I was interested to see the work of Figueroa-Munoz and colleagues
showing an association between obesity and wheeze.[1] I would like to
caution against their conclusion. In their study asthma is defined
according to "asthma attack" and parental reports of wheeze. Several
studies have shown parental reporting of wheeze to be unreliable.[2][3][4]
Please can the authors clarify who defined, "asthma att...
I was interested to see the work of Figueroa-Munoz and colleagues
showing an association between obesity and wheeze.[1] I would like to
caution against their conclusion. In their study asthma is defined
according to "asthma attack" and parental reports of wheeze. Several
studies have shown parental reporting of wheeze to be unreliable.[2][3][4]
Please can the authors clarify who defined, "asthma attack?" I see that
their data independent of reported wheeze supports their conclusion but it
would be a stronger argument if parents were not the only ones relied on
to report asthma symptoms. The assumption that all that wheezes is asthma
may lead to the omission of other diagnoses or the inappropriate
prescription of inhaled corticosteroids.
May I be so bold as to suggest an
alternative title for this important work: "Association of obesity and
respiratory symptoms in children"?
References
(1) Figueroa-Munoz JI, Chinn S, Rona RJ. Association of obesity and asthma in 4-11 year old children in the UK Thorax 2001;56:133-7.
(2) Elphick HE, Sherlock P, Foxall G et al. Survey of respiratory sounds in infants. Arch Dis Child 2001;84:35-9.
(3) Cane RS, McKenzie SA. Parents' interpretations of children's respiratory symptoms on video Arch Dis Child 2001;84:31-4.
(4) Cane RS, Ranganathan SC, McKenzie SA. What do parents' of wheezy
children understand by "wheeze". Arch Dis Child 2000;82:327-32.
The observational data presented by Macfarlane et al on the aetiology of
acute lower respiratory tract illness in the community[1] confirm that the
often stated assertion that these illnesses are usually caused by viral
infection is incorrect. The high prevalence of bacteriological and
atypical pathogens, and in particular the high prevalence of C pneumoniae
in these patients is of interest and points to the n...
The observational data presented by Macfarlane et al on the aetiology of
acute lower respiratory tract illness in the community[1] confirm that the
often stated assertion that these illnesses are usually caused by viral
infection is incorrect. The high prevalence of bacteriological and
atypical pathogens, and in particular the high prevalence of C pneumoniae
in these patients is of interest and points to the need for further
studies to clarify the clinical significance of these isolates. The lack
of correlation between indirect evidence of infection (radiographic and
CRP levels), GP assessment of the need for antibiotics and pathogen
isolation are also of great interests and have important messages for
those working in the community.
The outcome conclusions from this study do however need to be treated with
some caution.
The authors state that outcomes were similar whether or not
antibiotics were used, but as this was an unrandomised observational
study, we cannot say that the groups of patients who were and were not
given antibiotics by the GPs in the study were comparable. The experienced
GP researchers in this study may well have had particular reasons for
giving or withholding antibiotics, and the significance of similar
reconsultation rates in these groups is open to interpretation.
In the accompanying editorial,[2] the authors state that systematic
reviews of randomised controlled trials of antibiotic prescription for
acute bronchitis do not support antibiotic treatment, and evidence based
educational initiatives aimed at GPs are advocated as one of the
strategies to alter clinical behaviour.
Having recently reviewed the
literature on this important clinical topic myself,[3] I cannot agree with
their assessment of the current evidence. The more recent review they
quote[4] has been criticised on methodological grounds, and the most
recent and extensive systematic review of this clinical problem, published
on the Cochrane database,[5] comes to very different conclusions,
commenting that "the review confirmed the impression of clinicians that
antibiotics have some beneficial effects in acute bronchitis". The
benefits are probably small and confined to certain patient subgroups, but
the quantification of benefit and the definition of the characteristics of
responder groups need further studies to delineate.
The world literature
currently consists of eight randomised controlled trials of variable
quality, some 20 years old, that use different antibiotic regimens and
different outcome measures. Several of these studies have concluded that
the antibiotic regimens used did improve outcomes.
The recent enquiry into community acquired pneumonia deaths in young
adults published in this journal,[6] revealed that the primary care
management of these patients at the severe end of lower respiratory tract
infection spectrum was deficient in many cases - three quarters of patients
had seen their GP for the illness without a correct diagnoses and few had
received antibiotics from their GP. There are many areas of uncertainty
remaining in this field, and while observational studies such as this help
to bring some clarity into this confused area of daily clinical practice,
well designed randomised controlled trials are still needed to produce the
evidence based guidance that GPs require. The current evidence is
inadequate to meet the challenge identified by Macfarlane et al,[1] that
of identifying the cohort of patients who will benefit from antibiotics.
Dr Mike Thomas
Clinical Research Fellow
Department of Primary Care Respiratory Medicine
University of Aberdeen, UK
References
(1) Macfarlane J, Holmes W, Gard P, Macfarlane R, Rose D, Weston V.
et al. Prospective study of the incidence, aetiology and outcome of lower
respiratory tract illness in the community. Thorax 2001;56:109-14.
(2) Steele K, Gormley G, Webb CH. Management of adult lower
respiratory tract infection in primary care. Thorax 2001;56:88.
(3) Thomas M. The management of acute respiratory tract infection in
adults in primary care. Primary Care Respiratory Journal 200;9:4-7.
(4) Fahey T, Stocks N, Thomas T. Quantitative systematic review of
randomised controlled trials comparing antibiotic with placebo for acute
cough in adults. BMJ 1998;316:910.
(5) Becker L, Glazier R, McIsaac W, and et al. Antibiotics for acute
bronchitis. Douglas R, Bridges-Webb C, Glasziou P, and et al. (1). 1998.
Oxford, Update software. Acute Respiratory Infections Module of the
Cochrane database of systematic reviews.
(6) Simpson JCG, Macfarlane JT, Watson J, Woodhead M. A national
confidential enquiry into community acquired pneumonia deaths in young
adults in England and Wales. Thorax 2000;55:1040-5.
I read with great interest the article of Nakayama et al about tuberculin
responses and risk of pneumonia in immobile elderly patients. It is known
that TH1 cells are important in delayed type hypersensitivity responses to
tuberculin. The authors' findings are important in assessment of
pathogenesis of pneumonia in elderly patients. But I have some doubts
about the analysis of data. The groups were compared...
I read with great interest the article of Nakayama et al about tuberculin
responses and risk of pneumonia in immobile elderly patients. It is known
that TH1 cells are important in delayed type hypersensitivity responses to
tuberculin. The authors' findings are important in assessment of
pathogenesis of pneumonia in elderly patients. But I have some doubts
about the analysis of data. The groups were compared by using Student's t
test although the groups were less than 30. So Mann Whitney U test must be
used instead of Student t test.
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.
I was interested to see the work of Figueroa-Munoz and colleagues showing an association between obesity and wheeze.[1] I would like to caution against their conclusion. In their study asthma is defined according to "asthma attack" and parental reports of wheeze. Several studies have shown parental reporting of wheeze to be unreliable.[2][3][4]
Please can the authors clarify who defined, "asthma att...
The observational data presented by Macfarlane et al on the aetiology of acute lower respiratory tract illness in the community[1] confirm that the often stated assertion that these illnesses are usually caused by viral infection is incorrect. The high prevalence of bacteriological and atypical pathogens, and in particular the high prevalence of C pneumoniae in these patients is of interest and points to the n...
I read with great interest the article of Nakayama et al about tuberculin responses and risk of pneumonia in immobile elderly patients. It is known that TH1 cells are important in delayed type hypersensitivity responses to tuberculin. The authors' findings are important in assessment of pathogenesis of pneumonia in elderly patients. But I have some doubts about the analysis of data. The groups were compared...
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...
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