect of
tomatoes, carrots, and leafy vegetables in reducing asthma.
A large-scale experiment to test these theories in practice, would be
to obtain the statistics for the population of Italy, where tomatoes
(especially) are an integral part of the national diet, and basil (a green
leafy vegetable) is nearly always included in tomato dis...
I was very interested to read of your research on the effect of
tomatoes, carrots, and leafy vegetables in reducing asthma.
A large-scale experiment to test these theories in practice, would be
to obtain the statistics for the population of Italy, where tomatoes
(especially) are an integral part of the national diet, and basil (a green
leafy vegetable) is nearly always included in tomato dishes.
This could then also be compared with other countries, such as
Switzerland & Austria (countries near to or neighbouring Italy), but
where tomatoes do not play such a prominent role in the diet.
And in case factors other than diet are influencing the outcome, then
several other countries could also be used for comparison eg, Finland,
Scotland, Kenya, South Africa, Paraguay, Fiji, and Australia.
Sherriff and colleagues report an apparent association between
mothers’ self-reported frequency of use of assorted household ‘chemicals’
during pregnancy and ‘persistent wheeze’ in their offspring. Since their
paper suggests this may help explain recent rises in asthma, the
robustness of the data and other explanations for the observed statistical
association need careful consideration.
Sherriff and colleagues report an apparent association between
mothers’ self-reported frequency of use of assorted household ‘chemicals’
during pregnancy and ‘persistent wheeze’ in their offspring. Since their
paper suggests this may help explain recent rises in asthma, the
robustness of the data and other explanations for the observed statistical
association need careful consideration.
We see several concerns, including both exposure and outcome
measures, lack of a plausible biological mechanism for the suggested in
utero effect, and the possibility of both recall and selection bias.
The definition of persistent wheeze is weak, and far removed from
criteria currently considered to define asthma . Offspring are
categorised as having ‘persistent wheeze’ if mothers’ responses indicate
one instance of wheezing in three consecutive 12 month periods.
It is curious that the association appears using frequency of use
scores which treat 11 disparate product types as equal, irrespective of
composition, and remains when each in turn was removed from the analysis.
Some product types have nothing at all in common: we can see no
significant ingredient that is common even to the majority, nor any likely
shared toxic mode of action. Contrary to the authors’ suggestion
formaldehyde is little used in the products surveyed.
Self-reported frequency of use is a very poor measure of exposure:
variations in quantity of product used, duration of use and routes of
exposure (inhalation, dermal, ingestion etc) can yield scores which run
contrary to actual exposure.
We see little justification for aggregating disparate product
exposures as ‘Total Chemical Burden’ by analogy with particulate air
pollution: the action of particulates is plausibly associated more with
size, geometry and/or absorptive capacity than with chemical composition.
This concept cannot simply be extrapolated to vapours or non-particulates,
and the term itself unfortunately suggests some absorbed, retained load:
‘sum of reported product use frequencies’ would have been more
appropriate.
We are not aware of any substantiated toxicological effect that is
shared by all chemicals irrespective of composition, especially given that
the notion of a ‘chemical’ is essentially subjective. All matter,
natural or synthetic, is composed of atoms and molecules. How do the
products considered differ from the many household chemicals not
considered, and chemicals that make up the natural environment to which
people are continuously exposed?
It seems unlikely that the association is driven by one product type
since it remained when each in turn was removed from the analysis.
Further, previous analyses of these questionnaires for two specific types
(aerosols and air fresheners) found no association with wheeze . Per
capita consumption of cleaning products in different European countries
also shows no correlation with the patterns of asthma .
Other than chance, how else might the observed association have
arisen? Apart from confounding by other chemicals in the built or
natural environment, certain mothers may have over-reported both chemical
use and wheezing symptoms. While ‘chemicals’ are heterogeneous in terms
of composition and toxicology, the term perhaps has some homogeneous
psychological significance for certain people. We understand the question
about frequency of use was headed “Chemicals …… in your environment”.
The authors acknowledge some selection bias: “those excluded from the
analysis due to lack of chemical use data were more likely to have wheezed
at all ages than those included, and those excluded from the analysis due
to missing symptom data had, on average, higher TCB scores than those in
the analysis”. This is potentially significant since the numbers
excluded from the study for missing data (50%) are large.
Scrutinising household products for any possible role in the rise in
asthma is important but, to be meaningful, exposures must be properly
defined.
--------------------------------
References
1.Sherriff A, Farrow A, Golding A, the ALSPAC Study Team, Henderson
J. Frequent use of chemical household products is associated with
persistent wheezing in pre-school age children. Thorax 2005; 60: 45-49
2.Asher MI and Weiland SK on behalf of the ISAAC Steering Committee
(1998) The International Study of Asthma and Allergies in Childhood
(ISAAC). Clin Exp Allergy 28, Suppl 5, 52-66.
3. Farrow A, Taylor H, Northstone K, Golding J. Symptoms of Mothers
and Infants Related to Total Volatile Organic Compounds in Household
Products. Arch Environ Health. 2003 Oct;58(10):633-41.
4. Pickup J. Trends in home and consumer hygiene. In 'Are we too
clean? - a question of immunity balance'. RIPH Symposium Report. Published
as a supplement to Health & Hygiene. London: Royal Institute of Public
Health 2003: 6-7.
Dear Editor,
I read with interest the paper by Alfageme and colleagues (1) who investigated the efficacy of anti-pneumococcal vaccination in patients with COPD. To have new data in an area which has suffered from a surfeit of meta-analysis and even analysis of the meta-analysis is good and their results are quite clear. Although they do not specifically comment I presume that their primary end point was accum...
Dear Editor,
We appreciate the comments made by Prof. Quanjer concerning our manuscript (1) and fully agree with his comments. In his letter to the editor Prof. Quanjer gives valuable background information to the reasons why pulmonary function tests are relatively insensitive to track pulmonary changes in the longitudinal follow up of cystic fibrosis (CF) lung disease (2). We agree with his arguments that this is...
Dear Editor,
We would like to comment to the limitations of the Christopher-study (JAMA 2006;295) mentioned by Dr. Bari. He states that “the limitations of this study include the use of two different kinds of CT scanner (multi- detector and single-detector) with potentially different pick up rates”. The other limitation stated is: “the prevalence of PE of 23.2% in the ‘clinically unlikely PE and abnormal D-dimer’...
Dear Editor,
We congratulate Elkington and Friedland on their excellent review which gives an overview of matrix metalloproteinases (MMPs) in various destructive pulmonary diseases.[1] MMPs and neutrophil elastase do indeed play instrumental roles in the development of ARDS and lung injury following cardiopulmonary bypass (CPB), however, the mechanisms presented may be too simplified.[2]
Apart from...
Dear Editor,
We read with great interest the article published in Thorax by Dickinson et al (February 2006)(1) investigating the response of FEF50 following EVH (Eucapnic voluntary hyperventilation) or exercise challenges in elite athletes as an adjunct to FEV1.0. We were however, slightly confused as to the research design selected by the researchers. It appears from the stated methods that the researchers used...
Dear Editor,
The editorial by Cullinan suggests that the relationship between allergy, birth order and family size may not be completely explained by the hygiene hypothesis.[1] A role for infection in protecting against allergy has been under consideration for some years, although a credible mechanism has not been identified. It has been suggested that reduced exposure to infection in childhood shifted the balanc...
Dear Editor,
Imperatori et al. make a detailed comparison of lung cancer patients, management and survival in two hospitals, one in England and one in Italy, in an attempt to throw some light on the differences in published survival between these nations[1]. In collecting similar data we have found between 5 and 10% of the patients in our geographical catchment area have not attended our hospital either as in-patie...
Dear Editor,
The correction by Zollner diverts the main issue we raised from incorrectly citing our study as supporting the decrease/leveling off of asthma and allergies in Germany when our study showed an increase, to a reference order error [1]. Also, in Zollner's reply our data were again misinterpreted, as we showed clearly for example that symptoms of asthma, rhinitis, and rhino-conjunctivitis increased sig...
Dear Editor,
I was very interested to read of your research on the effect of tomatoes, carrots, and leafy vegetables in reducing asthma.
A large-scale experiment to test these theories in practice, would be to obtain the statistics for the population of Italy, where tomatoes (especially) are an integral part of the national diet, and basil (a green leafy vegetable) is nearly always included in tomato dis...
Dear Editor,
Sherriff and colleagues report an apparent association between mothers’ self-reported frequency of use of assorted household ‘chemicals’ during pregnancy and ‘persistent wheeze’ in their offspring. Since their paper suggests this may help explain recent rises in asthma, the robustness of the data and other explanations for the observed statistical association need careful consideration.
We...
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