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Rapid Responses to:
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Rapid Responses published:
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Hiroshi Kawane, Professor The Japanese Red Cross Hiroshima College of Nursing, Hatsukaichi City, Hiroshima, 738-0052, Japan
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The research by Parkes et al[1] may suggest that people tend to care about their age and want to be looking younger. Morris et al[2] reported the usefulness of lung age for motivating smoking cessation. We also made a calculation formula of lung age for the Japanese and found it useful for smokers with mild airflow obstruction[3]. If the lung age was calculated for patients with chronic obstructive pulmonary disease, it may be estimated at 100 or over. Thus in some cases, using lung age for smoking cessaton advice proved to be impractical. References [1]Parkes G, Greenhalgh T, Griffin M, Dent R. Effect on smoking quit ratio of telling patients their lung age: the Step2quit randomised controlled trial. BMJ 2008;0:bmj.39503.582396.25v1 [2]Morris JF, Temple W. Spirometric "lung age" estimation for motivating smoking cessation. Prev Med 1985;14:655 [3]Kawane H, Kojima K. Calculation of "lung age" from lung function. Rinshokensa 1998;42:248 Competing interests: None declared |
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Rajasree Pai R, Lecturer Dr SMCSI MCh
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The study does not compare the effect of patient counselling with showing images of lung age. The paper compares FeV1 with lung age which points to the fact that patients tend to understand simpler terms and images than complicated parameters like FeV1. Competing interests: None declared |
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John J. Kivlighan, Retired Marlborough, MA 01742
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Is there a chart/scale of age to peak flow readings that a layman could use? Many ex-smokers and smokers with asthma have personal peak flow meters and such a chart could be very useful to laymen at large. Regards, John K. Competing interests: None declared |
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Xiaofeng Ren, Associate Professor Microbiology Lab, Northeast Agricultural University, 59 Mucai Street, 150030 Harbin, China
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The work of Parkes et al. proves the positive effect of telling smokers their lung age significantly improves the likelihood of them quitting smoking[1], however, their report just highlights a phenomenon. The question "why" is not clear currently. In my opinion, the "lung age" do display the physical condition of the smokers and it is detectable by clincal examination and can be used as evidences for related evaluation and therapy. Nevertheless, once the smokers were informed on the status of their "lung age", it would be a very important mental stress that is usually difficult to be found and will lead to different response to any advices and intervention. The expected responses may be dependent on the good or bad status of smokers' lung age. Correspondingly, under most circumstances, the smokers may give rise to a very positive response, if they know that they have poor "lung age" . Although "lung age" should be both physical and mental index for patients including long-history smokers, some of the patients usually do not know the exact status of their "lung age". Particularly, some of the patients do not wish to express the weakness of their mentalness frankly. In other words, some of them may do not accept/believe the doctors' advices. Therefore,cooperation between the clincian and psychologists is needed for helping the patients in therapy and also for elucidating the hypothesis furtherly. Reference [1] Parkes G et al., Effect on smoking quit rate of telling patients their lung age: the Step2quit randomised controlled trial. BMJ, doi:10.1136/bmj.39503.582396.25 (published 6 March 2008). Competing interests: None declared |
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Gary Parkes, GP.Researcher EN118EP
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Some attempts have been made by other researchers to correlate FEV1 with PEFR but this has never become an established method. Therefore there is no reliable formula to make the conversion from PEFR into lung age. There are well-established diagnostic criteria for diagnosing COPD using spirometry measurements (FEV1 and FEV1/FVC ratio) but PEFR cannot be used for this purpose. PEFR is very valuable for diagnosis and monitoring of asthma.1 Lung age estimation was developed from reference linear regression equation tables and found to be correlated best with FEV1.(Morris and Temple)2 Reference List 1.Diagnosing COPD. Thorax 59.90001 (2004): i27-i38. 2.Morris, J. F. and W. Temple. "Spirometric "lung age" estimation for motivating smoking cessation." Preventive Medicine 14 (1985): 655-62. Competing interests: Author of the article |
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Anthony N Glaser, Assistant Professor of Family Medicine Medical University of South Carolina, SC 29483
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Parkes et al's paper is encouraging. I have been doing routine spirometry on smokers for some time, and showing patients the Fletcher curve, and anecdotally it seems to have some impact. But it would be helpful to be able to tell patients their lung age. The formulae are cumbersome and the statement "In practice, the lung age is automatically generated by adjustment of the settings of the spirometer" is not very revealing. Just how can lung age be automatically generated by the spirometer? Orr can someone please write a small Palm program that calculates lung age with the stated formulae? Competing interests: None declared |
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Gary Parkes, GP & Researcher Limes Surgery, Hoddesdon
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The Step2quit project used modern spirometers capable of displaying, downloading and/or printing graphs and has settings that can be adjusted to convert FEV1(knowing height and gender) into lung age.However, older models and hand held spirometers do not have that option. I agree that the mathematical formula (as per Morris and Temple) is not practical for daily use in a busy clinic. However, I can supply a calculator (in microsoft excel), which you should be able to keep on your computer desktop or palmcomputer. You only have to type-in the height and FEV1 to get the result. Just e mail me on the address given in the article and I will send you a copy. Gary Parkes Competing interests: Author of the article |
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Dr Manoj K. Saraswat, SpR General/Geriatric Medicine Scarborough Gen.Hospital YO12 5DX, Dr Shweta Saraswat, ST1 Psychiatry:Royal Edinburgh Hospital
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Dear Sir, We read the results and methodology of Step2quit randomised controlled trial by Parkes etal with great interest. The study results are encouraging as significantly more participants quit smoking in the intervention arm, which were explained their lung age based on spirometric results of their lung function tests. Smoking cessation advise is something that almost all clinicians routinely deliver across the specialities and to date most of the guidance suggested to use combination of Intensive behavioural support and nicotine replacement treatment to achieve highest quit rate(1) Although the results from Step2quit randomised trial are encouraging several questions remain to be answered: 1. The study included a very select population from a distinct geographic area of UK. 2.Patients with mental health problems were not Included in the study,this group has particularly high Prevalenc(2) 3. Outcome data are limited to point prevalence on abstinence and relapse rate after Quitting smoking are quite high(3) 4. We are not sure how applicable is to calculate lung age from the seemingly complex formulae given in the article We think more research is needed to clearly validate the usefulness of one strategy over the other in different population groups and patients with different background Social- Medical conditions References: 1.Raw etal Thorax 1998;53(suppl 5,part1)S1-19 2.Karen Lasser etal, JAMA 2000;284:2606-2610 3.Results from NHANES Population Survey:The health benefits of smoking cessation:Washington DC,DHHS,1990 Competing interests: None declared |
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Jay R. Schrand, Systems Engineer, Independent Researcher Enid, OK 73701
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Parkes(1) et al tested the use of a psychological persuasion technique on those who smoke. Revealing a hypothetical age of the lungs increased the percentage of quitters from 6.4% to 13.6%. Stress is indeed a motivator. A strong dose of guilt with claims of better health does sell medicine and procedures. However as with other cessation methods, a failure rate of 86.4%, is still abysmal, and reflects a lack of understanding of the complete relationship between tobacco use and the respiratory system. Stress, Respiration and Tobacco Use (see Figure 1) Traumatic stress in the presence of chronic stress induces asthma attacks(2). Felitti et al found a strong relationship between the stress of Adverse Childhood Experiences (ACE’s) and several of the leading causes of death in adults such as stroke (ACE’s >4, OR= 2.4) and Chronic Obstructive Pulmonary Disease(COPD) (ACE’s >4, OR= 3.9) (3). These exposed to the stress of ACE’s, have a strong graded relationship with eventual tobacco initiation(4). Tobacco has been used for 2000 years by the Native American population to treat respiratory disorders(5) and by physicians in the late 1800’s to treat asthma(6). Nicotine is a CNS and respiratory stimulant, increasing respiratory drive(7). Differences in respiratory symptoms appear in childhood before tobacco initiation(8). However, Tobacco Control (TC) studies appear to ignore the likelihood that many of those who smoke tobacco are unknowingly self-medicating stress induced respiratory disorders. Asthma, COPD and Smoking Data from a recent study(9) by Silva et al. indicates that when asthma is included in the model, the risk factor for smoking on COPD drops from the usual 5-13 range to a still significant but meager 2.9 compared with 12.5 for lifetime asthma. Though not discussed in the text, the newly discovered confounding relationship suggests that asthma is a greater risk factor for COPD rather than smoking. This is consistent with nicotine’s positive influence on respiration. The Insula and Tobacco Control Methods The insula translates sensory perceptions (smell, sight, etc) into feelings [love << like << ambivalence >> disgust >> hate] that motivate human choice. A stroke in the insular area often results in a shift of this reference point. What was once pleasurable now elicits no feelings or even disgust. Naqvi et al discovered that those with an insular stroke find it easy to quit(10). While recognizing that brain surgery to produce an insular stroke for the purpose of cessation would be unethical, the authors speculate that further experiments are warranted in the "human laboratory". In the Parkes et al study(1), the high number with CVA and stroke in the control group at baseline with an increased likelihood of cessation would tend to decrease the apparent program effect. It would likely be an artifact. However, the TC program depends heavily on social force and psychological guilt. This negative reinforcement combined with the low likelihood of successful cessation induces stressful conflict. This would be especially felt by the most vulnerable with a high number of ACE’s and have difficulty with the program. Stress induction, so similar to the methods used in dysfunctional family environments, increases the risk for stress related illnesses including stroke, and may actually be the basis for many of the current cessations. This analysis indicates that insular stroke likely plays a part in the natural and program tobacco cessation process. The only question is: "How much?" Any experimental techniques in the human laboratory must test for potential iatrogenic effects. Follow-up needs to occur to determine how many of the cessation successes are because of (silent) insular stroke.
REFERENCES 1. Parkes G, Greenhalgh T, Griffin M, Dent R. Effect on smoking quit rate of telling patients their lung age: the Step2quit randomized controlled trial. BMJ, doi:10.1136/bmj.39503.582396.25 2. Sandberg S, Paton JY, Ahola S, et al. The role of acute and chronic stress in asthma attacks in children. Lancet. 2000 Sep 16;356(9234):982-7. 3. Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Koss MP, Marks JS. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998 May;14(4):245-58. 4. Anda RF, Croft JB, Felitti VJ, Nordenberg D, Giles WH, Williamson DF, Giovino GA. Adverse childhood experiences and smoking during adolescence and adulthood. JAMA. 1999 Nov 3;282(17):1652-8. 5. Gandevia B. Historical review of the use of parasympatholytic agents in the treatment of respiratory disorders. Postgrad Med J. 1975;51(7 SUPPL):13-20. 6. National Library of Medicine - Elizabeth Fee, Ph.D. Exhibition Director Breath of Life - Asthma: From Symptom to Disease - Smoking Your Asthma Away http://www.nlm.nih.gov/hmd/breath/breath_exhibit/Asthma/smoking/smokingframe.html (accessed 03/13/08) 7. Haxiu M A, van Lunteren E, Van de Graff W B, Strohl K P. Action of nicotine on the respiratory activity of the diaphragm and genioglossus muscles and the nerves that innervate them. Respir Physiol 1984; 57: 153 8. Lebowitz MD. Smoking habits and changes in smoking habits as they relate to chronic conditions and respiratory symptoms. Am J Epidemiol. 1977 Jun;105(6):534-43. 9. Silva GE, Sherrill DL, Guerra S, et al. Asthma as a Risk Factor for COPD in a Longitudinal Study. Chest. 2004 Jul;126(1):59-65. 10. Naqvi NH, Rudrauf D, Damasio H, Bechara A. Damage to the insula disrupts addiction to cigarette smoking. Science. 2007 Jan 26;315(5811):531-4. Figure 1 - GraphicCompeting interests: In 1994, the author requested an educational grant from the Council for Tobacco Research to study the relationship between tobacco use and sleep apnea. This request was denied. However the letter seems to have become part of the tobacco archives: http://tobaccodocuments.org/ctr/60024574-4574.html Aside from this, the author has no financial interest in the tobacco, diet, or health industries other than as a consumer of their products and services. |
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Kathy Hartley, Specialist Trainee in Public Health Suffolk PCT, Rushbrook House, Papermill Lane, Bramford, Ipswich, IP8 4DE, Daniel G Showell, and Padmanabhan Badrinath
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We have some methodological reservation about the recent and important randomised controlled trial, Step2quit[1]. There are two threats to the internal validity of this study. Firstly, the additional verbal interaction (page 599) given to the intervention group as compared to minimal interaction given to the control (page 599) may have biased the outcome. It is plausible that this difference in the way participants received the intervention could have changed their behaviour to some extent. Secondly, the intervention was not the single intervention of telling smokers their lung age. It consisted of giving graphical as well as personalised information about lung age. Either or both of these may be responsible for the outcome. Indeed the Fletcher and Peto graph[2] is used in group smoking cessation classes without personalised data. It was helpful to have the numbers needed to treat (NNT) of 14 though the 95% confidence intervals for this would also have been of interest. We make these to be 8 to 51. We feel that it is important that there is more clarity on the first two issues above before this intervention is adopted widely in practice. [1] Parkes G, Greenhalgh T, Griffin M, Dent R. Effect on smoking quit ratio of telling patients their uc age: the stpe2quit randomised controlled trial. 2008;336:598-600 [2] Fletcher C, Peto R. The natural history of chronic airflow obstruction. BMJ 1977;i:1645-8. Competing interests: None declared |
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Gary Parkes, GP.Researcher EN118EP, Trisha Greenhalgh, Mark Griffin
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Dr Kathy Hartley et al are correct in their statement that the intervention in the step2quit study is more than just giving lung age measurements.(1) However, it is not correct to say that this is methodological bias. Bias is defined as ‘any systematic error in the design, conduct or analysis of a study that results in a mistaken estimate of an exposure’s effect’.(2) Although the abstract summarizes the intervention as ‘giving results in terms of lung age’, it is always important t look beyond the abstract to fully understand the methodology of a piece of research. I hope Dr Hartley et al will agree that the full text version of the research intervention clearly and openly states that: ‘Participants in the intervention group were given their results verbally, immediately after randomisation, in the form of "lung age" with a graphic display’. And ‘Written results were given to the intervention group as lung age’. This is not bias, this IS the (complex) intervention. Anyone wanting to introduce the intervention in their own clinical practice must be careful not to shortcut the intervention to just a verbal delivery of ‘lung age’. The complex intervention that produced the dramatic effect on quit rate in this study has three important components: verbal information, graphic information, and an individualised results letter. Together, these interventions seem to help people think about their health in a personalised way. We are continuing to explore the psychological literature to develop a theory of change as to why this may be. Clinicians will need to consider the ‘whole package’ if they wish to get similar favourable outcomes. To this end, I have requested the assistance of Health Enterprise East (http://www.hee.org.uk/) to create a clinical pack to make it easy to deliver the triple intervention on a wider scale. Based on our 95% CI for the ARR (2.2% to 12.1%) the 95% CI for the NNT comes out to be 9 to 46. Gary Parkes, Trisha Greenhalgh and Mark Griffin Even if you do not have a spirometer which can be set to display lung age the calculation derived from Morris and Temple(3) can be done easily using the excel spreadsheet now downloadable for free at www.step2quit.co.uk , and the graphics can be downloaded as Powerpoint slides from BMJ.com. Reference List (1) Parkes G, Greenhalgh T, Griffin M, Dent R. Effect on smoking quit rate of telling patients their lung age: the Step2quit randomised controlled trial. BMJ 2008; 336(7644):598-600. (2) Gordis L. Bias ,Confounding, and Interaction. Epidemiology. Second ed. Philadelphia: W.B.Saunders Company; 2000. (3) Morris JF, Temple W. Spirometric "lung age" estimation for motivating smoking cessation. Preventive Medicine 1985; 14:655-662. Competing interests: Authors of the original research |
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Alberto Donzelli, Director of Health Education Service - ASL Città di Milano - Italy via Ricordi 1 - 20131 Milano - Italy
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A Cochrane Sistematic Review (1) concluded “Current evidence of lower quality does not … support the hypothesis that biomedical risk assessment increases smoking cessation in comparison with standard treatment”. Exaled CO measurement and spirometry were used together in three trials, no one resulting in statistically significant differences between intervention and control groups. Two out of three trials even show a trend towards a worsening in the ORs (95% CI) of smoke quitting: 2.45 (0.73 to 8.25) and 3.50 (0.88 to 13.92) with CO measurement plus spirometry. Another RCT with only spirometry has an OR 1.21 (0,60-2,42) (and another with ultrasonography of carotid and femoral arteries performed in light smokers, smoking on average 10 to 12 cigarettes a day, significantly worsened the OR of smoke quitting: 3.15 (1.06 to 9.31), showing the actual risk to raise costs and harms at the same time (1). Parkes et al (2) state that NICE guidelines (which do not mention spirometry testing at all) should be reviewed and that “lung age” testing should be considered a part of a brief intervention package either in all smokers over 35 or all smokers. And they recommend that the new UK NHS general practitioner contract should include incentives for spirometric assessment accompanied by individualised communication of lung age in smokers. Conclusions (and claim) expressed in such way seem very little supported by trial results. Indeed Parkes et al performed a spirometric assessment to all participants smokers, and another after a year. What made the difference between the intervention and the control group was the communication: an information given immediately, in the form of “lung age” with a graphic display, followed by a written personalised letter in the intervention group; a letter delayed by several weeks with results given as simple FEV1 with no further explanation in the control group. The trial does not support neither the belief that the information of a worse spirometric lung age raises the patient chances of quitting smoking. On the contrary, the opposite seems true as trend (the mean lung age deficit was 8.7 years and 9.4 years in the quitters and non-quitters). Thus, what are the data telling us? 1) How the authors acknowledge, the success was likely to depend on communication: how the information was conveyed and understood, also using graphic displays and individualised letters. Yet, is questionable if a spirometric assessment is needed, instead of less expensive tools. n.b.: a more effective communication has perhaps also caused, as trend, a wider use of effective clinical and pharmacological support to quit: 7.8% in control group and 10.7% in the intervention group. Anyhow, quit rates at 12 months in the intervention group (13,6%) are similar to those obtained with effective available treatments, and less than the results achieved in a trial performed in the primary care setting (3)). 2) On the basis of existing evidence it is hard to recommend a spirometric assessment (and with which interval?) for all smokers over 35 (or all smokers at all). A spirometer is a technological device involving various costs: price (about € 1000-2000 in the Italian market), necessity of training to use it correctly, reimbursement fees of € 51,65 by Italian NHS or fees payed out of pocket by patients, and a performing time (30 minutes for every spirometry) which goes unavoidably in competition with other services of proven effectiveness. If the GP wants support for his/her quitting advice and counselling, with a graphic display, this could be the illustration/delivery of risk charts (in Italy there are specific and impressive colourful charts elaborated by Superior Institute of Health, by age, sex and smoking status for COPD, for lung cancer and for global cardiovascular risk, usable also in combination). It is questionable if we need a spirometry to convey an effective message on the almost sure effects (either pulmonary, or cardiovascular, or tumoral, or overall) for smokers who do not want to quit: a more direct, simple, multimedial educational intervention may be a real research priority. For GPs who want a technological support and to follow the evidence of Parkes’ trial, can be enough a simple FEV1 meter (about € 50 in the Italian market), which gives the essential information needed to show in colourful graphs the “lung age” (n.b.: the high reliability of measure is not the determinant factor). Finally, in my opinion the incentives (in proper amounts) should be better deserved by GPs whose formally reported interventions can document the real outcome of interest, that is a long term quitting status in every patient who was a previously certified smoker. Instead, incentives should not be provided for services or processes which per se are not a guarantee of outcome, and that can lead to technological abuse and interest-driven behaviours of providers. Dr. Alberto Donzelli
(1) Bize R et al. Biomedical risk assessment a san aid for smoking cessation. Cochrane Database of Systematic Reviews 2005, issue 4. Art. N°: CD004705 (2) Parkes G et al. Effect on smoking quit rate of telling patients their lung age: the Step2quit randomised controlled trial. BMJ 2008; 336: 598- 600 (3) Fossati R et al. A double-blind, placebo controlled, randomized trial of bupropion for smoking cessation in primary care. Arch Intern Med 2007; 167:1791-7 Competing interests: None declared |
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Philip H Quanjer, retired 7443 GT Nijverdal, the Netherlands
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I read with interest Parkes’ study [1] about lung age and fully sympathise with efforts to make people give up smoking. However, should doctors use biased information to persuade smokers? Example: a man, height 178 cm, age 50 year, FEV1 3.20 litre. Predicted FEV1 according to ECCS/ERS [2], Crapo [3] and Morris [4] comes to 3.71, 3.94 and 3.59 litre, respectively. The observed FEV1 is well within the normal range for healthy lifelong nonsmokers. “Lung age” according to the above 3 reference equations is 68, 83 and 62 year, respectively; so, what is this person’s “lung age”? If the person does not smoke we regard the FEV1 as being within the normal range and unremarkable. If the subject smokes, we no longer attribute the difference between measured and predicted value to normal variation but suggest that it is all accounted for by smoking. We introduce further bias by only attributing a difference from predicted to smoking if the recorded FEV1 is less than predicted. We inform only smokers about a fictitious lung age and withhold information about the normal range. Does the end really justify the means, is this a desirable role model for the doctor-patient relation? 1. Parkes G, Greenhalgh T, Griffin M, Dent R. Effect on smoking quit rate telling patients their lung age: the Step2quit randomized controlled trial. BMJ. 2008;336:598-600. 2. Quanjer PhH, Tammeling GJ, Cotes JE, Pedersen OF, Peslin R, Yernault JC. Lung volume and forced ventilatory flows. Report Working Party Standardization of lung function tests; Official Statement European Respiratory Society. Eur Respir J 1993; 6 Suppl 16:15-40. 3. Crapo RO, Morris AH, Gardner RM. Reference spirometric values using techniques and equipment that meet ATS recommendations. Am Rev Respir Dis 1981;123:659-664. 4. Morris JF, Temple WP, Koski A. Normal values for the ratio of one- second forced expiratory volume to forced vital capacity. Am Rev Resp Dis 1973;108:1000-1003. Philip H. Quanjer Competing interests: None declared |
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Kenneth W Lin, Medical Officer Agency for Healthcare Research and Quality, Rockville, Maryland USA 20850
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Although this is an interesting study, the results only support the conclusion that for asymptomatic smokers who undergo spirometry, communication about lung age is a more effective motivator for tobacco cessation than uninterpreted spirometry measurements. It does not establish the independent motivational effectiveness of doing spirometry screening vs. not doing it, which would require a randomized trial in which the control arm did not receive spirometry at all. Only 2 randomized controlled trials of this type have been conducted and both had negative results. For this and other reasons, the U.S. Preventive Services Task Force recently recommended against screening adults (regardless of smoking status) for COPD using spirometry (1). 1. U.S. Preventive Services Task Force. Screening for chronic obstructive pulmonary disease using spirometry: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2008;148:529-34. Competing interests: None declared |
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Rei Suganaga, senior resident Kameda Medical Center, Kamogawa Chiba 296-8602 Japan, Makito Yaegashi
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Parks et al have shown the usefulness of lung age in smoking cessation. However, is there an easier way to tell patients understandable numbers? There are 9 randomized-controlled trials addressing whether the use of spirometry will contribute to smoking cessation [1]. However, some study did not state how the result conveyed to patients [2], while other conveyed only whether patients had obstruction or not [3]. Since this is a matter of education, how the results conveyed to the patients should be clearly stated. FEV1 presented as percent predicted (i.e. 70% predicted) for their age, height, sex and race are always included in the spirometry reports. Knowledgeable physicians are using percentage rather than raw numbers while they are explaining the spirometry results. Instead of comparing lung age to FEV1 percent predicted, Parks et al used FEV1 presented as a raw number (i.e. 1.5L). Lay people would not understand the meaning and normal value of FEV1. The significant difference presented in this study could be solely from the use of a number that has little meaning to most patients. Lung age should therefore be compared to FEV1 percent predicted to elucidate the more effective way to convey understandable information to patients. 1)Kenneth Lin et al. Screening for Chronic Obstructive Pulmonary Disease Using Spirometry: Summary of the Evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2008; 148 : 535-543 2)Johan Buffels et al. Spirometry and smoking cessation advice in general practice: A of randomized clinical trial. Respiratory Medicine. 2006; 100: 2012-017 3)Jeffrey M. Sippel et al. Smoking Cessation in Primary Care Clinics. J Gen Intern Med. 1999; 14: 670-676 Competing interests: None declared |
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