Ghuysen et al in their recent retrospective study demonstrated the
potential value of CTPA RV/LV ratio in predicting in-hospital mortality
related to pulmonary embolism.[1] I wondered if they assessed ECG evidence
of acute right heart strain and/or serum cardiac biomarkers of injury in
the same study and what the relative prognostic value of these indices
versus the CTPA RV/LV ratio was, assuming th...
Ghuysen et al in their recent retrospective study demonstrated the
potential value of CTPA RV/LV ratio in predicting in-hospital mortality
related to pulmonary embolism.[1] I wondered if they assessed ECG evidence
of acute right heart strain and/or serum cardiac biomarkers of injury in
the same study and what the relative prognostic value of these indices
versus the CTPA RV/LV ratio was, assuming that the ability to correlate
with the degree of RV dysfunction is the most important factor here.
Yours sincerely,
Andrew RL Medford
References:
1. Ghuysen A, Ghaye B, Willems V et al. Computed tomographic
pulmonary angiography and prognostic significance in patients with acute
pulmonary embolism. Thorax 2005; 60: 956-61.
Regarding the article by Culpitt et al.[1] I wish to comment on the use of Resveratrol and the claims made with regard to COPD. I would interested in learning what evidence the authors
have for the claims made. I have, after reading the report and as a patient,
tested Resveratrol for 9 weeks without absolutely any result! There were
no indications of influence on the immune system or
inflammato...
Regarding the article by Culpitt et al.[1] I wish to comment on the use of Resveratrol and the claims made with regard to COPD. I would interested in learning what evidence the authors
have for the claims made. I have, after reading the report and as a patient,
tested Resveratrol for 9 weeks without absolutely any result! There were
no indications of influence on the immune system or
inflammatory system.
The test was done as per: 1. 3 capsulas , 25 mg Resveratrol/capsule) a day for 3 weeks
after that 2. 6 capsulas per day for 3 weeks
and after that 3. 9 capsulas per day for 3 weeks
Measurements were taken with an FEV-meter and an
oxygen-saturation meter for the duration of the test. No effect was measured.
I think it is of vital interest that results as those in this article can be repeated in vivo. Otherwise, valuable and costly scientific work could be lost.
I am looking forward hearing from the authors.
Reference
(1)
SV Culpitt, DF Rogers, PS Fenwick, P Shah, C De Matos, RE K Russell, PJ Barnes, and LE Donnelly. Inhibition by red wine extract, resveratrol, of cytokine release by alveolar macrophages in COPD. Thorax 2003; 58: 942-946.
We read with great interest the paper by Wickremasinghe et al. on the
prevalence of nontuberculous mycobacteria (NTM) in patients with
bronchiectasis.[1] They showed that the prevalence of NTM was uncommon
(only 2%) both in 50 newly referred patients and 50 follow up patients.
However, the authors stated in the Discussion that it is now our
practice to screen our patients routinely once a year bec...
We read with great interest the paper by Wickremasinghe et al. on the
prevalence of nontuberculous mycobacteria (NTM) in patients with
bronchiectasis.[1] They showed that the prevalence of NTM was uncommon
(only 2%) both in 50 newly referred patients and 50 follow up patients.
However, the authors stated in the Discussion that it is now our
practice to screen our patients routinely once a year because a large
number of NTM isolates (28%) were detected by routine surveillance in
their retrospective analysis of 71 patients with NTM sputum isolates.[1]
NTM pulmonary infection associated with bronchiectasis is increasing
worldwide.[2] However, should routine periodic screening for NTM
infection be necessary for all adult patients with bronchiectasis? Is
sputum culture a sufficiently sensitive method to exclude active NTM
infection? Are negative sputum studies sufficient to dissuade one from the
diagnosis of active NTM infection?
Bronchiectasis, in general, can manifest in one of two forms: as a
local or focal obstructive process of a lobe or segment of a lung or as a
diffuse process involving most of the lungs.[3] In patients with diffuse
bronchiectasis, the disease is more likely to be associated with specific
causes, such as infection (NTM infection, Aspergillus infection),
congenital conditions (primary ciliary dyskinesia, cystic fibrosis), or
immunodeficiency.[3]
High-resolution computed tomography (HRCT) has proven to be a
reliable and noninvasive method for the diagnosis of bronchiectasis. The
pattern and distribution of abnormalities revealed by HRCT are influenced
by the underlying cause of bronchiectasis. Multiple small nodules (and
sometimes cavity or cavities) combined with diffuse (or widespread)
bronchiectasis are reported to be the typical HRCT findings of NTM
pulmonary infection associated with bronchiectasis,[4-6] which was also
suggested by Wickremasinghe et al.[1] In patients with these
characteristic HRCT findings, 34-50% of patients have active NTM pulmonary
infection, especially M. avium complex infection.[4,6] These
abnormalities are usually confined to, or most severe in, the right middle
lobe and the lingular segment of the left upper lobe in NTM pulmonary
infection. Therefore, this presentation is now referred to as ¡°nodular
bronchiectatic disease.[2] Multiple small nodules around ecstatic
bronchi on HRCT scan have been reported to represent peribronchial
granuloma and caseous material.[4,5]
Diagnosis of this type of NTM pulmonary infection is often delayed;
this is because symptoms are mild, and excretion of NTM in sputum is
intermittent with few colonies retrievable in culture. Therefore, many
patients require bronchoscopy or lung biopsy for diagnosis of NTM
pulmonary disease.[7]
Therefore, in clinical practice, HRCT scans should be performed in
patients with suspected bronchiectasis. NTM pulmonary infection could be
suspected in selected patients who have multiple pulmonary nodules
combined with diffuse bronchiectasis on HRCT scans. Multiple sputum
specimens should be examined in these patients. However, the poor
sensitivity of sputum cultures suggests that in that situation where
multiple sputum cultures are nondiagnostic, bronchoscopy should be
performed to adequately exclude or diagnose NTM pulmonary disease. We
consider that there is no clear evidence to support the routine
surveillance for NTM infection in all adult patients with bronchiectasis.
References
1. Wickremasinghe M, Ozerovitch LJ, Davies G, et al. Non-tuberculous
mycobacteria in patients with bronchiectasis. Thorax 2005;60:1045-51.
2. American Thoracic Society. Diagnosis and treatment of disease
caused by nontuberculous mycobacteria. Am J Respir Crit Care Med
1997;156:S1-25.
3. Barker AF. Bronchiectasis. N Engl J Med 2002;346:1383-93.
4. Tanaka E, Amitani R, Niimi A, et al. Yield of computed tomography
and bronchoscopy for the diagnosis of Mycobacterium avium complex
pulmonary disease. Am J Respir Crit Care Med 1997;155:2041-6.
5. Jeong YJ, Lee KS, Koh WJ, et al. Nontuberculous mycobacterial
pulmonary infection in immunocompetent patients: comparison of thin-
section CT and histopathologic findings. Radiology 2004;231:880-6.
6. Koh WJ, Lee KS, Kwon OJ, et al. Bilateral bronchiectasis and
bronchiolitis at thin-section CT: diagnostic implications in
nontuberculous mycobacterial pulmonary infection. Radiology 2005;235:282-8.
7. Huang JH, Kao PN, Adi V, et al. Mycobacterium avium-intracellulare
pulmonary infection in HIV-negative patients without preexisting lung
disease: diagnostic and management limitations. Chest 1999;115:1033-40.
We thank Andreas von Glehn for his interest in our paper, sufficient
that he took resveratrol capsules for his own condition, presumably COPD.[1]
His short course of treatment (9 weeks) highlights the difficulties
in evaluating therapies for the treatment of COPD. COPD is a slowly
progressive inflammatory condition of the lungs and, as such, clinical
trials using lung function measurements a...
We thank Andreas von Glehn for his interest in our paper, sufficient
that he took resveratrol capsules for his own condition, presumably COPD.[1]
His short course of treatment (9 weeks) highlights the difficulties
in evaluating therapies for the treatment of COPD. COPD is a slowly
progressive inflammatory condition of the lungs and, as such, clinical
trials using lung function measurements as endpoints are generally
considered inadequate unless they are in large numbers of patients and of
at least 3 years duration.[2] The length of studies could be shortened if
adequate surrogate markers were available. However, at present there is
debate concerning the usefulness in COPD of most of these markers.[3]
Consequently, it is unsurprising that von Glehn reported that taking
resveratrol for 9 weeks was 'without absolutely any result'. It would have
been interesting to have had a more formal quality of life assessment, as
improvement in patient well-being is a valid end point in COPD.[4]
Although we found that resveratrol effectively inhibited cytokine
release by alveolar macrophages in vitro from patients with COPD, it is
unlikely that oral dosing would have a similar effect. This is because of
the low bioavailibility of resveratrol.[5] Consequently, resveratrol
analogues such as piceatannol are under investigation for improved
bioavailibilty.[6]
Finally, in the present climate of the debatable efficacy of
pharmacotherapy for COPD,[3] we understand the eagerness of von Glehn to
test the benefit of any proposed new treatment for his COPD. However, we
wish to highlight that our study examined the effect of resveratrol on
specific responses by a specific population of inflammatory cells that may
have a role to play in the pathophysiology of COPD. Further studies are
clearly required on the effect of resveratrol on the underlying
inflammation in COPD before considering large scale clinical
investigations. At present we would emphasise that the only intervention
proven to alter disease progression in COPD is smoking cessation.[3] We
recommend this course of action to von Glehn and wish him well for the
future.
References
(1) A von Glehn. Resveratrol/COPD [electronic response to Culpitt et
al. Inhibition by red wine extract, resveratrol, of cytokine release by
alveolar macrophages in COPD] thoraxjnl.com 2004http://thorax.bmjjournals.com/cgi/eletters/58/11/942#153
(2) MJ Leckie, SA Bryan, TT Hansel, PJ Barnes. Novel therapy for
COPD. Exp Opin Invest Drugs 2000; 9: 3-23.
(3) LE Donnelly, DF Rogers. Therapy for chronic obstructive pulmonary
disease in the 21st century. Drugs 2003; 63: 1973-1998.
(4) PW Jones, FH Quirk CM Baveystock. Why quality of life measures
should be used in the treatment of patients with respiratory illness.
Monaldi Arch Chest Dis 1994; 49:79-82.
(5) DM Goldberg, J Yan, GJ Soleas.Absorption of three wine-related
polyphenols in three different matrices by healthy subjects. Clin Biochem
2003; 36:79-87.
(6) T Wieder, A Prokop, B Bagci, F Essmann, D Bernicke, K Schulze-
Osthoff, B Dorken, HG Schmalz, PT Daniel, G Henze. Piceatannol, a
hydroxylated analog of the chemopreventive agent resveratrol, is a potent
inducer of apoptosis in the lymphoma cell line BJAB and in primary,
leukemic lymphoblasts. Leukemia 2001; 15:1735-42
Broughton and colleagues state that consideration should be given to
use of prophylactic palivizumab to infants born at less than 32 weeks in
the case of maternal smoking or even if they have siblings. The authors
however present no data from their own or other studies to indicate that
this would be in any way cost effective or justified. Certainly the word
"consider" is fortunate given the stated fu...
Broughton and colleagues state that consideration should be given to
use of prophylactic palivizumab to infants born at less than 32 weeks in
the case of maternal smoking or even if they have siblings. The authors
however present no data from their own or other studies to indicate that
this would be in any way cost effective or justified. Certainly the word
"consider" is fortunate given the stated funding provided to one author by
the manufacturer.
The study demonstrated a relationship between lower respiratory
morbidity from RSV and smoking which has been widely shown elsewhere.
Numbers of smokers were in fact very small - surprisingly so at 18 per 126
babies given both their prematurity and the catchment population for this
hospital although 28 experienced smoking in the home. One wonders if the
61 non-consenters and non-attenders may have comprised a higher
proportion.
Perhaps because of the small numbers there was actually very little
relationship shown with smoking in pregnancy - the strong relationships
were instead with the 28 passive smokers in the home. Were palvizumab to
be given to this group the cost would be something over £56,000. I have
unfortunately had to extrapolate from other data in the paper which would
indicate that about 8 of the 16 hospital admissions (excluding the two who
were given palvizumab anyway)would have been from smoking families.
Assuming a halving of hospital admission rate from treatment this amounts
to £56000 to prevent 4 "admissions" (with a median length of stay of 0
days) whilst 24 babeis would have received 120 needless injections. No
savings are likely to acrue from this reduction as the effect on total RSV
workload would be miniscule.
Some might consider this a small price to pay but one might consider
whether £56,000 spent on providing smoke stop groups to antenatal mothers
and householders of premature babies could be a better use of resources.
Malignant mesothelioma (MM) is a rare, highly aggressive tumor,
accounting for less than 1% of all cancer deaths in the world. Although
the association between exposure to asbestos and the development of MM is
commonly accepted, the exact mechanism whereby asbestos induces MM is
unknown. Therefore, we agree with Dr Lange observation that the search
for other agents/factors causing this disease should...
Malignant mesothelioma (MM) is a rare, highly aggressive tumor,
accounting for less than 1% of all cancer deaths in the world. Although
the association between exposure to asbestos and the development of MM is
commonly accepted, the exact mechanism whereby asbestos induces MM is
unknown. Therefore, we agree with Dr Lange observation that the search
for other agents/factors causing this disease should be strengthened.
Our
research group is actually investigating the pathogenesis of MM looking
both at molecular events and environmental factors. We have a manuscript
in press on Thorax showing a possible implication of COX-2 in MM
pathogenesis through the effects on cell cycle regulatory proteins.[1]
Moreover, our group is collaborating with the Regional Mesothelioma
Registry instituted by the Campania Region, and entrusted in convention to
the II University of Naples under the direction of Professor Massimo
Menegozzo. Finally, in collaboration with the SAFU Dept of Regina Elena
Cancer Institute in Rome, we are setting up a canine model of spontaneous
MM Spontaneous canine neoplasms have been considered in the recent years a
valuable and highly underused resource to characterize several tumor types
and to evaluate new experimental therapeutics.[2-4] The advantages of
this model system include: 1. similarities between specific types of
canine and human cancer with regards to histopathological appearence,
biological behavior and response to therapy; 2. significant similarity in
drug metabolism between dogs and humans; 3. pet owners’ willingness to
enter their tumor bearing dogs in humanely conducted clinical trials due
to the absence of a well defined “standard” therapy for many canine
cancers; 4. the compressed life-span of dogs, which allows the completion
of clinical trials in a timely manner;
5. the fact that dogs share the
same environment of their owners but lack their unhealthy habits such as
alcohol consumption and cigarette smoking which act as “confounding” in
many clinical and epidemiological studies;
6. the larger size of dogs
compared to rodents which makes feasible to perform many medical
procedures; 7. novel interventional strategies developed in vitro or in
laboratory animals studies can be tested in dogs affected by cancer,
similar studies might be unacceptable or less feasible in human patients,
especially when a standard, yet only partially effective treatment exists.
In conclusion, defining all the factors involved in mesothelioma
pathogenesis is a very difficult task, that can be accomplished only by a
multidisciplinary approach.
References
1. Baldi A., Santini D., Vasaturo F., Santini M., Vicidomini G., Di
Marino M.P., Esposito V., Groeger A.M., Liuzzi G., Vincenzi B., Tonini G.,
Piccoli M., Baldi F., Scarpa S. Prognostic significance of Cyclooxygenase-
2 (COX-2) and cell cycle inhibitors p21 and p27 expression in human
pleural malignant mesothelioma. Thorax 2004 (in press)
2. MacEwen EG. Spontaneous tumors in dogs and cats: models for the
study of cancer biology and treatment. Cancer Met Rev 1990; 9: 125-136.
3. Hahn KA, Bravo L, Adams WH, Frazier DL. Naturally occurring tumors
in dogs as comparative models for cancer therapy research. In Vivo 1994;
8: 133-144.
4. Vail DM, Mac Ewen EG. Spontaneously occurring tumors of companion
animals as models for human cancer. Cancer Invest 2000; 18: 781-792.
We would agree with much of the content of the interesting letter
from Doctors Koh and Kwon, particularly the details of M.avium complex
infection and the use of CT scans in making the diagnosis.[1] We have
also had experience of bronchoscopy and biopsy being necessary to make the
diagnosis in some cases with suggestive radiology. The one point on which
we disagree is the value of routine annual scr...
We would agree with much of the content of the interesting letter
from Doctors Koh and Kwon, particularly the details of M.avium complex
infection and the use of CT scans in making the diagnosis.[1] We have
also had experience of bronchoscopy and biopsy being necessary to make the
diagnosis in some cases with suggestive radiology. The one point on which
we disagree is the value of routine annual screening of sputum for AFB,
and our practice of sending three samples in all patients with a
deterioration in their clinical condition which is not explained or not
reversed by usual treatment.
The value of this practice will require a large prospective study with
cost benefit analysis, and attention paid to false negative results.
However, we would argue in favour of this approach for the following
reasons. Most patients have a CT scan when bronchiectasis is first
suspected. Our study[2] has shown that these patients in the future may
(rarely) contract NTM infection which adversely affects their condition.
As Doctors Koh and Kwon state this may be insidious and go unsuspected for
long periods. In our study[2] most patients with infection (rather than
colonisation) had heavy bacterial load (smear positive), which would make
it likely that routine screening would detect the patient. Repeat CT scans
in all cases that might raise suspicion of NTM is impractical. Lastly,
about 50% of cases with diffuse bronchiectasis remain idiopathic even
after full investigation[3], and our understanding of NTM pathogenesis is
just begining to increase. The data produced from closely studying NTM in
our population of bronchiectatic patients may provide useful information
in the future.
R.Wilson, M. Wickremasinghe, L.J. Ozerovitch, G. Davies,
T. Wodehouse, M.V. Chadwick, S. Abdallah, P. Shah
References
(1). Hollings NP, Wells AU, Wilson R, Hansell DM Comparative
appearances of non-tuberculosis mycobacteria species: a CT study Eur
Radiol 2002; 12: 2211-7.
(2). Wickremasinghe M, Ozerovitch LJ, Davies G et al Non-tuberculous
mycobacteria in patients with bronchiectasis Thorax 2005: 60: 1045-1051.
(3). Pasteur MC, Helliwell SM, Houghton SJ et al An investigation into
causative factors in patients with bronchiectasis Am J Respir Crit Care
Med 2000; 162: 1277-1284.
We read with interest the recent article by Wu et al. [1] in which
they investigated a single nucleotide polymorphism at exon 1 of the
transforming growth factor beta1 (TGF-beta1) gene.
While we agree with their assumption that TGF-beta1 is a candidate
gene for COPD association study, we can not understand why they restricted
their study to only one polymorphism in that gene. There a...
We read with interest the recent article by Wu et al. [1] in which
they investigated a single nucleotide polymorphism at exon 1 of the
transforming growth factor beta1 (TGF-beta1) gene.
While we agree with their assumption that TGF-beta1 is a candidate
gene for COPD association study, we can not understand why they restricted
their study to only one polymorphism in that gene. There are several
registered polymorphisms within TGF-beta1 and its promoter [2] that might
be functional and might be associated with COPD. A polymorphism of special
interest is the promoter SNP at -509 C/T that had been shown to be
associated with elevated total IgE [3] and asthma severity [4]. Recently,
Silverman et al. [5] showed that this SNP is associated with the diagnosis
of asthma and may enhance TGF-beta1 gene transcription. Another
interesting SNP is that at codon 25 (Arg25Pro). This SNP had been shown to
be associated with levels of TGF-beta1 production,[6] the development of
lung fibrosis [6] and proliferative diabetic retinopathy.[7]
To our knowledge, the study by Wu et al. [1] is the first study to
search for association between TGF-beta1 polymorphisms and COPD. In our
laboratory, when we examine a gene -for the first time- for disease
association, we search for polymorphisms inside the gene and its promoter.
Then, we compare the genotype and allele frequencies between the patient
and control groups.[8] If a large number of polymorphisms were detected,
we also check the linkage disequilibrium and compare the haplotypes
between the different groups for the common polymorphisms [9]. We found
that haplotype analysis, testing associations using several polymorphisms,
sometimes demonstrates genetic influences that are not detected by the
analysis of single polymorphisms [9].
References
1. Wu L, Chau J, Young RP, Pokorny V, Mills GD, Hopkins R, McLean L,
Black PN. Transforming growth factor-beta1 genotype and susceptibility to
chronic obstructive pulmonary disease. Thorax 2004; 59: 126-9.
2. Watanabe Y, Kinoshita A, Yamada T, Ohta T, Kishino T, Matsumoto N,
Ishikawa M, Niikawa N, Yoshiura K. A catalog of 106 single-nucleotide
polymorphisms (SNPs) and 11 other types of variations in genes for
transforming growth factor-beta1 (TGF-beta1) and its signaling pathway. J
Hum Genet 2002;47: 478-83.
3. Hobbs K, Negri J, Klinnert M, Rosenwasser LJ, Borish L.
Interleukin-10 and transforming growth factor-beta promoter polymorphisms
in allergies and asthma. Am J Respir Crit Care Med 1998;158: 1958-62.
4. Pulleyn LJ, Newton R, Adcock IM, Barnes PJ. TGFbeta1 allele
association with asthma severity. Hum Genet. 2001 Dec;109(6):623-7.
5. Silverman ES, Palmer LJ, Subramaniam V, Hallock A, Mathew S, Vallone J,
Faffe DS, Shikanai T, Raby BA, Weiss ST, Shore SA. Transforming growth
factor-beta1 promoter polymorphism C-509T is associated with asthma. Am J
Respir Crit Care Med 2004; 169: 214-9.
6. Awad MR, El-Gamel A, Hasleton P, Turner DM, Sinnott PJ, Hutchinson
IV. Genotypic variation in the transforming growth factor-beta1 gene:
association with transforming growth factor-beta1 production, fibrotic
lung disease, and graft fibrosis after lung transplantation.
Transplantation 1998; 66: 1014-20.
7. Beranek M, Kankova K, Benes P, Izakovicova-Holla L, Znojil V,
Hajek D, Vlkova E, Vacha J. Polymorphism R25P in the gene encoding
transforming growth factor-beta (TGF-beta1) is a newly identified risk
factor for proliferative diabetic retinopathy. Am J Med Genet 2002; 109:
278-83.
8. Hirano K, Sakamoto T, Uchida Y, Morishima Y, Masuyama K, Ishii Y,
Nomura A, Ohtsuka M, Sekizawa K. Tissue inhibitor of metalloproteinases-2
gene polymorphisms in chronic obstructive pulmonary disease. Eur Respir J
2001; 18: 748-52.
9. Hegab AE, Sakamoto T, Uchida Y, Nomura A, Ishii Y, Morishima Y,
Mochizuki M, Kimura T, Saitoh W, Massoud HH, Massoud HM, Hassanein KM,
Sekizawa K. CLCA1 gene polymorphisms in chronic obstructive pulmonary
disease. J Med Genet 2004; 41: e27.
I read with interest the article by Broughton et al, and wish to
offer following
comments.
1. The duration of oxygen therapy (in both Table 1 and the text)
ranges from
30 to 107 weeks, thus qualifying every baby in the cohort as having BPD.
Even if this was in days, it would make every baby oxygen dependent 28
days
after birth, c...
I read with interest the article by Broughton et al, and wish to
offer following
comments.
1. The duration of oxygen therapy (in both Table 1 and the text)
ranges from
30 to 107 weeks, thus qualifying every baby in the cohort as having BPD.
Even if this was in days, it would make every baby oxygen dependent 28
days
after birth, compared to 19% in other studies(1).
2. The rate of BPD in this cohort was 40% - much higher than has been
reported for babies of similar gestation in recent years(1,2). In view of
this
high rate of BPD and prolonged oxygen dependency, the studied cohort
might have consisted of rather sick infants.
3. Since discharge home on oxygen is mentioned as one of the
explanatory
variables, it would be helpful to know its frequency and significance in
relation to the risk of hospital admission and RSV infection.
4. It is not clear if the healthcare utilisation includes all events
after discharge
from the neonatal unit, or only those after a RSV infection. The authors
have
elsewhere suggested that babies with lung function deficits at discharge
from
the neonatal unit are more likely to sustain symptomatic RSV
infections(3). If
the healthcare utilisation includes all post-discharge events, then is it
possible that the excessive healthcare utilisation of RSV-infected infants
a
manifestation of their underlying lung deficit rather than effect of RSV?
5. The authors suggest consideration of palivizumab for the two risk
factors
of RSV LRTI – maternal smoking during pregnancy and presence of school
aged siblings. However, palivizumab has been shown to be effective in
‘reducing hospitalisations from RSV’ rather than ‘preventing RSV
infection’
itself(4), and the validity of this extrapolation remains to be tested.
Indeed,
the indicator for healthcare utilisation (GP attendances) just reached
significance among non-admitted RSV-infected infants as compared to no
LRTI infants, the use of reliever medications being comparable in all
three
groups. I am not sure widening the indications for palivizumab to the
suggested groups will prove to be cost-effective.
Conflict of interest: I have previously questioned the cost-
effectiveness of palivizumab in relation to its recommended indications.
References
1. Manktelow BN, Draper ES, Annamalai S, Field D. Factors affecting
the incidence of chronic lung disease of prematurity in 1987, 1992, and 1997.
Arch Dis Child Fetal Neonatal Ed 2001;85(1):F33-5.
2. Smith VC, Zupancic JA, McCormick MC, Croen LA, Greene J, Escobar
GJ,
et al. Trends in severe bronchopulmonary dysplasia rates between 1994 and
2002. J Pediatr 2005;146(4):469-73.
3. Broughton S, Bhat R, Roberts A, Zuckerman M, Rafferty G, Greenough
A.
Diminished lung function, RSV infection, and respiratory morbidity in
prematurely born infants. Arch Dis Child 2006;91(1):26-30.
4. Palivizumab, a humanized respiratory syncytial virus monoclonal
antibody, reduces hospitalization from respiratory syncytial virus
infection in
high-risk infants. The IMpact-RSV Study Group. Pediatrics 1998;102(3 Pt
1):
531-7.
We read with interest the study by Park et al(1). We agree that non-
asthmatic eosinophilic bronchitis (EB), a condition characterised by
eosinophilic inflammation without evidence of variable airflow obstruction
is a powerful disease control group to study the mechanisms involved in
the development of airway hyperresponsiveness in asthma. Previous
comparative studies have demonstrated that asthma and...
We read with interest the study by Park et al(1). We agree that non-
asthmatic eosinophilic bronchitis (EB), a condition characterised by
eosinophilic inflammation without evidence of variable airflow obstruction
is a powerful disease control group to study the mechanisms involved in
the development of airway hyperresponsiveness in asthma. Previous
comparative studies have demonstrated that asthma and EB are
immunopathologically similar, but that there are key differences namely
mast cell localisation to the airway smooth muscle bundle(2) and increased
IL-13 expression in asthma. Park et al(1) have proposed in their recent
study that this list needs to be extended to include increased airway wall
area as a feature confined to asthma. This is an important observation as
other HRCT studies in asthma have suggested that increased airway wall
area may in fact protect against airway hyperresponsiveness(3). However,
the observed absence of increased airway wall area in the EB group study
may not reflect distinct differences between this disease and asthma, but
may simply reflect duration of disease.
The subjects with EB had participated in an earlier study(4) .In this
study duration of disease was on average about 7 months and very few
subjects had symptoms or evidence of inflammation for more than one year.
It is not clear from the current study the duration of disease in the
asthma group, but this is likely to be years in many cases. This point
needs to be clarified as conclusions made about possible differences in
remodelling between asthma and EB are undermined if the disease duration
is markedly different.
In our experience some patients with EB and prolonged eosinophilic
airway inflammation have a progressive decline in their lung function (5)
suggesting that airway wall remodelling is a feature in some patients with
this condition. Therefore whether airway remodelling and increased airway
wall thickness are features shared by asthma and EB or specific to the
asthma phenotype remains to be fully addressed.
References
1. Park SW, Park JS, Lee YM, Lee JH, Jang AS, Kim DJ et al.
Differences in radiological/HRCT findings in eosinophilic bronchitis
compared to asthma: implication for bronchial responsiveness. Thorax 2005.
2. Brightling CE, Bradding P, Symon FA, Holgate ST, Wardlaw AJ,
Pavord ID. Mast-cell infiltration of airway smooth muscle in asthma. New
England Journal of Medicine 2002;346(22):1699-705.
3. Niimi A, Matsumoto H, Takemura M, Ueda T, Chin K, Mishima M.
Relationship of airway wall thickness to airway sensitivity and airway
reactivity in asthma. American Journal of Respiratory and Critical Care
Medicine 2003;168(8):983-8.
4. Park SW, Lee YM, Jang AS, Lee JH, Hwangbo Y, Kim dJ et al.
Development of chronic airway obstruction in patients with eosinophilic
bronchitis: a prospective follow-up study. Chest 2004;125(6):1998-2004.
5. Berry MA, Brightling CE, Hargadon B, McKenna S, Wardlaw AJ,
Pavord ID. Observational study of the natural history of eosinophilic
bronchitis. Thorax 2003;58:46.
Dear Editor,
Ghuysen et al in their recent retrospective study demonstrated the potential value of CTPA RV/LV ratio in predicting in-hospital mortality related to pulmonary embolism.[1] I wondered if they assessed ECG evidence of acute right heart strain and/or serum cardiac biomarkers of injury in the same study and what the relative prognostic value of these indices versus the CTPA RV/LV ratio was, assuming th...
Dear Editor
Regarding the article by Culpitt et al.[1] I wish to comment on the use of Resveratrol and the claims made with regard to COPD. I would interested in learning what evidence the authors have for the claims made. I have, after reading the report and as a patient, tested Resveratrol for 9 weeks without absolutely any result! There were no indications of influence on the immune system or inflammato...
Dear Editor,
We read with great interest the paper by Wickremasinghe et al. on the prevalence of nontuberculous mycobacteria (NTM) in patients with bronchiectasis.[1] They showed that the prevalence of NTM was uncommon (only 2%) both in 50 newly referred patients and 50 follow up patients. However, the authors stated in the Discussion that it is now our practice to screen our patients routinely once a year bec...
Dear Editor
We thank Andreas von Glehn for his interest in our paper, sufficient that he took resveratrol capsules for his own condition, presumably COPD.[1]
His short course of treatment (9 weeks) highlights the difficulties in evaluating therapies for the treatment of COPD. COPD is a slowly progressive inflammatory condition of the lungs and, as such, clinical trials using lung function measurements a...
Dear Editor,
Broughton and colleagues state that consideration should be given to use of prophylactic palivizumab to infants born at less than 32 weeks in the case of maternal smoking or even if they have siblings. The authors however present no data from their own or other studies to indicate that this would be in any way cost effective or justified. Certainly the word "consider" is fortunate given the stated fu...
Dear Editor
Malignant mesothelioma (MM) is a rare, highly aggressive tumor, accounting for less than 1% of all cancer deaths in the world. Although the association between exposure to asbestos and the development of MM is commonly accepted, the exact mechanism whereby asbestos induces MM is unknown. Therefore, we agree with Dr Lange observation that the search for other agents/factors causing this disease should...
Dear Editor,
We would agree with much of the content of the interesting letter from Doctors Koh and Kwon, particularly the details of M.avium complex infection and the use of CT scans in making the diagnosis.[1] We have also had experience of bronchoscopy and biopsy being necessary to make the diagnosis in some cases with suggestive radiology. The one point on which we disagree is the value of routine annual scr...
Dear Editor
We read with interest the recent article by Wu et al. [1] in which they investigated a single nucleotide polymorphism at exon 1 of the transforming growth factor beta1 (TGF-beta1) gene.
While we agree with their assumption that TGF-beta1 is a candidate gene for COPD association study, we can not understand why they restricted their study to only one polymorphism in that gene. There a...
Dear Editor,
I read with interest the article by Broughton et al, and wish to offer following comments.
1. The duration of oxygen therapy (in both Table 1 and the text) ranges from 30 to 107 weeks, thus qualifying every baby in the cohort as having BPD. Even if this was in days, it would make every baby oxygen dependent 28 days after birth, c...
Dear Editor,
We read with interest the study by Park et al(1). We agree that non- asthmatic eosinophilic bronchitis (EB), a condition characterised by eosinophilic inflammation without evidence of variable airflow obstruction is a powerful disease control group to study the mechanisms involved in the development of airway hyperresponsiveness in asthma. Previous comparative studies have demonstrated that asthma and...
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