Thanks to all concerned for putting together a very useful and long
awaited guideline. I have the following questions and comments.
1. What does "All Patient Rate" in table 3B mean and when should one
use it, if at all for UK born patients (say white) as opposed to table 3A?
Does a UK born white of 75 have a risk of 11 (Table 3A) or 4 (Table
3B - All patient rate column)?
2. I think that an arrow is missing between "Tuberculin test
unreliable" in "On Immunosuppressant" group AND "Stratify for TB Risk" box
in Figure 1.
3. I assume that patients who develop TB whilst on Anti TNF Alfa
treatment would qualify for 4 drug treatment simply by virtue of being on
immunosuppressants.
4. What is the guidance about patients who have developed TB whilst
on treatment with Anti TNF Alfa drugs and have not been able to tolerate
full treatment with 4 drugs, with regards to concomitant treatment with
Anti TNF Alfa drugs in "Normal CXR group" or time lag before treatment can
be started in "abnormal/suspicious group"? I have a couple of such
patients.
My mother had a yearly chest x-ray in March 2003 which then showed a
mild kyphotic deformity in her thorax. In June 2004 she had another
yearly x-ray which showed a left hilar mass lesion. Needless to say a
week later she had a CT scan which showed that the cancer had metastized
to her adrenal glands and she also had numerous lesions on her liver. As
a physician would the kyphotic deformity be an indication to take fu...
My mother had a yearly chest x-ray in March 2003 which then showed a
mild kyphotic deformity in her thorax. In June 2004 she had another
yearly x-ray which showed a left hilar mass lesion. Needless to say a
week later she had a CT scan which showed that the cancer had metastized
to her adrenal glands and she also had numerous lesions on her liver. As
a physician would the kyphotic deformity be an indication to take further
tests seeing that my mother was a heavy smoker for 65 years? Her
diagnosis was small cell lung cancer.
We have read with interest the paper of Battaglia et al.[1] regarding the
relationship between small airways function and molecular markers of
inflammation in exhaled air in mild asthma. They concluded that fractional
exhaled nitric oxide (FeNo) and 8-isoprostane in exhaled air reflect small
airway inflammation, and that 8-isoprostane particularly is increased in
patients with more prominent airway closure....
We have read with interest the paper of Battaglia et al.[1] regarding the
relationship between small airways function and molecular markers of
inflammation in exhaled air in mild asthma. They concluded that fractional
exhaled nitric oxide (FeNo) and 8-isoprostane in exhaled air reflect small
airway inflammation, and that 8-isoprostane particularly is increased in
patients with more prominent airway closure. However, the authors
reported levels of 8-isoprostane in EBC in the controls that were higher
(2.9-7.6 pg/ml) than in mildly asthmatic patients (1.6-2.7 pg/ml).
These results are in agreement with a previous report [2] and with
our findings. In a group of 13 asthmatic children without acute symptoms,
we found a mean concentration of 8-isoprostane in EBC of 1.09 + 1.69
pg/ml. Seven patients had a concentration lower than the detection limit
(5 pg/ml). The mean concentrations were higher in healthy controls than
in asthmatic children. These data raise several concerns regarding the
measurement of 8-isoprostane in exhaled breath condensate. In both our and
Battaglia's study the 8-isorostane values are either below or just above
the limit of the assay used to detect 8-isoprostane and so should be
viewed with the utmost caution.
Furthermore, the low levels of 8- isoprostane in the EBC of asthmatic
patients in comparison with controls raises the question whether the
detection of this molecule can be a reliable marker of the functional
status of small airways. We think that data of Battaglia et al. provide
only preliminary evidence. We suggest that these data indicate that 8-
isoprostane cannot be considered associated with airway inflammation in
asymptomatic asthmatic patients at the present time. The measurement of
exhaled breath condensate and inflammatory markers are not standardised
which makes comparison between studies also difficult. Further evaluations
by a more accurate technique, such as gas chromatography/mass spectrometry
[3], will be necessary.
References
1. Battaglia S, den Hertog H, Timmers MC et al. Small airways
function and molecular markers in exhaled air in mild asthma. Thorax 2005;
60: 639-644.
2. Van Hoydonck PG, Wuyts WA, Vanaudenaerde BM, et al.
Quantitative analysis of 8-isoprostane and hydrogen peroxide in exhaled
breath condensate. Eur Respir J 2004; 23:189-92.
We read with great interest the article by Schanen[1] et al. - Asthma
and incident cardiovascular disease in which the authors have shown an
association between multivariate adjusted Hazard ratio and incident
stroke, but, not with Coronary heart disease in both model 1 and 2. One of
the most important risk factors for coronary heart disease in asthmatics
identified so far is the use of inhaled short-ac...
We read with great interest the article by Schanen[1] et al. - Asthma
and incident cardiovascular disease in which the authors have shown an
association between multivariate adjusted Hazard ratio and incident
stroke, but, not with Coronary heart disease in both model 1 and 2. One of
the most important risk factors for coronary heart disease in asthmatics
identified so far is the use of inhaled short-acting and long acting beta
2 agonists.[2]
More recently a meta analysis conducted by Shelley et al.[3]
reported that for trials lasting from 3 days to 1 year, ß2-agonist
treatment significantly increased the risk for a cardiovascular event
(relative risk [RR], 2.54; 95% CI, 1.59 to 4.05) compared to placebo.
Similar findings of increased risk of unstable angina, myocardial
infarction associated with inhaled beta- agonists were also reported by
Au et al.[4,5] It would have had tremendous clinical application if the
authors had studied the association between inhaled beta 2 agonist and
incident coronary heart disease in ever asthmatics.
Also studies have shown that rapid decline of FEV1 is an independent
risk factor for coronary heart disease.[6] Since this was a prospective
cohort study, it would be useful if the authors also analysed the
association between decline of FEV1 /Low quartiles of FEV1 and incident
coronary heart disease.
References
1. JG Schanen et al: Asthma and incident cardiovascular disease: the
Atherosclerosis Risk in Communities Study.
Thorax. 2005 Aug;60(8):633-8.
2. Suissa et al. Patterns of increasing beta-agonist use and the risk of
fatal or near-fatal asthma Eur Respir J 1994; 7: 1602-1609.
3. Shelley R. Salpeter, Thomas M. Ormiston, and Edwin E. Salpeter
Cardiovascular Effects of ß-Agonists in Patients With Asthma and COPD: A
Meta-Analysis
Chest, Jun 2004; 125: 2309 - 2321.
4. Au, DH, Curtis, JR, McDonell, MB, et al. Association between inhaled
beta-agonists and the risk of unstable angina and myocardial infarction.
Chest 2002;121,846-851.
5. Au, DH, Lemaitre, RN, Curtis, JR, et al. The risk of myocardial
infarction associated with inhaled beta-adrenoceptor agonists. Am J Respir
Crit Care Med 2000;161,827-830.
6. Tockman MS et al. A new risk factor for coronary heart disease
mortality. Am J Respir Crit Care Med 1995;151:390-398.
Matheson et al., in their article had shown that the occupational
exposure to biological dust was more associated with increased risk of
respiratory symptoms and COPD than the mineral dust and gas fumes. We
suppose that the subjects who had shown both mineral dust or gas and
biological dust exposure together in their occupational history could have
confounded these results.
Matheson et al., in their article had shown that the occupational
exposure to biological dust was more associated with increased risk of
respiratory symptoms and COPD than the mineral dust and gas fumes. We
suppose that the subjects who had shown both mineral dust or gas and
biological dust exposure together in their occupational history could have
confounded these results.
The statement that biological dust is more prone
to cause COPD and respiratory symptoms as compared to the mineral dust and
gas fumes, would have been more conclusive if the author had compared
subjects exposed purely to the biological fumes with the subjects purely
to the mineral dust or gas fumes.
Secondly the author had shown that women
are more prone to develop COPD on cumulative exposure of biological dust
in form of 1-12 years and >12 years, as compared to males. The author
had not shown the distribution of male and female gender in perspective of
both years of exposure and, high and low exposures. We suppose higher
number of females with high and longer duration of exposure than the
males, must have attributed to these results. Moreover predominance of
female COPDs could have been attributed to passive smoking.
McGhee et al.
had shown that passive smokers were 37% more likely to visit doctors for
respiratory symptoms[1] than the non-passive smokers. Svanes et al. had also
shown that intrauterine and environmental exposure to parental smoking was
related to more respiratory symptoms and poorer lung functions in
adulthood.[2] Lastly factors like poor living conditions could have
attributed to increase in COPD prevalence in subjects exposed to
biological dust. Recently Kim et al. in Korean population had shown low
income to be independent predictor with odds ratio of 2.13 for COPD.[3]
References
1. S M McGhee, AJ Hedley and LM Ho; Passive smoking and its imoact on
employers and employees in Hong Kong: Occup. Environ. Med. 2002; 59; 842-
846.
2. C Svanes, E Omennas, D Jarvis S Chinn, A Gulsvik, P Burney;
Parental Smoking in childhood and adult obstructive lung disease: results
from European Community Respiratory Health Survey; Thorax 2004: 295-302.
3. Dong Soon Kim, Young Sam Kim et al: Prevalence of Obstructive
Pulmonary Disease in Korea: A population based Spirometry Survey: Am J
Respir Crit Care Med. 2005 Jun 23.
I read with interest the study by Broekhuizen et al. in which they
described the beneficial effect of n-3 EPA/DHA. This reminded me of my own
study done few years back on the possible beneficial action of n-3 PUFAs
in bronchial asthma. In this study, I observed that asthmatics
supplemented with n-3 PUFAs had fewer episodes of asthmatic attacks and
the attacks tended to be mild. At that time, I thought...
I read with interest the study by Broekhuizen et al. in which they
described the beneficial effect of n-3 EPA/DHA. This reminded me of my own
study done few years back on the possible beneficial action of n-3 PUFAs
in bronchial asthma. In this study, I observed that asthmatics
supplemented with n-3 PUFAs had fewer episodes of asthmatic attacks and
the attacks tended to be mild. At that time, I thought that I am too
biased and hence the results were never published. Retrospectively, it is
now clear that n-3 PUFAs are beneficial both in asthma and COPD.
Although, the exact mechanism of action is not clear, it is likely
that anti-inflammatory actions of n-3 PUFAs need to be considered
seriously. The absence of any significant changes in the plasma
concentrations of CRP, TNF, and IL-6 in the study done by Broekhuizen et
al., suggests that in all probability local actions of these fatty acids
within the lungs needs to be taken into consideration. The other
possibility is that n-3 PUFAs may not alter the concentrations of pro-
inflammatory cytokines but may enhance the production of anti-inflammatory
cytokines such as IL-4 and IL-10 that may tilt the balance more towards
resolution of inflammation.
The other possibility is that n-3 PUFAs are known to reduce anxiety
and this may aid in the beneficial effect seen. N-3 PUFAs also enhance
endothelial nitric oxide (eNO) generation. NO is known to have
bronchodilator actions and reduce inflammation.
It is possible that long-term supplementation of n-3 PUFAs may offer
more clear-cut beneficial actions in asthma and COPD and this needs to be
studied.
We thank Dr. O'Driscoll for alerting us to an error in the text. The
correct figure for the worldwide mortality from lung cancer in 2000 was
0.85 million, not 328 million as originally stated in the article.
We read with particular interest an excellent paper of Swigris et
al.[1] systemically reviewed the published literature, to 1 April 2004, on
the important issue of health-related quality of life (HRQL) in patients
with idiopathic pulmonary fibrosis (IPF). We recently published a study
(2) investigated HRQL impairment of 25 patients with histologically proven
IPF using 3 HRQL questionnaires, 1 generic:...
We read with particular interest an excellent paper of Swigris et
al.[1] systemically reviewed the published literature, to 1 April 2004, on
the important issue of health-related quality of life (HRQL) in patients
with idiopathic pulmonary fibrosis (IPF). We recently published a study
(2) investigated HRQL impairment of 25 patients with histologically proven
IPF using 3 HRQL questionnaires, 1 generic: the Quality of Well-being
(QWB), 1 specific to assess psychological aspects: the Hospital Anxiety
and Depression questionnaire (HAD) and 1 specific for pulmonary diseases:
the St. George’s Respiratory Questionnaire (SGRQ). Three dyspnea scales
(MRC, Borg, and oxygen cost diagram-OCD), pulmonary function tests,
arterial blood gas measurements at rest and during exercise and the
duration of the disease were used for correlations with HRQL measurements.
Although SGRQ total and its all component’s scores were increased in
our population they were lower than the mean scores reported in the study
of Swigris et al. These discrepancies are most likely attributable to the
differences of the groups studied in terms of the severity and the
duration of the disease. The scores of the QWB (best: 1; worse: 0) in our
IPF patients was significantly lower than healthy controls, mean(SD)
0.59(0.29) versus 0.866 (0.05) while the HAD questionnaire (best:<_8 xmlns:worse="urn:x-prefix:worse" _="_" worse:_="worse:_"/>10) score although statistically significant different than
normal group did not reached clinically relevant level. The latter means
that IPF does not affect significantly the psychological status of the
patients with IPF.
According to our findings the SGRQ total score was
statistically significant correlated with TLC (r=-0.499), FEV1 (r=-0.545),
PaO2 at rest (r=-0.514), and with PaO2 on exertion (r=-0.597). All the
three dyspnea scales (MRC, Borg, OCD) used in our study were significantly
correlated with the duration of the disease, r=0.774, 0.687, and 0.687,
respectively. Finally we found significant correlations between duration
of the disease and SGRQ (r=0.483), Hospital anxiety (r=0.637), and
Hospital depression (r=0.629) scores. The relationships found between
duration of the disease and HRQL measurements indicate that maybe patients
does not adapt fully to their disease over time. However, we agree with
the conclusion of the paper of Swigris et al that more studies are needed
to verify whether this chronic disease affects quality of life
longitudinally, taking into account the lack of a specific questionnaire
in ILDs (3).
References
1. Swigris JJ, Kuschner WG, Jacobs SS, Wilson SR, Gould MK. Health-
related quality of life in patients with idiopathic pulmonary fibrosis: a
systematic review. Thorax. 2005; 60:588-94.
2. Tzanakis N, Samiou M, Lambiri I, Antoniou K, Siafakas N, Bouros D.
Evaluation of health-related quality-of-life and dyspnea scales in
patients with idiopathic pulmonary fibrosis. Correlation with pulmonary
function tests. Eur J Intern Med. 2005;16:105-112.
3. Bouros D., Psathakis K. Siafakas N. M. Quality of life in
interstitial lung disease. Eur Respir Rev 1997; 7:66-70.
Authors Nikolaos Tzanakis, Nikolaos Siafakas, Demosthenes Bouros
Departments of Thoracic Medicine
Medical School University of Crete and
Medical School Democritus University of Thrace Greece
Wassawa-Kintu and colleagues have performed a useful meta-analysis of
the effect of reduced FEV1 on the risk of developing lung cancer. However,
the authors, reviewers and editors failed to notice a major error of fact
which is repeated in the "Airwaves" section of the journal. They stated in
both articles that 328 million people died of lung cancer in 2000.
Wassawa-Kintu and colleagues have performed a useful meta-analysis of
the effect of reduced FEV1 on the risk of developing lung cancer. However,
the authors, reviewers and editors failed to notice a major error of fact
which is repeated in the "Airwaves" section of the journal. They stated in
both articles that 328 million people died of lung cancer in 2000.
The population of the world is about 6000 million people. If average
life expectancy is about 45 years, there would be only 133 million deaths
in the world from all causes in a single year! The correct figure from the
reference quoted is 0.85 million deaths from lung cancer in 2000.
Yours sincerely,
Dr B. Ronan O'Driscoll
Reference
1. Ezzati M, Lopez AD. Estimates of global mortality attributable to
smoking in 2000. Lancet. 2003; 362:847-52.
We read the study by Zollner and colleagues published recently in
Thorax about the leveling off of asthma and allergies among children in
Germany between 1992 and 2001.[1] We have published a study looking at
the same issue and using much of the same methodology (ISAAC) to assess
asthma and allergies symptoms, diagnosis, and severity in more than 15,000
children (6–7 and 13–14 year olds) between 199...
We read the study by Zollner and colleagues published recently in
Thorax about the leveling off of asthma and allergies among children in
Germany between 1992 and 2001.[1] We have published a study looking at
the same issue and using much of the same methodology (ISAAC) to assess
asthma and allergies symptoms, diagnosis, and severity in more than 15,000
children (6–7 and 13–14 year olds) between 1995 and 2000 in Muenster,
Germany.[2] We found a tendency towards an increase in current symptoms
of asthma and allergies in both age groups, but more so among girls.[2]
Indices of diagnosis either remained the same or increased in parallel to
the increase in symptoms, arguing against a change in diagnostic behaviour
as an explanation for our results. Indices of severity also showed a
homogenous increase in the 5-year study period pointing towards an
increase in the overall burden of asthma and allergies within the society.[2]
Regrettably, these results, coming from Germany, were not considered
either in the discussion of Zollner’s report nor in the affirmative title
that no increase in asthma and allergies occurred in Germany in the
nineties. Regrettably more so, when our study was alluded to in the
discussion and conclusion of Zollner’s report it was cited, contrary to
our results, as one of the studies (from China!!) showing a decrease or
leveling off of asthma and allergies among children. [1] Remarkably our
study had the word Germany in the title.
Regards
Wasim Maziak and Ulrich Keil,
Institute of Epidemiology and Social Medicine,
University Clinic of Muenster, Muenster, Germany
References
1. Zollner IK, Weiland SK, Piechotowski I, Gabrio T, von Mutius E,
Link B, Pfaff G, Kouros B, Wuthe J. No increase in the prevalence of
asthma, allergies, and atopic sensitisation among children in Germany:
1992-2001. Thorax 2005; 60(7):545-8.
2. Maziak W, Behrens T, Brasky TM, Duhme H, Rzehak P, Weiland SK,
Keil U. Are asthma and allergies in children and adolescents increasing?
Results from ISAAC phase I and phase III surveys in Munster, Germany.
Allergy 2003;58(7):572-579.
Dear Editor,
Thanks to all concerned for putting together a very useful and long awaited guideline. I have the following questions and comments.
1. What does "All Patient Rate" in table 3B mean and when should one use it, if at all for UK born patients (say white) as opposed to table 3A?
Does a UK born white of 75 have a risk of 11 (Table 3A) or 4 (Table 3B - All patient rate column)?
2. I...
My mother had a yearly chest x-ray in March 2003 which then showed a mild kyphotic deformity in her thorax. In June 2004 she had another yearly x-ray which showed a left hilar mass lesion. Needless to say a week later she had a CT scan which showed that the cancer had metastized to her adrenal glands and she also had numerous lesions on her liver. As a physician would the kyphotic deformity be an indication to take fu...
Dear Sir,
We have read with interest the paper of Battaglia et al.[1] regarding the relationship between small airways function and molecular markers of inflammation in exhaled air in mild asthma. They concluded that fractional exhaled nitric oxide (FeNo) and 8-isoprostane in exhaled air reflect small airway inflammation, and that 8-isoprostane particularly is increased in patients with more prominent airway closure....
Dear Editor,
We read with great interest the article by Schanen[1] et al. - Asthma and incident cardiovascular disease in which the authors have shown an association between multivariate adjusted Hazard ratio and incident stroke, but, not with Coronary heart disease in both model 1 and 2. One of the most important risk factors for coronary heart disease in asthmatics identified so far is the use of inhaled short-ac...
Dear Editor,
Matheson et al., in their article had shown that the occupational exposure to biological dust was more associated with increased risk of respiratory symptoms and COPD than the mineral dust and gas fumes. We suppose that the subjects who had shown both mineral dust or gas and biological dust exposure together in their occupational history could have confounded these results.
The statement that...
Dear Editor,
I read with interest the study by Broekhuizen et al. in which they described the beneficial effect of n-3 EPA/DHA. This reminded me of my own study done few years back on the possible beneficial action of n-3 PUFAs in bronchial asthma. In this study, I observed that asthmatics supplemented with n-3 PUFAs had fewer episodes of asthmatic attacks and the attacks tended to be mild. At that time, I thought...
We thank Dr. O'Driscoll for alerting us to an error in the text. The correct figure for the worldwide mortality from lung cancer in 2000 was 0.85 million, not 328 million as originally stated in the article.
Dear Editor,
We read with particular interest an excellent paper of Swigris et al.[1] systemically reviewed the published literature, to 1 April 2004, on the important issue of health-related quality of life (HRQL) in patients with idiopathic pulmonary fibrosis (IPF). We recently published a study (2) investigated HRQL impairment of 25 patients with histologically proven IPF using 3 HRQL questionnaires, 1 generic:...
Dear Editor,
Wassawa-Kintu and colleagues have performed a useful meta-analysis of the effect of reduced FEV1 on the risk of developing lung cancer. However, the authors, reviewers and editors failed to notice a major error of fact which is repeated in the "Airwaves" section of the journal. They stated in both articles that 328 million people died of lung cancer in 2000.
The population of the world is abou...
Dear Editor,
We read the study by Zollner and colleagues published recently in Thorax about the leveling off of asthma and allergies among children in Germany between 1992 and 2001.[1] We have published a study looking at the same issue and using much of the same methodology (ISAAC) to assess asthma and allergies symptoms, diagnosis, and severity in more than 15,000 children (6–7 and 13–14 year olds) between 199...
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