We fully appreciate Dr Furness's comments on the limitations of the
definition of asthma based on parents' reports of symptoms and we have
contributed on the subject.[1] Epidemiological studies of asthma have to
rely on reported symptoms,[2][3] but a better understanding of what
parents call wheeze would be of great importance, especially in a
multicultural society. The validity of reported asthma symptoms...
We fully appreciate Dr Furness's comments on the limitations of the
definition of asthma based on parents' reports of symptoms and we have
contributed on the subject.[1] Epidemiological studies of asthma have to
rely on reported symptoms,[2][3] but a better understanding of what
parents call wheeze would be of great importance, especially in a
multicultural society. The validity of reported asthma symptoms has been
demonstrated in adults[4] and the symptoms analysed in the validation were
not dissimilar from those used in our study.
We have discussed that parents' perceptions of asthma may vary
according to ethnicity and social background.[5][6] False positive and
false negative responses could arise if parents mislabel other respiratory
symptoms as wheeze or if persistent wheeze is unrecognised.[7] Persistent
wheeze is unrecognised as asthma in a large percentage of children from
the ethnic minorities and inner city areas. We performed the analysis
using either parental reports of persistent wheeze or asthma attacks in
order to overcome these differences and the results were consistent. We
adjusted for ethnicity and study area in the analysis of the inner city
sample to account for the variation in perception.
References
(1) Jones CO, Qureshi S, Rona RJ, et al. Exercise-induced bronchoconstriction by ethnicity and presence of asthma in British nine
year olds. Thorax 1996;51:1134-6.
(2) Burney PGJ, Chinn S, Rona RJ. Has the prevalence of asthma
increased in children? Evidence from the National Study of Health and
Growth 1973-86. BMJ 1990;300:1306-10.
(3) The International Study of Asthma and Allergies in Childhood
(ISAAC) Steering Committee. Worldwide variations in the prevalence of
asthma symptoms: The International Study of Asthma and Allergies in
Childhood (ISAAC). Eur Respir J 1998;12:315-35.
(4) Burney PG, Laitinen LA, Perdrizet S, et al. Validity and
repeatability of the IUATLD (1984) bronchial symptom questionnaire: an
international comparison. Eur Respir J 1989;2:940-5.
(5) Duran-Tauleria E, Rona RJ, Chinn S, Burney P. Influence of ethnic
group on asthma treatment in children in 1990-1: national cross sectional
study. BMJ 1996;313:148-52.
(6) Duran-Tauleria E, Rona RJ. Geographical and socioeconomic
variation in the prevalence of asthma symptoms in English and Scottish
children. Thorax 1999;54:476-81.
(7) Cane RS, Ranganathan SC, McKenzie SA. What do parents of wheezy
children understand by wheeze? Arch Dis Child 2000;82:327-32.
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.
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) rat...
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) ratio. We wish to reignite attention to the use of this uncomplicated measurement through presentation of an interesting clinical case.
A 57-year old lady presented to our respiratory clinic with a complaint of inspiratory stridor. She did not have any other significant respiratory symptoms. There were no overt symptoms of gastroesophageal reflux or oesophageal dysfunction. On direct questioning, she denied any symptoms consistent with collagen vascular disease or vasculitis, except Raynaud’s phenomenon. Her medications included losartan for hypertension and amitriptyline for depression. She is a never-smoker. Clinical examination was unremarkable apart from a soft inspiratory stridor, which was heard best above the suprasternal notch. Her blood biochemistry, haematology, autoimmune, and vasculitic screen were unremarkable. Spirometry showed FEV1 of 2.79L (110% predicted), forced vital capacity (FVC) of 3.57L (120% predicted), FEV1/FVC ratio of 78%, and PEF of 396L/min (105% predicted). Her calculated FEV1/PEF ratio was 7.05ml/L/min. The pattern of the expiratory flow-volume curve was normal with a slight plateau in the inspiratory flow-volume curve (Figure 1). Flexible fibre-optic bronchoscopy demonstrated a subglottic stenosis (Figure 2).
Several pioneering studies have previously determined the usefulness of the FEV1/PEF ratio in diagnosing UAO.1-3 FEV1 is defined as the volume measured during the initial 1 second of a forced expiration from full inspiration and PEF is defined as the maximum flow rate maintained for at least 10 milliseconds during a forced expiration from full inspiration. Therefore, in UAO where the embarrassment is in the pre-carina upper airway, one would intuitively expect the FEV1/PEF ratio to increase, as chronologically, PEF would be affected more than FEV1, with the former reflecting more proximal airway per se. Evidently, the FEV1/PEF ratio has been shown to be significantly higher in patients with UAO compared to patients with asthma, chronic obstructive pulmonary disease, and normal subjects.1;2 A value of above 10ml/L/min was initially thought to represent UAO,1;2 although this was subsequently found to vary between 7ml/L/min and 12ml/L/min depending on the different subgroups of UAO such as extrathoracic, fixed, and variable intrathoracic.3
Therefore, although definitive procedures such as flexible fibre-optic bronchoscopy are needed to confirm the diagnosis of UAO, straightforward practical measurements that are useful in day-to-day clinical practice such as the FEV1/PEF ratio, which is easily obtainable through simple spirometry, may aid in either prompting initial consideration or confirming clinical suspicion of such a diagnosis.
Daniel K C Lee, MB, BCh, MRCP, MD
Prashant S Borade, MB, BS, MD
Nicholas J Innes, MB, BS, FRCP
Department of Respiratory Medicine, Ipswich Hospital, Heath Road, Ipswich IP4 5PD, Suffolk, England, United Kingdom
Rotman HH, Liss HP, Weg JG. Diagnosis of upper airway obstruction by pulmonary function testing. Chest 1975; 68: 796-799.
Mellisant CF, Van Noord JA, Van de Woestijne KP, Demedts M. Comparison of dynamic lung function indices during forced and quiet breathing in upper airway obstruction, asthma, and emphysema. Chest 1990; 98: 77-83.
Figure 1
Expiratory and inspiratory flow-volume curve
Figure 2
Subglottic stenosis found on flexible fibre-optic bronchoscopy
The review of Pulmonary Rehabilitation in the UK (Thorax, 2001: 56:
827-834) by Dr MDL Morgan begins by noting the lag between the quality of
pulmonary rehabilitation services in the USA compared to their virtual
absence in the UK. Dr Morgan goes on to mention that psychology is one of
the disciplines included in the multiple disciplines that comprise an
effective pulmonary rehabilitation program. In fact, most of the le...
The review of Pulmonary Rehabilitation in the UK (Thorax, 2001: 56:
827-834) by Dr MDL Morgan begins by noting the lag between the quality of
pulmonary rehabilitation services in the USA compared to their virtual
absence in the UK. Dr Morgan goes on to mention that psychology is one of
the disciplines included in the multiple disciplines that comprise an
effective pulmonary rehabilitation program. In fact, most of the leading
hospitals in the US that have pulmonary rehabilitation programs are indeed
truly "multidisciplinary" and the psychosocial and emotional functioning
of the clients constitutes an important ingredient of such programs.
However, the "most recent definition of pulmonary rehabilitation" cited by
Dr Morgan waters down the role of psychology and the program that he
recommends for the UK appears to be primarily exercise based and
physiotherapy-led. In fact,the process and components of pulmonary
rehabilitation described by Dr Morgan comprise almost entirely of
exercise. Dr Morgan acknolwedges only that the "coexistence of reduced
self-efficacy and the affective component is likely to have an effect on
performance," and even so, in the next sentence he, astonishingly,
essentially dismisses the need for a psychologist in such programs:
"psychological and behavioural intervention is already embedded in the
structure of rehabilitation programmes through the delivery of education,
small group discussions and relaxation therapy.... The role of
specific, individual or group psychotherapy is also unclear." According
to him, the only area where psychologists may contribute is in the
assessment of motivation!
Dr Morgan recommends the usage of mental health
questionnaires, presumably psychosocial and mental health variables are
only to be measured not targeted for treatment -- as the presumtion sems
to be that with improved lung function, all such parameters will
automatically improve as well. If this were so, then we would hope that
problems in treatment compliance, severe panic attacks with or without
agoraphobia, debilitating anxiety, depression, fear of death and dying
frequently seen in COPD patients will also automatically resolve without
the need for a professional psychologist on a pulmonary rehabilitation
program. When read closely, the program described in this article does
not resemble a multidisciplinary program at all and hence it should simply
be called a Physiotherapy or Exercise-Based program. Sadly, the kind of
program described will fail many of the COPD patients and Pulmonary
Rehabilitation in the UK will continue to be well behind the well-rounded,
well-funded multidisciplinary prgrams in the US.
The Code of Practice (Control and prevention of tuberculosis in the United Kingdom)[1] provides us with evidence based gold
standards for best practice in this field. The exception is of promoting
routine immigrant screening and the context within which it is
recommended.
I welcome a general health check for immigrants on arrival, but does
routine screening for tuberculosis needs to be part of it?...
The Code of Practice (Control and prevention of tuberculosis in the United Kingdom)[1] provides us with evidence based gold
standards for best practice in this field. The exception is of promoting
routine immigrant screening and the context within which it is
recommended.
I welcome a general health check for immigrants on arrival, but does
routine screening for tuberculosis needs to be part of it? Emphasis on
such screening implies convincing evidence. The Code’s reference to
Ormerod contradicts that assumption.[2][3]
Ormerod states that most tuberculosis is not evident on arrival.
Birmingham stopped adult screening some years back. Birmingham is
arguably the largest receiver of immigrants from the Indian subcontinent
to the UK. It was rare for even a single case to be recorded annually
when screening was practised in the city.
We must also take into account the cumulative radiological hazards of
screening; comparative cost benefits and effectiveness of diagnosing an
active case and its subsequent management as against relying on a disease
management policy alone. Human rights issue of equating immigration with
tuberculosis cannot be ignored.[4] [5]
The context in which immigrant screening is recommended is also worth
noting. Increased number of tuberculosis cases in the country does not
necessarily mean increased incidence. We have very poor measures of the
population base against which rates could be determined.
The natural immigrant population increase (some communities have an
above average birth rate) added to the number of new arrivals is an
unknown quantity since the last census a decade ago. The immigrant
population has also aged and could account for a higher age-specific
number of tuberculosis cases. Race and age specific rates may indeed be
falling while overall prevalence shows an increase. Much higher prevalence
of age-related diabetes in the immigrant population is an additional risk
factor for tuberculosis.[6]
It may well be that the increase in numbers is accompanied by
decrease in age and race specific rates due to improved living conditions
and better treatment facilities. The Code does add to the confusion,
referring to geographical preponderance when in reality the increase is
due to the presence of inhabitants from different parts of the world.
Areas such as Liverpool, though densely populated but with fewer immigrants
of Indian subcontinent origin, have a much lower overall prevalence of
tuberculosis.[7]
Tuberculosis is a slow evolving disease. It will be decades before
those who have migrated in the second half of the last century come into
equilibrium with rest of the indigenous population. There is the urgent
need to show whether this population is progressing towards that end or
that there is reversal in the secular trend of decrease of tuberculosis.
The latter would indeed be most worrying and call for the most detailed of
measures including screening.
We do not yet know of the impact of any control strategy on the trend
of tuberculosis. A disease management policy in affluent countries will at
least reduce the burden of disease and suffering. Diverting resource to a
screening programme will be counter productive.[8]
References
(1) BTS guidelines. Control and prevention of tuberculosis in the
United Kingdom: Code of Practice 2000. Thorax 2000;55:887-901.
(2) Ormerod LP. Tuberculosis screening and prevention in new
immigrants 1983-88. Respir Med 1990;84:269-71.
(3) Ormerod LP. Is immigrant screening for tuberculosis still
worthwhile? J Infect 1998;37:39-40.
(4) Bakhshi SS. screening immigrants at risk of tuberculosis. BMJ 1994;308:416.
(5) Bakhshi S. Detecting tuberculosis in new arrivals to UK. BMJ 2000;321:569.
(6) Stead WW, Dutt AK. Tuberculosis in the elderly. Semin Respir Infect 1989;4:189-97.
(7) Jeremy IH, Bakhshi SS, Ali S, Farrington CP. Ecological analysis
of ethnic differences in relation between tuberculosis and poverty. BMJ 1999;319:1031-4.
(8) Bwire R, et al. Tuberculosis screening among immigrants in The Netherlands: what is its contribution to public health? The Netherlands J Med 2000;56:63-71.
If the abstract indicates correctly that children of totally non-smoking parents were not included in the study, I see that as a significant weakness.
The study found, as might be expected by many, an increase in contacts for asthma episodes among children most heavily exposed to environmental tobacco smoke (ETS).
However, it also found a non-significant but noteworthy decrease in asthma epi...
If the abstract indicates correctly that children of totally non-smoking parents were not included in the study, I see that as a significant weakness.
The study found, as might be expected by many, an increase in contacts for asthma episodes among children most heavily exposed to environmental tobacco smoke (ETS).
However, it also found a non-significant but noteworthy decrease in asthma episode contacts among those with "moderate" exposure as opposed to "low" exposure. If non-smoking parents (which would presumably usually
have children with *extremely* low exposure) had been included as a study group as well, we might have seen a continuation of the U-shaped curve indicating support for the idea that moderate levels of tobacco smoke in
the air might act in some way as a suppressor to asthma or asthma episodes
among children regularly exposed to such. Such a finding would also be in
line with the observed increase in asthma among American children over the
last few decades that seems to form a strikingly inverse relationship with
the exposure of American children to secondary smoke in the home and such
venues as fast-food restaurants and child care facilities.
Such a theory is of course anathema to the standard view that *any* exposure is "bad" for children and others, but it's possible that it could prove correct if properly studied.
Simler et al. raise an interesting possibility of the prognostic
value of plasma VEGF in interstitial lung disease. Meyer et al. in a
previous study [1] did not find any difference
in serum VEGF165 levels in patients with diffuse parenchymal lung disease.
It would have been interesting to know the BALF VEGF levels of these
patients as Meyer et al.and Koyama et al. [2] have shown reduced BAL fluid VEGF...
Simler et al. raise an interesting possibility of the prognostic
value of plasma VEGF in interstitial lung disease. Meyer et al. in a
previous study [1] did not find any difference
in serum VEGF165 levels in patients with diffuse parenchymal lung disease.
It would have been interesting to know the BALF VEGF levels of these
patients as Meyer et al.and Koyama et al. [2] have shown reduced BAL fluid VEGF levels in interstitial
lung disease. This might simply reflect damage to the alveolar epithelium
(a known major source) in this disease or indeed VEGF may have an
important role in the pathogenesis of interstitial disease. Interestingly,
VEGF receptor blockade has been shown to lead to an induction of apoptosis
and an emphysema-like histological appearance in rats but with no evidence
of fibrosis or inflammatory cells [3].
In addition, it is interesting to speculate the cellular source of
the elevated plasma VEGF in the more fibrotic patients? Could this
represent alveolar-capillary membrane damage with leakage of intra-
alveolar VEGF which is known to be compartmentalised [4] and hence lower BALF levels as described in the previous
studies? Or does it represent an inflammatory cell source of systemic VEGF
correlating with an inflammatory response that is here associated with a
poorer outcome? Or is there some other mechanism.
Finally, Koyama et al. have shown smokers also have reduced BAL VEGF
levels and this may be of relevance (if intrapulmonary VEGF is postuated
as having a role in this disease) given the DIP group had all smoked
compared to 50% of the NSIP, and only 20% of the controls.
References
(1) J Lab Clin Med 2000;135:332-8.
(2) Am J Resp Crit Care Med 2002;166: 382-5.
(3) Kasahara et al. J Clin Invest. 2000
Dec;106(11):1311-9.
We read with interest the recent article from Simler et al in Thorax
investigating angiogenic cytokines in patients with idiopathic
interstitial pneumonia [1]. We were surprised by their reported high
levels of plasma VEGF in the normal control group. Previously, several
other groups, including the manufacturers of the ELISA (R&D systems)
quote normal plasma VEGF levels in the range of 36-76 pg/...
We read with interest the recent article from Simler et al in Thorax
investigating angiogenic cytokines in patients with idiopathic
interstitial pneumonia [1]. We were surprised by their reported high
levels of plasma VEGF in the normal control group. Previously, several
other groups, including the manufacturers of the ELISA (R&D systems)
quote normal plasma VEGF levels in the range of 36-76 pg/ml[2, 3]. Indeed
one of the authors of the paper previously quoted normal VEGF levels as 76
pg/ml using a matched pair ELISA [4]. It is clear, therefore that the
levels quoted of 648 pg/ml for normal controls are nearly 10 fold higher
than reported previously.
One possible explanation for this finding is the low centrifugal
force used for preparation of plasma (300g for 12 minutes). The
manufacturer of the ELISA recommends 1000 g for 15 minutes as a way to
reduce platelet contamination of plasma. Platelet secretion of VEGF is the
reason for elevated serum levels of VEGF when compared to plasma and might
therefore explain the extraordinarily high levels of VEGF found in these
normal subjects [4]. Interestingly 14/49 (28.5%) of patients included were
on immunosuppressant drugs that potentially reduce platelet count. This
offers an alternative explanation as to why there was no difference
between normal patients and those with pulmonary fibrosis in contrast to
earlier reports in connective tissue disease related pulmonary fibrosis
from 1998 [5].
Although the plasma levels of VEGF correlated with fibrosis based
upon CT score it is difficult to fully appreciate the relevance of this
finding, without knowing the concentration of VEGF actually within the
lung compartment. This is because in the normal individual, epithelial
lining fluid levels of VEGF at 9-11 ng/ml are several orders of magnitude
greater than that found in the circulation [6, 7]. Furthermore, previous
investigators have reported reduced levels of alveolar VEGF in patients
with IPF [8]. Low BALF VEGF levels are also seen in patients with acute
lung injury, sarcoidosis, emphysema and the transplanted lung. Thus it
would appear that a reduced alveolar level of VEGF is a common feature of
diseases associated with alveolar epithelial damage. Indeed, in ARDS,
alveolar levels of VEGF are lowest in those with the worst lung injury.
This is probably a result of reduced epithelial cell secretion of VEGF and
increased expression of its soluble receptor sVEGFR-1, which acts as a
natural inhibitor to the bioactivity of VEGF. The trophic role of VEGF
within the lung is supported by the fact that VEGF acts as a proliferative
factor for fetal pulmonary epithelial cells (9) and because lung-targeted
VEGF inactivation leads to an emphysema phenotype in mice[10]. These
studies suggest that reduced alveolar levels of VEGF may inhibit
epithelial repair in a wide variety of lung diseases.
To summarize, we have some concerns about the
validity/reproducibility of the VEGF levels reported in this study.
Furthermore, based upon the available evidence, we believe it is
inappropriate to suggest that antagonizing VEGF would be a successful
potential therapy for patients with pulmonary fibrosis. To the contrary we
believe this would hasten epithelial cell apoptosis and promote alveolar
septal cell loss with resultant honeycombing and functional deterioration.
References
(1) Simler, N. R., P. E. Brenchley, A. W. Horrocks, S. M. Greaves, P.
S. Hasleton, and J. J. Egan. 2004. Angiogenic cytokines in patients with
idiopathic interstitial pneumonia. Thorax 59(7):581-585.
(2) Thickett, D. R., L. Armstrong, S. J. Christie, and A. B. Millar. 2001.
Vascular endothelial growth factor may contribute to increased vascular
permeability in acute respiratory distress syndrome. Am J Respir Crit Care
Med 164(9):1601-5.
(3) Himeno, W. 2001. Angiogenic growth factors in patients with cyanotic
congenital heart disease and in normal children. Kurume Med J 48(2):111-6.
(4) Webb, N. J., M. J. Bottomley, C. J. Watson, and P. E. Brenchley. 1998.
Vascular endothelial growth factor (VEGF) is released from platelets
during blood clotting: implications for measurement of circulating VEGF
levels in clinical disease. Clin Sci (Lond) 94(4):395-404.
(5) Kikuchi, K., M. Kubo, T. Kadono, N. Yazawa, H. Ihn, and K. Tamaki.
1998. Serum concentrations of vascular endothelial growth factor in
collagen diseases. Br J Dermatol 139(6):1049-51.
(6) Kaner, R. J., and R. G. Crystal. 2001. Compartmentalization of vascular
endothelial growth factor to the epithelial surface of the human lung. Mol
Med 7(4):240-6.
(7) Thickett, D. R., L. Armstrong, and A. B. Millar. 2002. A role for
vascular endothelial growth factor in acute and resolving lung injury. Am
J Respir Crit Care Med 166(10):1332-7.
(8) Koyama, S., E. Sato, M. Haniuda, H. Numanami, S. Nagai, and T. Izumi.
2002. Decreased level of vascular endothelial growth factor in
bronchoalveolar lavage fluid of normal smokers and patients with pulmonary
fibrosis. Am J Respir Crit Care Med 166(3):382-5.
(9) Brown, K. R., K. M. England, K. L. Goss, J. M. Snyder, and M. J.
Acarregui. 2001. VEGF induces airway epithelial cell proliferation in
human fetal lung in vitro. Am J Physiol Lung Cell Mol Physiol 281(4):L1001
-10.
(10) Tang, K., H. B. Rossiter, P. D. Wagner, and E. C. Breen. 2004. Lung-
targeted VEGF inactivation leads to an emphysema phenotype in mice. J Appl
Physiol.
I read the article by Janssen-Heijnen et al with interest [1]. There are
large differences in the reported survival of patients presenting with
lung cancer. Those presenting in the United states and Spain are reported
to have up to twice the chance of surviving five years when compared to
those presenting in the United Kingdom [2-4]. This may be due to differences
in disease, differences in performanc...
I read the article by Janssen-Heijnen et al with interest [1]. There are
large differences in the reported survival of patients presenting with
lung cancer. Those presenting in the United states and Spain are reported
to have up to twice the chance of surviving five years when compared to
those presenting in the United Kingdom [2-4]. This may be due to differences
in disease, differences in performance status or co-morbidity, differences
in treatment, or differences in recording, but it demands a critical
analysis of current practice. This study informs the discussion suggesting
that age and co-morbidity do not significantly alter prognosis but it
includes only those with a histologically confirmed non small cell lung
cancer. It seems likely that age and significant co-morbidity might reduce
the chances of getting histology. Do the authors know the rate of
histological confirmation in the population described and, if so, is it
influenced by age or co-morbidity? It is hard to base any conclusion on
the role of these factors in outcomes for the whole population on those
with confirmed histology without first quantifying age and co-morbidity in
those without histological confirmation.
References
(1) Janssen-Heijnen MLG. Effect of comorbidity on the treatment and prognosis of elderly patients with non-small cell lung cancer. Thorax 2004; 59: 602-607
(2) Berrino F, Capocaccia R, Estève T, et al. Survival of cancer
patients in Europe- the EUROCARE 2 Study. (IARC Scientific Publications
No. 151) International Agency for Research on Cancer (Lyon: 1999)
(3) Sikora K. Cancer survival in Britain. BMJ 1999; 319: 461-2
(4) American Cancer Society, Inc. Cancer Facts and Figures 2002.
Surveillance Research (2002)
The paper by Fitzgerald et al [1] raises important questions as to
what patients should be advised to do during periods of less well
controlled asthma. In other words, the commonly advised practice of
doubling the inhaled corticosteroid dose is not backed up by a wealth of
evidence, in turn resulting in an embarassing paucity of clear guidance
for patients.
The paper by Fitzgerald et al [1] raises important questions as to
what patients should be advised to do during periods of less well
controlled asthma. In other words, the commonly advised practice of
doubling the inhaled corticosteroid dose is not backed up by a wealth of
evidence, in turn resulting in an embarassing paucity of clear guidance
for patients.
It has become apparent in the management of chronic asthma, that
additional 2nd line controller therapy is generally more advantageous than
doubling the dose of inhaled corticosteroid. [2] In the treatment and
prevention of asthma exacerbations, a similar pharmacotherapeutic
rationale may also become the norm and be incorporated into individualised
asthma action plans. In other words, adding further 2nd line therapy for a
short period of time during deteriorating asthma control - while
maintaining the same inhaled corticosteroid dose - may be appropriate.
For example, the hybrid actions of leukotriene antagonism would
attenuate airway hyperresponsiveness and further dilate the airways, while
add on long acting ß2-agonist would maximally bronchodilate the airways
with the provision of an “airway stabilising effect”.[3] Indeed, Aalbers
et al demonstrated that the use of budesonide and eformoterol in
combination, with dose adjustment according to patients symptoms,
conferred benefit in terms of exacerbations, lung function and reliever
use. Perhaps in asthmatics already using an inhaled corticosteroid plus
long acting ß2-agonist, the addition of montelukast may be worthwhile, as
“triple therapy” has been shown to confer further benefit in terms of
surrogate inflammatory biomarkers and attenuating airway
hyperresponsiveness.[5]
In conclusion, studies evaluating the effects of “short bursts” of
leukotriene receptor antagonists or add-on long acting ß2-agonists
compared to doubling the inhaled corticosteroid dose during deteriorating
asthma control are urgently required.
Graeme P Currie
Daniel K C Lee †
Department of Respiratory Medicine, Aberdeen Royal Infirmary,
Foresterhill, Aberdeen AB25 2ZN, Scotland, United Kingdom
† Department of Respiratory Medicine, Ipswich Hospital, Heath Road,
Ipswich IP4 5PD, Suffolk, England, United Kingdom
References
1. FitzGerald JM, Becker A, Sears MR, et al. Doubling the dose of
budesonide versus maintenance treatment in asthma exacerbations. Thorax
2004;59:550–6
2. British Guideline on the Management of Asthma. Thorax 2003; 58
(Suppl 1):1-83.
3. Currie GP, Jackson CM, Ogston SA, Lipworth BJ. Airway-stabilising
effect of long-acting ß2-agonists as add-on therapy to inhaled
corticosteroids. QJM 2003;96: 435-40.
4. Aalbers R, Backer V, Kava TTK, et al. Adjustable maintenance
dosing with budesonide/formoterol compared with fixed-dose
salmeterol/fluticasone in moderate to severe asthma. Curr Med Research and
Opinion 2004; 20: 225-40.
5. Currie GP, Lee DKC, Haggart K, et al. Effects of montelukast on
surrogate inflammatory markers in corticosteroid treated patients with
asthma. Am J Respir Crit Care Med 2003; 167:1232-8.
We fully appreciate Dr Furness's comments on the limitations of the definition of asthma based on parents' reports of symptoms and we have contributed on the subject.[1] Epidemiological studies of asthma have to rely on reported symptoms,[2][3] but a better understanding of what parents call wheeze would be of great importance, especially in a multicultural society. The validity of reported asthma symptoms...
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...
Dear Editor,
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) rat...
The review of Pulmonary Rehabilitation in the UK (Thorax, 2001: 56: 827-834) by Dr MDL Morgan begins by noting the lag between the quality of pulmonary rehabilitation services in the USA compared to their virtual absence in the UK. Dr Morgan goes on to mention that psychology is one of the disciplines included in the multiple disciplines that comprise an effective pulmonary rehabilitation program. In fact, most of the le...
The Code of Practice (Control and prevention of tuberculosis in the United Kingdom)[1] provides us with evidence based gold standards for best practice in this field. The exception is of promoting routine immigrant screening and the context within which it is recommended.
I welcome a general health check for immigrants on arrival, but does routine screening for tuberculosis needs to be part of it?...
If the abstract indicates correctly that children of totally non-smoking parents were not included in the study, I see that as a significant weakness.
The study found, as might be expected by many, an increase in contacts for asthma episodes among children most heavily exposed to environmental tobacco smoke (ETS).
However, it also found a non-significant but noteworthy decrease in asthma epi...
Dear Editor
Simler et al. raise an interesting possibility of the prognostic value of plasma VEGF in interstitial lung disease. Meyer et al. in a previous study [1] did not find any difference in serum VEGF165 levels in patients with diffuse parenchymal lung disease. It would have been interesting to know the BALF VEGF levels of these patients as Meyer et al.and Koyama et al. [2] have shown reduced BAL fluid VEGF...
Dear Editor
We read with interest the recent article from Simler et al in Thorax investigating angiogenic cytokines in patients with idiopathic interstitial pneumonia [1]. We were surprised by their reported high levels of plasma VEGF in the normal control group. Previously, several other groups, including the manufacturers of the ELISA (R&D systems) quote normal plasma VEGF levels in the range of 36-76 pg/...
Dear Editor
I read the article by Janssen-Heijnen et al with interest [1]. There are large differences in the reported survival of patients presenting with lung cancer. Those presenting in the United states and Spain are reported to have up to twice the chance of surviving five years when compared to those presenting in the United Kingdom [2-4]. This may be due to differences in disease, differences in performanc...
Dear Editor,
The paper by Fitzgerald et al [1] raises important questions as to what patients should be advised to do during periods of less well controlled asthma. In other words, the commonly advised practice of doubling the inhaled corticosteroid dose is not backed up by a wealth of evidence, in turn resulting in an embarassing paucity of clear guidance for patients.
It has become apparent in the...
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