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We thank Professor Morice and his colleagues for their interest and
for the issues raised vis-a-vis our manuscript.
The main issue raised concerns the possibility that we may have
missed gastrooesophageal disorders such as reflux and dysmotility in our
cohort of chronic cough patients. In our assessment protocol, we state
that we used oesophageal pH measurements in most patients (32 out of 50)...
We thank Professor Morice and his colleagues for their interest and
for the issues raised vis-a-vis our manuscript.
The main issue raised concerns the possibility that we may have
missed gastrooesophageal disorders such as reflux and dysmotility in our
cohort of chronic cough patients. In our assessment protocol, we state
that we used oesophageal pH measurements in most patients (32 out of 50),
together with a trial of proton pump inhibitor. We are pleased to read
from Professor Morice that proton pump inhibitors “only improve symptoms
in a proportion of patients with reflux cough”, when they reported
previously a very excellent 82% therapeutic response in this group treated
with 'proton pump inhibitors, alginates and conventional advice regarding
diet and posture' [1]. We agree entirely that proton pump inhibitors are
not very efficacious in reflux cough. We have not performed oesophageal
manometry and are aware of Professor Morice’s interesting observations.
They also report that patients with abnormal oesophageal manometry respond
to proton pump inhibition, and therefore we would have picked up such
patients with a proton pump inhibitor trial of therapy. However, the
direct link between oesophageal dysmotility and chronic cough still
remains to be established.
We do not believe we have missed reflux as an associated cause of the
cough and therefore do not agree with the explanation that the reduced
exhaled breath condensate pH is a reflection of larngophargeal reflux
throughout the diagnostic categories. Rather, this is likely to be related
to the chronic inflammatory and remodelling process that is present in the
submucosa of chronic cough patients, associated with asthma or non-
asthmatic causes [2, 3, 4]. We must emphasise that we are assuming that
exhaled breath condensate is a reflection of the epithelial surface
liquid, which needs to be confirmed.
References
(1) Kastelik JA, Redington AE, Aziz I, Buckton GK, Smith CM,
Dakkak M
et al. Abnormal oesophageal motility in patients with chronic cough.
Thorax 2003;58:699-702.
(2) Niimi A, Matsumoto H, Minakuchi M, Kitaichi M, Amitani R.
Airway
remodelling in cough-variant asthma. Lancet 2000;356:564-5.
(3) Boulet LP, Milot J, Boutet M, St Georges F, Laviolette M.
Airway
inflammation in non-asthmatic subjects with chronic cough. Am J Respir Crit
Care Med 1994;149:482-9.
(4) Niimi, A., Cosio, B., Oates, T., Nicholson, A., and Chung,
K. F.
Airway inflammation and remodelling in non-asthmatic patients with chronic
cough: comparison with asthmatics. Amer J Resp Crit Care Med 2003; 167:
A353 (Abstract).
in a recent issue of the Journal, Gan WQ et al. published a systematic review
and meta-analysis of 14 reports which confirmed the strong association between
COPD and biological markers of systemic inflammation [1]. In 6 reports, COPD was
diagnosed according to the presence of a FEV1/FVC ratio lower than 0.7. However,
in the remaining 8 studies this measure was not available, and authors assumed
as affecte...
in a recent issue of the Journal, Gan WQ et al. published a systematic review
and meta-analysis of 14 reports which confirmed the strong association between
COPD and biological markers of systemic inflammation [1]. In 6 reports, COPD was
diagnosed according to the presence of a FEV1/FVC ratio lower than 0.7. However,
in the remaining 8 studies this measure was not available, and authors assumed
as affected by COPD all participants in the lowest quartile of FEV1% and, for
one study [2], of FVC%. In these cases, the corresponding highest quartile group
served as control. Since a COPD diagnosis based on the decreased FEV1/FVC ratio
was lacking in 8 reports, the possibility cannot be excluded that a certain
number of patients included in the meta-analysis did not have COPD, but a
restrictive ventilatory defect. This could be particularly true for participants
to the study by Engstrom [2], who were characterized only by a low FVC.
According to the current GOLD guidelines [3], only a FEV1/FVC ratio lower
than 0.7 indicates airflow obstruction, thus allowing a COPD diagnosis. Indeed,
in the absence of particular pulmonary diseases, many subjects show an
homogenous decrease of all dynamic lung volumes (FEV1, FVC, PEF), without any
alteration of FEV1/FVC ratio, and are thus considered as having “impaired lung
function”. The occurrence of respiratory symptoms [4], the systemic inflammation
[2] and the increased risk of cardiovascular disease [5] are the only features
that restrictive subjects share with COPD. In fact, whereas COPD is
characterized by a decrease in BMI and blood lipids, restrictive subjects often
have abdominal obesity, insulin-resistance and other metabolic risk factors [6].
Although we believe that most of the included patients were really affected
by COPD, the possible inclusion of restrictive patients may have altered the
statistical conclusions of the meta-analysis. In addition, the choice of
selecting patients in the lowest quartile of FEV1 or FVC hindered the authors
from confirming the absence of inflammation in mild COPD (GOLD stage I and II),
a finding previously reported by the same group in a study not included in this
meta-analysis [7].
Because the two groups of restrictive and COPD patients have different
features, the generic term ”impaired lung function” should not be used. Future
studies about the role of inflammation and other cardiovascular risk conditions
in respiratory patients, as well as those investigating the outcome of these
subjects, should clearly distinguish restrictive from COPD patients.
References
(1) Gan WQ, Man SFP, Senthilselvan A, Sin DD. Association between chronic
obstructive pulmonary disease and systemic inflammation: a systematic review and
a meta-analysis. Thorax 2004; 59: 574-580
(2) Engstrom G, Lind P, Hedblad B et
al. Lung function and cardiovascular risk. Relationship with
inflammatory-sensitive plasma protein. Circulation 2002; 106: 2555-2560
(3)
Global Initiative for Chronic Obstructive Lung Disease (GOLD). Publication no.
2701. Bethesda, National Institute for Health, 2001 (2004 update).
(4) Mannino
DM, Ford ES, Redd SC. Obstructive and restrictive lung disease and functional
limitation: data from the Third national Health and Nutrition Examination.
Journal of Internal Medicine 2003; 254: 540-547
(5) Hole DJ, Watt GC, Davey-Smith
G et al. Impaired lung function and mortality risk in men and women: findings
from the Renfrew and Paisley prospective population study. BMJ 1996; 313:
711-715
(6) Lawlor DA, Ebrahim S, Davey-Smith G. Associations of measures of lung
function with insulin resistance and type 2 diabetes: findings from the British
Women’s heart and health Study. Diabetologia 2004; 47: 195-203
(7) Sin DD, Man SFP. Why are patients with obstructive pulmonary disease at increased risk of
cardiovascular diseases? The potential role of systemic inflammation in Chronic
Obstructive Pulmonary Disease. Circulation 2003; 107: 1514-1519
Morten Dahl and Børge G. Nordestgaard argue against selection bias,
if genotyping is performed after lung function tests because a newborn
with PiMZ genotype does not change to PiZZ later in life. The latter is
obviously true and not the issue. The reason for possible selection bias
is that some persons may fail to have genotype performed due to a
characteristic of the lung function tests under stud...
Morten Dahl and Børge G. Nordestgaard argue against selection bias,
if genotyping is performed after lung function tests because a newborn
with PiMZ genotype does not change to PiZZ later in life. The latter is
obviously true and not the issue. The reason for possible selection bias
is that some persons may fail to have genotype performed due to a
characteristic of the lung function tests under study and this may affect
the result of a longitudinal study.
If we assume that PiMZ persons have a very fast FEV1 decline with
premature death, a number of PiMZ persons may have attended the first
examinations, but did not live long enough to show up to the last visit
with genotyping. These persons would not be included in the analysis of
FEV1 decline and the result would be an underestimate of FEV1 decline with
the possible conclusion that PiMZ is not a risk factor for lung disease.
This is usually called a survivor effect.
The opposite may also be true. Suppose a reverse relationship between
pulmonary function and compliance to study visits, that is persons with
normal FEV1, normal FEV1 decline, and no lung symptoms may not show up to
the last visit because they feel well. This would tend to exaggerate any
increased decline in FEV1 and the conclusion could be that PiMZ is an
important risk factor for lung disease.
These are just two of many examples of possible biases. They show
that even if the risk factor (PiMZ) is present from birth, it is vital to
postpone the collection of tests for analysis after genotyping has been
performed.
Anti TNF treatment should be given after screening for latent
tuberculosis as this may result active tuberculosis in these cases [1]. The
World Health Organization estimates that at least one-third of the world’s
population are infected with TB [2], [3]. 95% of tuberculosis cases and
98% tuberculosis deaths are in the developing countries [2], [3]. It is
difficult to rule out latent tuberculosis infection...
Anti TNF treatment should be given after screening for latent
tuberculosis as this may result active tuberculosis in these cases [1]. The
World Health Organization estimates that at least one-third of the world’s
population are infected with TB [2], [3]. 95% of tuberculosis cases and
98% tuberculosis deaths are in the developing countries [2], [3]. It is
difficult to rule out latent tuberculosis infection in developing
countries like India, as positive tuberculin reaction is very common in
person needing health care. So use of anti TNF treatment should be
restricted as this may be a high-risk gamble with health system of this
region.
References
(1) Keane J, Gershon S, Wise R P et al.Tuberculosis associated with
infliximab, a tumor necrosis factor á-neutralizing agent. N Eng J Med
2001;345:1098-1104.
(2) Raviglione MC, Snider DE, Kochi A. Global epidemiology of
tuberculosis. Morbidity and mortality of a worldwide epidemic. JAMA 1995;
273:220-226
(3) Dolin PJ, Raviglione MC, Kochi A.Global tuberculosis incidence and
mortality during 1900-2000. Bull. World Health Organ. 1994; 72(2): 213-220
Heinzer et al. report cases of severe respiratory effects
following exposure to aerosol waterproofing sprays in Switzerland [1].
They report that while there are reports from elsewhere in Europe there
are no reports yet from the UK. We report the experience of the National
Poisons Information Service (London) [NPIS(L)] with these products in
2003.
Heinzer et al. report cases of severe respiratory effects
following exposure to aerosol waterproofing sprays in Switzerland [1].
They report that while there are reports from elsewhere in Europe there
are no reports yet from the UK. We report the experience of the National
Poisons Information Service (London) [NPIS(L)] with these products in
2003.
The European Association of Poisons Centres and Clinical
Toxicologists (EAPCCT) issued a warning regarding the risk of respiratory
distress developing in people using aerosol waterproofing agents. Subsequently NPIS(L) received an enquiry concerning a patient who
had developed Adult Respiratory Distress Syndrome (ARDS) following the use of an
aerosol waterproofing product in a confined space. This patient developed
respiratory failure and despite supportive treatment died [2].
Since this date the NPIS(L) has undertaken enhanced surveillance of
enquiries regarding such products. There were 43 enquiries to the NPIS(L)
concerning 33 cases of inhalation of aerosol waterproofing agents in 2003.
Of these cases, 31 (94%) involved adults and 2 (6%) children. All cases
were accidental exposures, with 27 (82%) exposures occurring at home, 4
(12%) at work and 2 (6%) in cars. All patients were or had been
symptomatic (symptoms were scored using the IPCS/EAPCCT Poisoning Severity
Score [3] following their exposure; 22 (67%) with mild symptoms and 10
(30%) with moderate symptoms, mostly respiratory in nature. One patient
had severe symptoms leading to death [2].
Although the number of enquiries to NPIS(L), from 2000 to 2003,
regarding aerosol waterproofing agents was very small compared with total
enquiry load, the number of enquiries concerning these products has
increased each year from 18 in 2000 [0.011%] to 43 in 2003 [0.067%]. This
is despite a significant decrease in total call load and represents a
proportional increase of 5.6 fold from 2000 to 2003. 2003 saw the most
serious case reported to NPIS(L) [2].
The manufacturer of the product implicated in the death [2] informed
the NPIS of a recent change in formulation. A high-odour solvent had been
replaced by a low-odour solvent blend. This change may have allowed greater
exposure to the product than is recommended, as there would be less olfactory
warning compared with the original solvent (i.e. allowing heavier exposures to
be tolerated). This is despite the manufacturer’s instructions on the package
indicating that indoor use is not recommended. This low-odour variant has since
been withdrawn [4]. 11
further cases in 2003, many in the early part of the year (1 case in
2002), involved this particular product. The high incidence may have been
related to the new low-odour variant, however, the variant involved in
these cases was either not known or not specified by the enquirer.
It seems likely that the fluorocarbon compounds in these products
cause the pulmonary problems [5,6,7] however the reason for this is not
clear. Nor is it clear why there has been an increase in cases in the UK
and elsewhere in Europe and unexpectedly severe effects. Some products
may generate smaller aerosol droplets, allowing the fluorocarbons to
penetrate deeper into the pulmonary tract [8,9,10] or that exposure is
prolonged because the products are less noxious due to different carrier
solvents. The cases reported to NPIS(L) involved at least 14 different
waterproofing brands and products and in some cases the exact product and
therefore ingredients are not known, the exact cause of the respiratory
problems is difficult to assess and is possibly due to a combination of
these factors.
References
(1) Heinzer R, Fitting JW, Ribordy V, Kuzoe B, Lazor R. Recurrence of
acute respiratory failure following use of waterproofing sprays
[Correspondence]. Thorax 2004;59:541-542
(2) Malik M. Acute respiratory syndrome associated with extreme superpruf
aerosol [Correspondance]. Anaesthesia 2003;58:1037-8.
(3) The International Program on Chemical Safety/European Association of
Poison Centres and Clinical Toxicologists Poisoning Severity Score
(http://www.intox.org/pagesource/intox%20area/other/pesticide/annex3pss.htm)
(4) Communication from Grangers International Ltd to NPIS(UK)
(5) Jinn Y, Akizuki N, Ohkouchi M, Inase N, Ichioka M, Marumo F. Acute
lung injury after inhalation of water-proofing spray while smoking a
cigarette. Respiration 1998;65:486-8.
(6) Kupfershcmidt H. Epidemy of acute respiratory illness linked to use of
waterproofing textile and leather spray [Abstract No. 59]. Clinical
Toxicology 2003;41:665.
(7) Laliberte M, Sanfacon G, Blais R. Acute pulmonary toxicity linked to
use of a leather protector. Annals of Emergency Medicine 1995;25:841-4.
(8) Yamashita M, Tanaka J. Pulmonary collapse and pneumonia due to
inhalation of a waterproofing aerosol in Female CD-1 mice. Clinical
Toxicology 1995;33(6):631-7.
(9) Yamashita M, Tanaka J, Yamashita M, Hirai H, Suzuki M, Kajigaya H.
Mist particle diameters are related to the toxicity of waterproofing
sprays: Comparison between toxic and non-toxic products. Veterinary and
Human Toxicology 1997;39(2):71-4.
(10) Yamashita M, Yamashita M, Tanaka J, Hirai H, Suzuki M, Kajigaya H.
Toxicity of waterproofing spray is influenced by the mist particle size.
Veterinary and Human Toxicology 1997;39(6):332-4.
Like Dr. Silvestri, I support a model of shared
decision making when considering chemotherapy [1]. Unfortunately, many
patients don’t realize that the advantages of chemotherapy are not shared
equally by those treated. For example, Spiro et al. show that
chemotherapy reduces the risk of death from lung cancer by 9% and 5% at
one and two years, respectively [2]. The fact that the reduction benefits
o...
Like Dr. Silvestri, I support a model of shared
decision making when considering chemotherapy [1]. Unfortunately, many
patients don’t realize that the advantages of chemotherapy are not shared
equally by those treated. For example, Spiro et al. show that
chemotherapy reduces the risk of death from lung cancer by 9% and 5% at
one and two years, respectively [2]. The fact that the reduction benefits
only a fraction of those treated is sure to be misunderstood by many. A
more straightforward (and honest) way to describe these data is the number
needed to treat (NNT)[3], which would allow patients to consider that 11
individuals would need chemotherapy for one to survive an additional year,
and 20 would need treatment for one to survive an additional two. The NNT
is a useful concept for patients to incorporate into their decisions about
whether the chemotherapy glass is half empty or half full.
References
(1) Silvestri G. Chemotherapy for advanced lung cancer: is the glass half
full or half empty? Thorax 2004; 59:821.
(2) Spiro SG, Rudd RM, Souhami RL, et al.Chemotherapy versus supportive
care in advanced non-small cell lung cancer: improved survival without
detriment to quality of life. Thorax 2004;59:828–36.
(3) Cook RJ and Sackett DL. The number needed to treat: a clinically useful
measure of treatment effect. BMJ 1995;310:452-4.
In a recent otherwise excellent editorial in Thorax [1], Dr. Seersholm indicated that our previous results on FEV1 decline based on the
Copenhagen City Heart Study [2] are biased. We disagree, and rather
believe that our study of the general population is prone to less bias
than case-control or family-based studies.
Dr. Seersholm argues that because we genotyped study participants
after measuremen...
In a recent otherwise excellent editorial in Thorax [1], Dr. Seersholm indicated that our previous results on FEV1 decline based on the
Copenhagen City Heart Study [2] are biased. We disagree, and rather
believe that our study of the general population is prone to less bias
than case-control or family-based studies.
Dr. Seersholm argues that because we genotyped study participants
after measurement of FEV1 in 1976-1978, 1981-1984, and 1991-1994, our
results are biased [1]. Certainly, if conventional risk factors are
measured after development of disease, the disease might be the cause of
the risk factor, rather than vice versa. However, an alpha1-antitrypsin MZ genotype in a newborn does not change into a ZZ genotype by age.
Therefore, Pi MZ genotype preceded FEV1 outcomes in our study, even though
genotypes were determined after FEV1 measurements. Using identical logic,
genotype preceded outcomes in a similar manner in other previous studies
[3-6].
Selection bias could potentially be a reason for discrepancies
between studies on Pi MZ and COPD [1,7]. In our study where genotype
distribution was in Hardy Weinberg equilibrium, we found no evidence for
selection against any alpha1-antitrypsin genotype [2,8]. Therefore, as
also pointed out by Dr. Seersholm [1], selection bias is more likely in
case-control and family-based studies than in cohort studies of the
general population.
Morten Dahl and Børge G. Nordestgaard. Dept of Clinical
Biochemistry, Herlev University Hospital, Copenhagen, Denmark.
References
(1) Seersholm N. Pi MZ and COPD:
will we ever know? Thorax 2004;59:823-825.
(2) Dahl M, Tybjærg-Hansen A, Lange P, Vestbo J, Nordestgaard BG.Change in lung function and morbidity from chronic obstructive pulmonary disease in alpha1-antitrypsin MZ heterozygotes. A longitudinal study of
the general population. Ann Intern Med 2002;136:270-279.
(3) Juul K, Tybjærg-Hansen A, Steffensen R, Kofoed S, Jensen G,
Nordestgaard BG. Factor V leiden: The Copenhagen City Heart Study and 2
meta-analyses. Blood 2002;100:3-10.
(4) Bojesen SE, Tybjærg-Hansen A, Nordestgaard BG. Integrin beta3Leu33Pro homozygosity and risk of cancer. J Natl Cancer Inst
2003;95:1150-1157.
(5) Dahl M, Tybjærg-Hansen A, Schnohr P, Nordestgaard BG. A population
-based study of morbidity and mortality in mannose-binding lectin
deficiency. J Exp Med 2004;199:1391-1399.
(6) Wadsworth MEJ, Vinall LE, Jones AL, Hardy RJ, Whitehouse DB,
Butterworth SL, Hilder WS, Lovegrove JU, Swallow DM. Alpha-1-antitrypsin
as a risk factor for infant and adult respiratory outcomes in a national
birth cohort. Am J Respir Cell Mol Biol (in press).
(7) Hersh CP, Dahl M, Ly CS, Nordestgaard BG, Silverman EK. Chronic
obstructive pulmonary disease in alpha1-antitrypsin PI MZ heterozygotes: a
meta-analysis. Thorax 2004;59:843-849.
(8) Dahl M, Tybjærg-Hansen A, Sillesen H, Jensen G, Steffensen
R, Nordestgaard BG. Blood pressure, risk of ischemic cerebrovascular and
ischemic heart disease, and longevity in alpha1-antitrypsin deficiency:
the Copenhagen City Heart Study. Circulation 2003;107:747-752.
The aim of our study was to study ‘the effect of 6 weeks regular
supplementation with vitamin E on the clinical control of asthma’ [1]. We
thus used a combination of objective and subjective measures of asthma as
our outcomes. The entry criteria were designed to be as inclusive as
possible and to cover a population with mild to moderate asthma.
However, as Currie et al highlight our study pop...
The aim of our study was to study ‘the effect of 6 weeks regular
supplementation with vitamin E on the clinical control of asthma’ [1]. We
thus used a combination of objective and subjective measures of asthma as
our outcomes. The entry criteria were designed to be as inclusive as
possible and to cover a population with mild to moderate asthma.
However, as Currie et al highlight our study population had few
symptoms, with a median daytime and night time symptoms score of 0. A
similar intervention study of vitamin C and magnesium from our group
covering a comparable population also recruited a population with few
asthma symptoms [2], which was why we used bronchial responsiveness to methacholine as one of our entry criteria in the current study. We
considered this the best measure of bronchial responsiveness when we
designed the study, but agree that an alternative technique may have
resulted in a different result.
We also agree with Currie et al that further studies of vitamin E are
required those with asthma, including symptomatic asthmatics, particularly
with regard to clinically relevant outcomes such as exacerbations.
Philip Pearson,
Andrew Fogarty
Division of Respiratory Medicine, University of Nottingham, Clinical
Science Building, Nottingham City Hospital, Nottingham, NG5 1PB.
John Britton
Division of Epidemiology and Public Health, University of Nottingham,
Clinical Science Building, Nottingham City Hospital, Nottingham, NG5 1PB.
References
(1) Pearson P, Fogarty A, Lewis S, Britton J. Vitamin E
supplementation in the treatment of asthma: a randomised controlled trial.
Thorax 2004; 59:652-656.
(2) Fogarty A, Lewis S, Scrivener S, Antoniak M, Pacey S, Pringle M
et al. Oral magnesium and vitamin C supplements in asthma: a parallel
group randomised placebo-controlled trial. Clin Exper Allergy 2003;
33:1355-1359.
As my Title suggests, I have considered the possibility which would be
analogue to a detonation causing ARDS (Adult Respiratory Distress
Syndrome). In contrast to the ears, where the middle ear reflex until a
certain limit prevents destruction of the tympanic membrane with a time
constant of 35 microseconds, the lungs have no reflex damping sudden
bursts from heavy sub-woofers working together with...
As my Title suggests, I have considered the possibility which would be
analogue to a detonation causing ARDS (Adult Respiratory Distress
Syndrome). In contrast to the ears, where the middle ear reflex until a
certain limit prevents destruction of the tympanic membrane with a time
constant of 35 microseconds, the lungs have no reflex damping sudden
bursts from heavy sub-woofers working together with tweeters. Such
environment can also be found in discotheques where a sudden ARDS could be
assumed as caused by drug abuse.
Gupta and colleagues [1] present the epidemiology of pneumothorax in
England using national data from the Hospital Episode Statistics for
emergency hospital admissions, which in turn is reliant on information
provided from local National Health Service (NHS) trusts. However, little
is known of the reliability of these locally collected data on the
incidence of pneumothorax.
Gupta and colleagues [1] present the epidemiology of pneumothorax in
England using national data from the Hospital Episode Statistics for
emergency hospital admissions, which in turn is reliant on information
provided from local National Health Service (NHS) trusts. However, little
is known of the reliability of these locally collected data on the
incidence of pneumothorax.
We prospectively evaluated data from The Ipswich Hospital NHS Trust
over a four-year period (2001 – 2004). Data for episodes of pneumothorax
were obtained from hospital records identified through the appropriate
discharge codes. Chest X-ray reports which demonstrated the presence of
pneumothorax, acted as the ‘gold-standard’ of which the reliability of
data was assessed, as every pneumothorax episode would have required
radiological confirmation.
The number of pneumothorax episodes as recorded by the hospital
database was 135 compared to 210 reported on chest radiographs, indicating
that the former correctly identified 64% of pneumothorax episodes compared
to the latter.
Formal data recording of pneumothorax episodes is unreliable in our
locality, and if our experience is mirrored in other local NHS trusts,
this may well influence the national epidemiology of pneumothorax as a
whole in England. A more reliable method of identifying pneumothorax
episodes is now urgently needed.
References
(1) Gupta D, Hansell A, Nichols T, et al. Epidemiology of pneumothorax
in England. Thorax 2000;55:666-71.
Dear Editor
We thank Professor Morice and his colleagues for their interest and for the issues raised vis-a-vis our manuscript.
The main issue raised concerns the possibility that we may have missed gastrooesophageal disorders such as reflux and dysmotility in our cohort of chronic cough patients. In our assessment protocol, we state that we used oesophageal pH measurements in most patients (32 out of 50)...
Dear Editor
in a recent issue of the Journal, Gan WQ et al. published a systematic review and meta-analysis of 14 reports which confirmed the strong association between COPD and biological markers of systemic inflammation [1]. In 6 reports, COPD was diagnosed according to the presence of a FEV1/FVC ratio lower than 0.7. However, in the remaining 8 studies this measure was not available, and authors assumed as affecte...
Dear Editor
Morten Dahl and Børge G. Nordestgaard argue against selection bias, if genotyping is performed after lung function tests because a newborn with PiMZ genotype does not change to PiZZ later in life. The latter is obviously true and not the issue. The reason for possible selection bias is that some persons may fail to have genotype performed due to a characteristic of the lung function tests under stud...
Dear Editor
Anti TNF treatment should be given after screening for latent tuberculosis as this may result active tuberculosis in these cases [1]. The World Health Organization estimates that at least one-third of the world’s population are infected with TB [2], [3]. 95% of tuberculosis cases and 98% tuberculosis deaths are in the developing countries [2], [3]. It is difficult to rule out latent tuberculosis infection...
Dear Editor
Heinzer et al. report cases of severe respiratory effects following exposure to aerosol waterproofing sprays in Switzerland [1]. They report that while there are reports from elsewhere in Europe there are no reports yet from the UK. We report the experience of the National Poisons Information Service (London) [NPIS(L)] with these products in 2003.
The European Association of Poison...
Dear Editor
Like Dr. Silvestri, I support a model of shared decision making when considering chemotherapy [1]. Unfortunately, many patients don’t realize that the advantages of chemotherapy are not shared equally by those treated. For example, Spiro et al. show that chemotherapy reduces the risk of death from lung cancer by 9% and 5% at one and two years, respectively [2]. The fact that the reduction benefits o...
Dear Editor
In a recent otherwise excellent editorial in Thorax [1], Dr. Seersholm indicated that our previous results on FEV1 decline based on the Copenhagen City Heart Study [2] are biased. We disagree, and rather believe that our study of the general population is prone to less bias than case-control or family-based studies.
Dr. Seersholm argues that because we genotyped study participants after measuremen...
Dear Editor
The aim of our study was to study ‘the effect of 6 weeks regular supplementation with vitamin E on the clinical control of asthma’ [1]. We thus used a combination of objective and subjective measures of asthma as our outcomes. The entry criteria were designed to be as inclusive as possible and to cover a population with mild to moderate asthma.
However, as Currie et al highlight our study pop...
Dear Editor
As my Title suggests, I have considered the possibility which would be analogue to a detonation causing ARDS (Adult Respiratory Distress Syndrome). In contrast to the ears, where the middle ear reflex until a certain limit prevents destruction of the tympanic membrane with a time constant of 35 microseconds, the lungs have no reflex damping sudden bursts from heavy sub-woofers working together with...
Dear Editor
Gupta and colleagues [1] present the epidemiology of pneumothorax in England using national data from the Hospital Episode Statistics for emergency hospital admissions, which in turn is reliant on information provided from local National Health Service (NHS) trusts. However, little is known of the reliability of these locally collected data on the incidence of pneumothorax.
We prospectively...
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