****Please note that BMJ Open received this response on 10 September 2018, but it was not published until 14 January 2019***
We note the letter from Mr Donnay accusing us of committing research fraud in our 2012 paper [1].
First, Mr Donnay states that we incorrectly used both arterial and venous COHb. It is clear from the published human literature that there is no significant clinical difference between arterial and venous COHb levels after 10-15 minutes of exposure due to admixture [2-12], although I acknowledge that this message has not got through to some front-line clinicians [13].
His second point is more pertinent. We became aware of some discrepancies between the non-invasive and venous results. We subsequently became aware of concerns raised by other researchers about the Rad-57 device [14] so we did analyse the data separately in the report to the Department of Health. However, the separate analyses did not alter the fundamental conclusion of our study that a proportion of patients do present to Emergency Departments with higher than expected COHb levels and our hope to raise awareness of possible CO exposure in these people. We stressed that the figures obtained should not be extrapolated more widely and we were careful to avoid confusing higher than expected COHb levels with exposure to non-smoking exogenous sources of CO. We also discussed in depth the limitations of COHb as a biomarker.
On the note of patient safety our definition of...
****Please note that BMJ Open received this response on 10 September 2018, but it was not published until 14 January 2019***
We note the letter from Mr Donnay accusing us of committing research fraud in our 2012 paper [1].
First, Mr Donnay states that we incorrectly used both arterial and venous COHb. It is clear from the published human literature that there is no significant clinical difference between arterial and venous COHb levels after 10-15 minutes of exposure due to admixture [2-12], although I acknowledge that this message has not got through to some front-line clinicians [13].
His second point is more pertinent. We became aware of some discrepancies between the non-invasive and venous results. We subsequently became aware of concerns raised by other researchers about the Rad-57 device [14] so we did analyse the data separately in the report to the Department of Health. However, the separate analyses did not alter the fundamental conclusion of our study that a proportion of patients do present to Emergency Departments with higher than expected COHb levels and our hope to raise awareness of possible CO exposure in these people. We stressed that the figures obtained should not be extrapolated more widely and we were careful to avoid confusing higher than expected COHb levels with exposure to non-smoking exogenous sources of CO. We also discussed in depth the limitations of COHb as a biomarker.
On the note of patient safety our definition of ‘positive’ and ‘negative’ cases and their respective subgroups was based on a previously published paper (15), clearly described, and agreed by the Barking and Havering Ethics Committee. In addition, all subjects, including those defined as negative, were verbally advised about the availability of domestic CO detectors and the benefits of having their fossil fuel appliances checked annually by appropriately qualified engineers. We highlighted cases where such people defined as negative discovered faulty appliances at home showing our concern for safety and reinforcing the message about the limitations of COHb as a biomarker.
Lastly, we discussed the limitations of the study in both our paper and final report; extreme caution has to be exercised about overanalysing our data, tempting as that may be. We are more than happy for both the BMJ Open and Department of Health to independently scrutinise the study data. We feel that we have nothing to hide.
Simon Clarke
Patricia Ward
Stephen Bush
Joanne Zamani
References
1. Clarke S, Keshishian C, Murray V, Kafatos G, Ruggles R, Coultrip E, Oetterli S, Earle D, Ward P, Bush S, and Porter C. Screening for carbon monoxide exposure in selected patient groups attending rural and urban emergency departments in England: a prospective observational study. Br Med J Open. 2012; 2; e000877
2. Benignus VA, Hazucha MJ, Smith MV, and Bromberg PA. Prediction of carboxyhemoglobin formation due to transient exposure to carbon monoxide. J Appl Physiol. 1994; 76; 1739-1745
3. Garvican LA, Burge CM, Cox AJ, Clark SA, Martin DT, and Gore CJ. Carbon monoxide uptake kinetics of arterial, venous and capillary blood during CO rebreathing. 2010; 95; 1156-1166
4. Bruce EN and Bruce MC. A multicompartment model of carboxyhemoglobin and carboxymyoglobin responses to inhalation of carbon monoxide. J Appl Physiol. 2003; 95; 1235-1247
5. Chada KE and Bruce EN. Computational analyses of CO-rebreathing methods for estimating haemoglobin mass in humans. Exp Physiol. 2011; 97; 141–154
6. Touger M, Gallagher EJ and Tyrell J. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med. 1995; 25; 481-483
7. Yasuda H, Sasaki T, Yamaya M, Ebihara S, Maruyama M, Kanda A, and Sasaki H. Increased arteriovenous carboxyhemoglobin differences in patients with inflammatory pulmonary diseases. Chest. 2004; 125; 2160-2168
8. Eletr D, Reich A, Stubbe HD, Booke M, Daudel F, Erren M, and Westphal M. Arteriovenous carboxyhemoglobin difference is not correlated to TNF-a, IL-6, PCT, CRP and leukocytes in critically ill patients. Clinica Chimica. 2004; 349; 75-80
9. Yasuda H, Yamaya M, Nakayama K, Ebihara S, Sasaki T, Okinaga S, Inoue D, Asada M, Nemoto M, and Sasaki H. Increased arterial carboxyhemoglobin concentrations in chronic obstructive pulmonary disease. Am J Resp Crit Care Med. 2005; 171; 1246-1251
10. van Staden SR, Groenewald M, Engelbrecht R, Becker PJ, and Hazelhurst LT. Carboxyhaemoglobin levels, health and lifestyle perceptions in smokers converting from tobacco cigarettes to electronic cigarettes. S Afr Med J. 2013; 11; 865-868
11. Ergun D, Ergun R, Ersoy Ortac, E, Ozdemir C, Yuce G, and Ardic S. The measurement of exhaled carbon monoxide and arterial carboxyhemoglobin concentrations in middle-aged and elderly patients with COPD. Turk J Geri. 2014; 17; 223-227
12. Naples R, Laskowski D, McCarthy K, Mattox E, Comhair SAA, and Erzurum SC. Carboxyhemoglobin and methemoglobin in asthma. Lung. 2015; 193; 183-187
13. Bloomer C, Kairam N, Fiesseler F, Riggs R, and Salo D. Are venous carboxyhemoglobin levels being utilized by physicians? Ann Emerg Med. 2009; 54; S115
14. Wilcox SR and Richards JB. Non-invasive carbon monoxide detection: insufficient evidence for broad clinical use. Respir Care. 2012; 58; 376-379
15. Mandal S, Ruggles R, Leonardi G, Goodfellow F, Bradley N and Murray V. Developing best practice response to carbon monoxide incidents: a toolkit for health protection front-line staff. Pub Health. 2011; 125; 148-156
I am writing to correct false and misleading claims in the reply of Dr. Clarke, two of his co-authors, and Ms. Zamani to my letter of 25 August 2018 documenting evidence of scientific misconduct in their 2012 study of carbon monoxide (CO) poisoning (1).
For the record, my original letter did not accuse them of “committing research fraud” as they claim. I was open to the possibility that all their misconduct—including not fully reporting their ethics committee approvals, methods, and results—may have been inadvertent or unwitting.
But this seems less likely in light of their reply, which does not address any of my specific concerns while making new false and misleading claims. They say I allege that they “incorrectly used both arterial and venous COHb,” but my complaint was that they incorrectly used one to validate the other. I assumed this was because they mistook the arterial Rad57 measure for venous. However from their reply it appears they recognized the difference but simply ignored it, based on their mistaken belief that “there is no significant clinical difference [emphasis added] between arterial and venous COHb levels after 10-15 minutes of exposure due to admixture [2-12].”
In fact, 8 of the 11 studies they cite for this reported just the opposite, finding both clinically and statistically significant differences, including the only study that, like Clarke et al, compared Rad57 measures with venous COHb (12). Only three reported...
I am writing to correct false and misleading claims in the reply of Dr. Clarke, two of his co-authors, and Ms. Zamani to my letter of 25 August 2018 documenting evidence of scientific misconduct in their 2012 study of carbon monoxide (CO) poisoning (1).
For the record, my original letter did not accuse them of “committing research fraud” as they claim. I was open to the possibility that all their misconduct—including not fully reporting their ethics committee approvals, methods, and results—may have been inadvertent or unwitting.
But this seems less likely in light of their reply, which does not address any of my specific concerns while making new false and misleading claims. They say I allege that they “incorrectly used both arterial and venous COHb,” but my complaint was that they incorrectly used one to validate the other. I assumed this was because they mistook the arterial Rad57 measure for venous. However from their reply it appears they recognized the difference but simply ignored it, based on their mistaken belief that “there is no significant clinical difference [emphasis added] between arterial and venous COHb levels after 10-15 minutes of exposure due to admixture [2-12].”
In fact, 8 of the 11 studies they cite for this reported just the opposite, finding both clinically and statistically significant differences, including the only study that, like Clarke et al, compared Rad57 measures with venous COHb (12). Only three reported finding no significant difference among mean a-vCOHb differences (6, 9 and 10), but they only tested blood samples; focused only on the statistical significance of the CO difference; and said nothing about the obvious clinical significance of finding either a positive or negative gap. This clearly distinguishes people who are taking up CO from their lungs into tissues (when a>v) from those who are net excreting CO (when v>a), as occurs after any exogenous CO exposure stops until healthy equilibrium is re-established.
Critically, all the studies that Clarke et al now cite published some comparison of their arterial and venous COHb results, including two that reported a-v correlations over 0.91 (6, 10), while Clarke et al withheld from publication the results of their analysis that found a correlation of just 0.03–less than expected by chance—which they only reported to their funder (13).
They also did not disclose their decision to combine rather than contrast their (arterial) Rad57 and (venous) COHb results in their published analyses, which none of these other studies did. They nevertheless reported the “accuracy” of the Rad57 was within +/- 2% of blood COHb, referencing two papers that they only added at the recommendation of their reviewers, without disclosing--except to their funder--that they found differences up to 31%. (13).
In their defence, Clarke et al now claim they “subsequently became aware of concerns raised by other researchers about the Rad-57 device [14], so we did analyse the data separately in the report to the Department of Health,” but this is not possible. The study they cite (14) was only published in 2013, not 2012 as they claim, while their final report to the Department of Health was submitted in 2011 (13).
Also misleading is their claim that “the separate analyses did not alter the fundamental conclusion of our study that a proportion of patients do present to Emergency Departments with higher than expected COHb levels…” The proportion of ED patients they reported with high CO exposure was only 4.3%, while the actual rate—including the 293 cases they mistakenly dismissed as “false positive”—was 21%, which is five-fold higher .
The claim that they “discussed in depth the limitations of COHb as a biomarker” also rings hollow given that their paper did not mention any of these false positives while disclosing just 3 false negatives.
Finally, the authors’ claim that their “definition of ‘positive’ and ‘negative’ cases and their respective subgroups was based on a previously published paper [15], clearly described, and agreed by the Barking and Havering Ethics Committee” is false. The study was granted ethics approval by this committee in 2009 and conducted in 2010, one year before the cited paper [15] was published. Even if this paper was shared with Clarke et al prior to publication (and VM is a co-author of both), it was not submitted until February 2010, one month after the study began testing subjects, and it only specifies one COHb threshold for CO poisoning of 5%, while Clarke et al added a lower threshold of 2.5% for non-smokers.
Since the authors now claim they have “nothing to hide” and are “more than happy for both the BMJ Open and Department of Health to independently scrutinize the study data,” I hope they will promptly provide BMJO with both their unpublished final report (13) and an electronic file containing all their individual COHb results.
According to another paper (16) that some of the same authors published in 2012 with different methods and results from the same study; these included at least an initial Rad57 measure taken “at triage,” an arterial COHb taken 2 hours later, and another arterial COHb taken prior to discharge. (see Table 1). Clarke et al also should release their initial and revised protocols so reviewers can take into account whatever changes were introduced when the authors abandoned their original case-control design after just four months.
No such review is needed, however, for BMJ Open to decide whether the authors’ withholding of so much relevant information about their methods and results warrants retraction. Whether this was done deliberately or inadvertently makes no difference to the scientific record.
Albert Donnay
References
1. Clarke S, Keshishian C, Murray V, Kafatos G, Ruggles R, Coultrip E, Oetterli S, Earle D, Ward P, Bush S, and Porter C. Screening for carbon monoxide exposure in selected patient groups attending rural and urban emergency departments in England: a prospective observational study. Br Med J Open. 2012; 2; e000877
2. Benignus VA, Hazucha MJ, Smith MV, and Bromberg PA. Prediction of carboxyhemoglobin formation due to transient exposure to carbon monoxide. J Appl Physiol. 1994; 76; 1739-1745
3. Garvican LA, Burge CM, Cox AJ, Clark SA, Martin DT, and Gore CJ. Carbon monoxide uptake kinetics of arterial, venous and capillary blood during CO rebreathing. 2010; 95; 1156-1166
4. Bruce EN and Bruce MC. A multicompartment model of carboxyhemoglobin and carboxymyoglobin responses to inhalation of carbon monoxide. J Appl Physiol. 2003; 95; 1235-1247
5. Chada KE and Bruce EN. Computational analyses of CO-rebreathing methods for estimating haemoglobin mass in humans. Exp Physiol. 2011; 97; 141–154
6. Touger M, Gallagher EJ and Tyrell J. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med. 1995; 25; 481-483
7. Yasuda H, Sasaki T, Yamaya M, Ebihara S, Maruyama M, Kanda A, and Sasaki H. Increased arteriovenous carboxyhemoglobin differences in patients with inflammatory pulmonary diseases. Chest. 2004; 125; 2160-2168
8. Eletr D, Reich A, Stubbe HD, Booke M, Daudel F, Erren M, and Westphal M. Arteriovenous carboxyhemoglobin difference is not correlated to TNF-a, IL-6, PCT, CRP and leukocytes in critically ill patients. Clinica Chimica. 2004; 349; 75-80
9. Yasuda H, Yamaya M, Nakayama K, Ebihara S, Sasaki T, Okinaga S, Inoue D, Asada M, Nemoto M, and Sasaki H. Increased arterial carboxyhemoglobin concentrations in chronic obstructive pulmonary disease. Am J Resp Crit Care Med. 2005; 171; 1246-1251
10. van Staden SR, Groenewald M, Engelbrecht R, Becker PJ, and Hazelhurst LT. Carboxyhaemoglobin levels, health and lifestyle perceptions in smokers converting from tobacco cigarettes to electronic cigarettes. S Afr Med J. 2013; 11; 865-868
11. Ergun D, Ergun R, Ortac E, Ersoy E, Ozdemir C, Yuce G, and Ardic S. The measurement of exhaled carbon monoxide and arterial carboxyhemoglobin concentrations in middle-aged and elderly patients with COPD. Turk J Geri. 2014; 17; 223-227
12. Naples R, Laskowski D, McCarthy K, Mattox E, Comhair SAA, and Erzurum SC. Carboxyhemoglobin and methemoglobin in asthma. Lung. 2015; 193; 183-187
13. Clarke et al. (co-authors are not specified but second page lists contributors by type starting with [Chief Investigator] Clarke S; [Study Site Researchers] Coultrip E, Oetterli S, Earle D; [Project Management Group] Keshishian C, Murray V, Ruggles R, Ward P, Bush S, Zamani J, Mason A; [Statistical Support] Kafatos G; [Advisory Group] Harrison P, Bielby C, Edwards N, Karalliedde L; [Consulted] Baker D, Leonardi G, Volans G, Croxford B, Griffiths L. [Names in italics are also co-authors of Clarke et al 2012, along with Porter C, who is not listed here]. Non-invasive screening for carbon monoxide exposure in selected patient groups attending rural and urban emergency departments in England. Final Report Revised 30 June 2011. Department of Health, Policy Research Programme, Carbon Monoxide, PR-CO-0907-10003. https://www.coportal.org/wp-content/uploads/gst_attachments/26a118120deb... [accessed August 2018; backup archived at https://www.dropbox.com/s/b5cs338h2k96z72/24122014100805-Dept%20of%20Hea...
14. Wilcox SR and Richards JB. Non-invasive carbon monoxide detection: insufficient evidence for broad clinical use. Respir Care. 2013; 58; 376-379
15. Mandal S, Ruggles R, Leonardi G, Goodfellow F, Bradley N and Murray V. Developing best practice response to carbon monoxide incidents: a toolkit for health protection front-line staff. Pub Health. 2011; 125; 148-156
16. Clarke S, Stephens C, Farhan M, Ward P, Keshishian C, Murray V, and Zenner D. Multiple patients with carbon monoxide toxicity from water-pipe smoking. Prehospital and Disaster Medicine, 2012; 27; 612-614.
After reading the study thoroughly it comes as a surprise that patients would be actually assessing about there treating physicians and surgeon's knowledge and competence also on basis of there attire rather than handling of affairs, discussions and discourse. The high percentage of preference for White Coats was also indeed refreshing to see in US. Even though in United Kingdom, NHS has embraced the concept of bare elbow for many years now and almost completely let go of the white coat culture, which once used to be a sense of identification and source of pride for doctors everywhere. I believe if such a study is carried out across trusts in United Kingdom the results would be convincingly different. Especially because use of Caucasian models would result in significant bias for the study since NHS is multicultural and not just consisting of Caucasian doctors.. It would be interesting if the same study model is repeated with doctors representing the BAME(Black Asian Minority Ethnicity) as patients preferences regarding there attire would be a stark difference from Caucasian fellow doctors. Also effect of attire would have much greater influence on patients perceiving there doctor as being knowledgeable or not.
We write to express our concern about the prevalence estimate of plagiarism in African medical journals in the study reported by Rohwer et al.(1) The authors’ finding that 63% of African medical journal articles are plagiarized to some degree is a gross overestimate.
The study definitions of “some,” “moderate,” and “extensive” plagiarism are unvalidated and, as the authors admit in the fourth paragraph of their Discussion section, lack inter-rater reliability and precision. Articles were classified as having “some” plagiarism if there were as few as 1-2 sentences that included identical words or sentences in another article by different authors even if the sentences were properly referenced. Numerous publishing organizations, including the Council of Science Editors,(2) the World Association of Medical Editors,(3) and the US Office of Research Integrity,(4) reserve the use of plagiarism for instances when another’s words are used without proper credit or attribution. The authors developed their definition based on suggestions from the Committee on Publication Ethics (COPE), yet even COPE’s Flowchart for managing suspected plagiarism in a submitted manuscript defines plagiarism as “unattributed use of large portions of text and/or data.”(5)
In fairness to the African journals implicated in the study, we request the authors go back to their data, identify all instances in which identical wording with formal source citations were defined as plagiarism, recalcu...
We write to express our concern about the prevalence estimate of plagiarism in African medical journals in the study reported by Rohwer et al.(1) The authors’ finding that 63% of African medical journal articles are plagiarized to some degree is a gross overestimate.
The study definitions of “some,” “moderate,” and “extensive” plagiarism are unvalidated and, as the authors admit in the fourth paragraph of their Discussion section, lack inter-rater reliability and precision. Articles were classified as having “some” plagiarism if there were as few as 1-2 sentences that included identical words or sentences in another article by different authors even if the sentences were properly referenced. Numerous publishing organizations, including the Council of Science Editors,(2) the World Association of Medical Editors,(3) and the US Office of Research Integrity,(4) reserve the use of plagiarism for instances when another’s words are used without proper credit or attribution. The authors developed their definition based on suggestions from the Committee on Publication Ethics (COPE), yet even COPE’s Flowchart for managing suspected plagiarism in a submitted manuscript defines plagiarism as “unattributed use of large portions of text and/or data.”(5)
In fairness to the African journals implicated in the study, we request the authors go back to their data, identify all instances in which identical wording with formal source citations were defined as plagiarism, recalculate their plagiarism estimates with instances of proper attribution excluded, and formally correct their article. Only then will the study estimate be credible and useful to the journals included in this study.
Moreover, the singling out of 7 journals from the African Journal Partnership Program (AJPP) is unfair, and some of the comments made about AJPP journals are erroneous. Specifically, the authors claim that only 1 AJPP journal has a stated policy on plagiarism. In fact 3 journals have specific stated policies in their guides for authors,(6-8) and all journals indicate they follow the policies of the International Committee of Medical Journal Editors, which identifies plagiarism as a form of scientific misconduct. When the authors correct their prevalence estimate they should also issue an additional correction for that inaccurate statement about the AJPP journal author guides.
Audits like Rohwers’ et al can be useful for journals considering how to improve their editorial processes and standards. The AJPP journals, with very limited resources, are working to improve their editorial practices and support for and education of authors, and the journal editors are looking for an affordable way to implement software to assess for similarity, duplication, and actual plagiarism as part of their workflows and plans for process improvement. It is unfortunate that the AJPP journals only recently received notification from the study authors with claims of serious plagiarism for 4 articles - at least 6 weeks after publication of the study and after media coverage of the misleading findings. We note that the communication from the study authors to a few AJPP journal editors includes a link to the COPE flowchart that defines clear plagiarism with the term “unattributed.” This further reinforces the problems with the published study and the need to correct the misleading estimate of the prevalence of actual plagiarism and the misrepresentation of AJPP journal policies.
Annette Flanagin, JAMA and the JAMA Network
David Ofori-Adjei, Ghana Medical Journal
Co-Directors, African Journal Partnership Program (AJPP), on behalf of AJPP Journal Editors
References
1. Rohwer A, Wager E, Young T, et al Plagiarism in research: a survey of African medical journals BMJ Open 2018;8:e024777. doi: 10.1136/bmjopen-2018-024777
I worked on emergency ambulances in London from 1974 to 1978. I attended several bomb calls during the IRA campaign and it was terrifying to sit in a fibreglass ambulance knowing that there was a real risk of being right next to a car bomb that might be detonated with the intention of harming the emergency services. I was 19 at the time. Looking back, with my current knowledge, I can see that the experience was quite harmful for me. In addition to the existential threat there was also the fear of failing to perform and letting people down and being seen to be a coward. This also took its toll.
Other things also took a toll and they were not so obvious. Dealing with sick elderly patients was incredibly depressing. I came to fear growing old, because the only old people that I was meeting were ill and depressed and really not enjoying life. I saw so many old people living sad lives in grinding poverty.
Again, with maturity, this seems totally absurd, but as a 19 year old with no experience of healthy older people (my grandparents were all dead) ambulance work made me very sad. I was surrounded by other ambulance workers who I think tended to be able to cope by having sociopathic tendencies. A very toxic milieu!
My point here is that when I compared notes with ambulance workers with similar seniority in more rural settings and away from the IRA bombs, their experiences were entirely different. They attended the occasional serious RTC, but mos...
I worked on emergency ambulances in London from 1974 to 1978. I attended several bomb calls during the IRA campaign and it was terrifying to sit in a fibreglass ambulance knowing that there was a real risk of being right next to a car bomb that might be detonated with the intention of harming the emergency services. I was 19 at the time. Looking back, with my current knowledge, I can see that the experience was quite harmful for me. In addition to the existential threat there was also the fear of failing to perform and letting people down and being seen to be a coward. This also took its toll.
Other things also took a toll and they were not so obvious. Dealing with sick elderly patients was incredibly depressing. I came to fear growing old, because the only old people that I was meeting were ill and depressed and really not enjoying life. I saw so many old people living sad lives in grinding poverty.
Again, with maturity, this seems totally absurd, but as a 19 year old with no experience of healthy older people (my grandparents were all dead) ambulance work made me very sad. I was surrounded by other ambulance workers who I think tended to be able to cope by having sociopathic tendencies. A very toxic milieu!
My point here is that when I compared notes with ambulance workers with similar seniority in more rural settings and away from the IRA bombs, their experiences were entirely different. They attended the occasional serious RTC, but mostly their calls were somehow nicer. I went on to experience this in rural France later on.
I applaud the study and hope that it will be the first of many and that its findings will be acted upon. However, to improve the case pick-up rate, I wonder whether it would be worth considering gathering information on the subjects' contact with psychologically traumatic events. It might also be worth considering an exploration of the sociological stresses that they encounter and their view of more experienced colleagues' coping strategies.
This is a useful study. May I suggest that the Output Area Classification (OAC) offers similar insights based on social groupings. Several studies have explored the use of the OAC relating to A&E attendance and Critical Care admission [1-3]. I suspect that your data is amenable to further helpful analysis using the OAC.
1. Beeknoo N, Jones R. Factors influencing A&E attendance, admissions and waiting times at two London hospitals. British Journal of Medicine and Medical Research 2016; 17(10): 1-29. doi : 10.9734/BJMMR/2016/28783
2. Beeknoo N, Jones R. Using Social Groups to Locate Areas with High Emergency Department Attendance, Subsequent Inpatient Admission and Need for Critical Care. British Journal of Medicine and Medical Research 2016; 18(6): 1-23. doi: 10.9734/BJMMR/2016/29208
3. Beeknoo N, Jones R. Using social groups to locate areas of high utilization of critical care. BBritish Journal of Healthcare Management 2016; 22(11): 551-560.
We have read with interest the article by Ball et al (2018) recently published in BMJ Open and note that they refer to our letter (Pereira Gray and Wilkie, 2017) which listed disadvantages of this system from the point of view of patients and where we reported the opposition of the National Association of Patient Participation (N.A.P.P.) to this system.
We agree with the authors that ‘telephone first’ system is a “fundamental” change in the provision of general practice.
The authors refer in detail to the independent review of this system Newbould et al (2017), which was published on the BMJ in 2017 and in which three of the authors were the same. We are puzzled by the way they summarise it.
Authors’ statements in 2018 can be contrasted with the published results in Newbould et al 2017. For example, Ball et al write “No evidence of reduced secondary care costs.” Whereas Newbould et al wrote “we found a significant increase of cost of admissions… leading to an estimated overall increase in secondary care costs of £11,766 per 10,000 patients (i.e. over £1 per patient registered in the general practices).
Secondly, Ball et al write “Little overall improvement in patient satisfaction as expressed in patient surveys” when Newbould et al reported:
1.GP communication composite-Significant fall (P<0.001)
2. Would you recommend your surgery?- Significant fall (P<0.001) 3.Seeing preferred GP- Significant fall (P<0.035)
We have read with interest the article by Ball et al (2018) recently published in BMJ Open and note that they refer to our letter (Pereira Gray and Wilkie, 2017) which listed disadvantages of this system from the point of view of patients and where we reported the opposition of the National Association of Patient Participation (N.A.P.P.) to this system.
We agree with the authors that ‘telephone first’ system is a “fundamental” change in the provision of general practice.
The authors refer in detail to the independent review of this system Newbould et al (2017), which was published on the BMJ in 2017 and in which three of the authors were the same. We are puzzled by the way they summarise it.
Authors’ statements in 2018 can be contrasted with the published results in Newbould et al 2017. For example, Ball et al write “No evidence of reduced secondary care costs.” Whereas Newbould et al wrote “we found a significant increase of cost of admissions… leading to an estimated overall increase in secondary care costs of £11,766 per 10,000 patients (i.e. over £1 per patient registered in the general practices).
Secondly, Ball et al write “Little overall improvement in patient satisfaction as expressed in patient surveys” when Newbould et al reported:
1.GP communication composite-Significant fall (P<0.001)
2. Would you recommend your surgery?- Significant fall (P<0.001) 3.Seeing preferred GP- Significant fall (P<0.035)
Why have the authors summarised Newbould et al. by twice writing that there was “ no evidence or little overall improvement” when Newbould et al. provided important evidence that telephone-first system is associated with increased costs for the general practices (which pay for the system), increased costs for the hard-pressed hospital service, and significantly worse satisfaction for patients on three key questions?
Ball et al support the conclusion of the ESTEEM study, which also used telephone triage, “there is considerable potential in using telephone consultations in general practice”, but omit the important consequence that GP triage in that study was associated with a 22% increase in the use of out-of-hours services by patients - a bad outcome for patients (Pereira Gray and Wilkie 2015; Campbell et al., 2015).
The patients’ actions in the ESTEEM study and their responses to the 2017 study have not been properly valued. We appreciate the need to explore methods of making the most appropriate and cost-effective use of GP time. However, N.A.P.P. believes that there is a real need to independently evaluate the various uses of this service before they are more widely introduced.
References
Ball SL Newbould J Corbett J et al Qualitative study of patient views on a ‘telephone-first’ approach in general practice in England: speaking the GP by telephone before making face to face appointments BMJ Open 2018; 8 :e026197
Campbell J Warren F Taylor R et al (2015) Authors’ reply Lancet 2015; 385 :688
Newbould J Abel G Ball S et al. (2017) Evaluation of telephone first approach to demand management in English general practice: observational study BMJ 2017; 358 : j4197
Pereira Gray D and Willkie P Patient perspectives on telephone triage in general practice [Letter] Lancet 2015; 385: 687
Pereira Gray D and Wilkie P Patient perspectives on telephone first system BMJ 2017; 359 :j4925
We recently reported on brain tumour incidence time trends in 20 to 59 year old Australians, from 1982 to 2013, and analysed these in terms of mobile phone usage patterns and diagnostic improvements over that interval1. This was designed to determine whether claims that mobile phone use causes brain tumours, are consistent with the pattern of brain tumour incidence in Australia, and in particular to compare such incidence patterns with the results of the multinational Interphone case control study2. In summary, we reported that: 1/ Overall brain tumour incidence rates did not change over time; 2/ Increased glioblastoma incidence was seen during intervals that coincided with improvements in diagnostic technologies (CT, MRI); 3/ Decreased incidence of ‘unspecified’ tumours was seen during the same intervals; and 4/ No evidence of increased tumour incidence (including glioblastoma) related to mobile phone use was found (based on incidence rates seen during the period of substantial mobile phone use and on modelling using a range of hypothetical relative risks and latency periods).
Philips submitted a Letter to the Editor3 of BMJ Open, where he purports to show that there are ‘significant flaws and unjustifiable conclusions’ in the above paper. Although he may firmly hold this view, his letter does not provide any evidence of this, and we strongly disagree with his statement. We have addressed the substance of his letter below to hopefully obviate potential misunderstan...
We recently reported on brain tumour incidence time trends in 20 to 59 year old Australians, from 1982 to 2013, and analysed these in terms of mobile phone usage patterns and diagnostic improvements over that interval1. This was designed to determine whether claims that mobile phone use causes brain tumours, are consistent with the pattern of brain tumour incidence in Australia, and in particular to compare such incidence patterns with the results of the multinational Interphone case control study2. In summary, we reported that: 1/ Overall brain tumour incidence rates did not change over time; 2/ Increased glioblastoma incidence was seen during intervals that coincided with improvements in diagnostic technologies (CT, MRI); 3/ Decreased incidence of ‘unspecified’ tumours was seen during the same intervals; and 4/ No evidence of increased tumour incidence (including glioblastoma) related to mobile phone use was found (based on incidence rates seen during the period of substantial mobile phone use and on modelling using a range of hypothetical relative risks and latency periods).
Philips submitted a Letter to the Editor3 of BMJ Open, where he purports to show that there are ‘significant flaws and unjustifiable conclusions’ in the above paper. Although he may firmly hold this view, his letter does not provide any evidence of this, and we strongly disagree with his statement. We have addressed the substance of his letter below to hopefully obviate potential misunderstandings that his letter may generate.
1/ A substantial portion of the Letter is dedicated to describing aspects of a paper published by Philips and colleagues4. Philips does not relate that description to Karipidis et al. (2018)1, and as his restatement of his paper does not raise any issues that were not considered in our work, we do not comment on that here.
2/ There are a number of factual inaccuracies in Philips’ letter.
For example, in relation to our report of an increased incidence in glioblastoma over the 1993-2002 period, he claims that Karipidis et al. concluded that it “was due to diagnostic improvements”. If Philips was correct, we would agree that this would represent an oversimplification of the data. However, we have been very careful to appropriately interpret the results and the level of certainty the evidence provided from the analyses; indeed we stated that the elevated glioblastoma incidence from 1993 to 2002, with no significant increase from 2003 to 2013, was “most likely due to improved diagnosis from MRI” (p. 10). Further, in support of this we gave substantial reasons for why diagnostic improvements are a far more likely explanation than radiofrequency exposure from mobile phone use.
Similarly, Philips’ letter says that “Karipidis et al incorrectly state that we did not analyse different time periods to investigate the impact of mobile phone use”, and then goes on to show that different time periods were reported separately. However, our statement is correct in that, although some breakdown of time periods was given, these time periods do not correspond to periods relevant for determining whether incidence changes were related to mobile phone use (such as intervals relating to diagnosis change or mobile phone usage patterns), and no data is provided to address the issue of mobile phone use. Indeed Philips et al. did not even claim to have addressed cancer incidence in terms of mobile phone use specifically, and Karipidis et al. has merely noted this.
3/ Philips asks how rapidly developing tumours can be misdiagnosed and recorded. This has been dealt with in our paper, which includes consideration of the fact that there is no increase in glioma overall, that the increase in glioblastoma is paralleled by a reduction in ‘unspecified’ tumours, that the increase in glioblastoma incidence occurs during a period of improved diagnosis and changes to the tumour classification scheme, and that it precedes the period of rapid mobile phone use. Further, Philips does not provide any argument for his apparent view that we are erroneous in our conclusion that the temporary rise in glioblastoma incidence is most likely due to improved diagnosis and classification.
4/ Philips states that changes in antenna position on different phones, and different communication technologies (e.g. 2G, 3G, 4G) “should have been discussed by Karipidis et al.” However, Karipidis et al. states that we could not take changes in technology and patterns of individual use into account, as we had no representative data on the effects of such changes on individual exposure; and discussion could thus be no more than speculation.
5/ Philips’ letter criticised our paper for assessing data for 20-59 year olds, rather than for all ages. Although Philips may see benefit in conducting a study quite different to ours, there are many benefits in the method that we used, and these were described in Karipidis et al. For example, our study was designed to compare cancer incidence with that that would be expected based on different interpretations of the Interphone2 results, and this is the age range used in the Interphone study (which in turn was chosen to “maximise the likelihood of exposure”5). Beyond that, more-general methodological considerations point to the appropriateness of this age range: 1/ As cases older than 60 would be more affected by the diagnostic issues described above, 60+ year olds were not included as their inclusion would reduce the chance of seeing mobile phone related changes to tumour incidence; 2/ As we wanted to test whether tumour onset latencies of > 10 years could explain observed tumour incidence rates, and as this would require cases < 20 years old to have substantial mobile phone usage before the age of 10 (which they do not), those < 20 were not suitable for the purposes of this study. The relatively small number of cases in the < 20 year age group (being far rarer than in adults), would also increase data instability, making it less likely to observe meaningful changes in tumour incidence.
6/ Philips criticises Karipidis et al. for using the World Health Organization’s (WHO) world standard population to standardize our data, as he believes that a different method should have been sought. However the purpose of this standardisation is to ensure age-comparability of each year’s data, and the WHO world population provides comparability with much of the international literature, which is very useful in addressing this issue. We do not believe that the use of other standards would change the time trends appreciably.
7/ It is noteworthy that Philips is the Technical Director of a company that derives income from selling devices which were “mainly designed by Alasdair Philips”, “to protect people from the ever-increasing levels of Electromagnetic radiation, or electrosmog, in our environment” (https://emfields-solutions.com/aboutus.asp). Thus although he fails to declare any conflict of interest in relation to his letter, this activity would normally be seen as a direct conflict of interest; whether radiofrequency exposure due to mobile phone use is seen as being related to cancer induction or promotion would have a tangible effect on whether people purchased devices to ‘protect’ themselves from such radiofrequency exposure.
In conclusion, Philips’ Letter to the Editor does not raise any cogent issues with Karipidis et al. Instead it provides a series of claims that Karipidis et al. is inadequate, but does not provide relevant argumentation in support of this. We maintain that the data presented in Karipidis et al. does not provide any indication of mobile phone-related increases in cancer incidence, but conversely that it does suggest that changes to glioblastoma diagnostic and classification practices in Australia are a more likely explanation for the reported increase in glioblastoma incidence rates in Australia.
References:
1. Karipidis K, Elwood M, Benke G, Sanagou M, Tjong L, Croft RJ. Mobile phone use has not increased the incidence of brain tumour histological types, grading or anatomical location: A population-based ecological study. BMJ Open, 2018, 8(12):e024489.
2. INTERPHONE Study Group. Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study. Int J Epidemiol, 2010(39):675–94.
3. Philips A. Significant flaws and unjustifiable conclusions. Letter to the Editor, BMJ Open, 2019.
4. Philips A, Henshaw DL, Lamburn G, et al. Brain tumours: rise in Glioblastoma Multiforme incidence in England 1995–2015 suggests an adverse environmental or lifestyle factor. J of Environment and Public Health, 2018:7910754.
5. Cardis E, Richardson L, et al. The INTERPHONE study: design, epidemiological methods, and description of the study population. Eur J Epi, 2007, 22(9):647-664.
****Please note that BMJ Open received this response on 10 September 2018, but it was not published until 14 January 2019***
We note the letter from Mr Donnay accusing us of committing research fraud in our 2012 paper [1].
Show MoreFirst, Mr Donnay states that we incorrectly used both arterial and venous COHb. It is clear from the published human literature that there is no significant clinical difference between arterial and venous COHb levels after 10-15 minutes of exposure due to admixture [2-12], although I acknowledge that this message has not got through to some front-line clinicians [13].
His second point is more pertinent. We became aware of some discrepancies between the non-invasive and venous results. We subsequently became aware of concerns raised by other researchers about the Rad-57 device [14] so we did analyse the data separately in the report to the Department of Health. However, the separate analyses did not alter the fundamental conclusion of our study that a proportion of patients do present to Emergency Departments with higher than expected COHb levels and our hope to raise awareness of possible CO exposure in these people. We stressed that the figures obtained should not be extrapolated more widely and we were careful to avoid confusing higher than expected COHb levels with exposure to non-smoking exogenous sources of CO. We also discussed in depth the limitations of COHb as a biomarker.
On the note of patient safety our definition of...
I am writing to correct false and misleading claims in the reply of Dr. Clarke, two of his co-authors, and Ms. Zamani to my letter of 25 August 2018 documenting evidence of scientific misconduct in their 2012 study of carbon monoxide (CO) poisoning (1).
For the record, my original letter did not accuse them of “committing research fraud” as they claim. I was open to the possibility that all their misconduct—including not fully reporting their ethics committee approvals, methods, and results—may have been inadvertent or unwitting.
But this seems less likely in light of their reply, which does not address any of my specific concerns while making new false and misleading claims. They say I allege that they “incorrectly used both arterial and venous COHb,” but my complaint was that they incorrectly used one to validate the other. I assumed this was because they mistook the arterial Rad57 measure for venous. However from their reply it appears they recognized the difference but simply ignored it, based on their mistaken belief that “there is no significant clinical difference [emphasis added] between arterial and venous COHb levels after 10-15 minutes of exposure due to admixture [2-12].”
In fact, 8 of the 11 studies they cite for this reported just the opposite, finding both clinically and statistically significant differences, including the only study that, like Clarke et al, compared Rad57 measures with venous COHb (12). Only three reported...
Show MoreAfter reading the study thoroughly it comes as a surprise that patients would be actually assessing about there treating physicians and surgeon's knowledge and competence also on basis of there attire rather than handling of affairs, discussions and discourse. The high percentage of preference for White Coats was also indeed refreshing to see in US. Even though in United Kingdom, NHS has embraced the concept of bare elbow for many years now and almost completely let go of the white coat culture, which once used to be a sense of identification and source of pride for doctors everywhere. I believe if such a study is carried out across trusts in United Kingdom the results would be convincingly different. Especially because use of Caucasian models would result in significant bias for the study since NHS is multicultural and not just consisting of Caucasian doctors.. It would be interesting if the same study model is repeated with doctors representing the BAME(Black Asian Minority Ethnicity) as patients preferences regarding there attire would be a stark difference from Caucasian fellow doctors. Also effect of attire would have much greater influence on patients perceiving there doctor as being knowledgeable or not.
We write to express our concern about the prevalence estimate of plagiarism in African medical journals in the study reported by Rohwer et al.(1) The authors’ finding that 63% of African medical journal articles are plagiarized to some degree is a gross overestimate.
The study definitions of “some,” “moderate,” and “extensive” plagiarism are unvalidated and, as the authors admit in the fourth paragraph of their Discussion section, lack inter-rater reliability and precision. Articles were classified as having “some” plagiarism if there were as few as 1-2 sentences that included identical words or sentences in another article by different authors even if the sentences were properly referenced. Numerous publishing organizations, including the Council of Science Editors,(2) the World Association of Medical Editors,(3) and the US Office of Research Integrity,(4) reserve the use of plagiarism for instances when another’s words are used without proper credit or attribution. The authors developed their definition based on suggestions from the Committee on Publication Ethics (COPE), yet even COPE’s Flowchart for managing suspected plagiarism in a submitted manuscript defines plagiarism as “unattributed use of large portions of text and/or data.”(5)
In fairness to the African journals implicated in the study, we request the authors go back to their data, identify all instances in which identical wording with formal source citations were defined as plagiarism, recalcu...
Show MoreI worked on emergency ambulances in London from 1974 to 1978. I attended several bomb calls during the IRA campaign and it was terrifying to sit in a fibreglass ambulance knowing that there was a real risk of being right next to a car bomb that might be detonated with the intention of harming the emergency services. I was 19 at the time. Looking back, with my current knowledge, I can see that the experience was quite harmful for me. In addition to the existential threat there was also the fear of failing to perform and letting people down and being seen to be a coward. This also took its toll.
Other things also took a toll and they were not so obvious. Dealing with sick elderly patients was incredibly depressing. I came to fear growing old, because the only old people that I was meeting were ill and depressed and really not enjoying life. I saw so many old people living sad lives in grinding poverty.
Again, with maturity, this seems totally absurd, but as a 19 year old with no experience of healthy older people (my grandparents were all dead) ambulance work made me very sad. I was surrounded by other ambulance workers who I think tended to be able to cope by having sociopathic tendencies. A very toxic milieu!
My point here is that when I compared notes with ambulance workers with similar seniority in more rural settings and away from the IRA bombs, their experiences were entirely different. They attended the occasional serious RTC, but mos...
Show MoreThis is a useful study. May I suggest that the Output Area Classification (OAC) offers similar insights based on social groupings. Several studies have explored the use of the OAC relating to A&E attendance and Critical Care admission [1-3]. I suspect that your data is amenable to further helpful analysis using the OAC.
1. Beeknoo N, Jones R. Factors influencing A&E attendance, admissions and waiting times at two London hospitals. British Journal of Medicine and Medical Research 2016; 17(10): 1-29. doi : 10.9734/BJMMR/2016/28783
2. Beeknoo N, Jones R. Using Social Groups to Locate Areas with High Emergency Department Attendance, Subsequent Inpatient Admission and Need for Critical Care. British Journal of Medicine and Medical Research 2016; 18(6): 1-23. doi: 10.9734/BJMMR/2016/29208
3. Beeknoo N, Jones R. Using social groups to locate areas of high utilization of critical care. BBritish Journal of Healthcare Management 2016; 22(11): 551-560.
We have read with interest the article by Ball et al (2018) recently published in BMJ Open and note that they refer to our letter (Pereira Gray and Wilkie, 2017) which listed disadvantages of this system from the point of view of patients and where we reported the opposition of the National Association of Patient Participation (N.A.P.P.) to this system.
We agree with the authors that ‘telephone first’ system is a “fundamental” change in the provision of general practice.
The authors refer in detail to the independent review of this system Newbould et al (2017), which was published on the BMJ in 2017 and in which three of the authors were the same. We are puzzled by the way they summarise it.
Authors’ statements in 2018 can be contrasted with the published results in Newbould et al 2017. For example, Ball et al write “No evidence of reduced secondary care costs.” Whereas Newbould et al wrote “we found a significant increase of cost of admissions… leading to an estimated overall increase in secondary care costs of £11,766 per 10,000 patients (i.e. over £1 per patient registered in the general practices).
Secondly, Ball et al write “Little overall improvement in patient satisfaction as expressed in patient surveys” when Newbould et al reported:
1.GP communication composite-Significant fall (P<0.001)
2. Would you recommend your surgery?- Significant fall (P<0.001) 3.Seeing preferred GP- Significant fall (P<0.035)
Why h...
Show MoreWe recently reported on brain tumour incidence time trends in 20 to 59 year old Australians, from 1982 to 2013, and analysed these in terms of mobile phone usage patterns and diagnostic improvements over that interval1. This was designed to determine whether claims that mobile phone use causes brain tumours, are consistent with the pattern of brain tumour incidence in Australia, and in particular to compare such incidence patterns with the results of the multinational Interphone case control study2. In summary, we reported that: 1/ Overall brain tumour incidence rates did not change over time; 2/ Increased glioblastoma incidence was seen during intervals that coincided with improvements in diagnostic technologies (CT, MRI); 3/ Decreased incidence of ‘unspecified’ tumours was seen during the same intervals; and 4/ No evidence of increased tumour incidence (including glioblastoma) related to mobile phone use was found (based on incidence rates seen during the period of substantial mobile phone use and on modelling using a range of hypothetical relative risks and latency periods).
Philips submitted a Letter to the Editor3 of BMJ Open, where he purports to show that there are ‘significant flaws and unjustifiable conclusions’ in the above paper. Although he may firmly hold this view, his letter does not provide any evidence of this, and we strongly disagree with his statement. We have addressed the substance of his letter below to hopefully obviate potential misunderstan...
Show MoreThis is a note to indicate that BMJ Open is still looking into the disagreement between Albert Donnay and the authors of the paper.
We will post further updates on the article in due course.
Page 8/9; Acknowledgements.
The spelling of research assistant Rohan Navani was misspelt as Rohan Navari.
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