Displaying 1-10 letters out of 273 published
Re:Reply to "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention"
Thanks to Rikke D. Maimburg for her comments and considerations to our study on stillbirths.
In real life, we very often have to rely on observational studies in the attempt to identify and quantify risk factors (causes) of diseases and deaths. Although the possibility of residual confounding in all such studies has to be considered, it is in our opinion too puritan to discard all observational studies in this regard. The vast majority of identified and quantified risk factors have actually been found by observational studies.
In the present study, we made a regression analysis, accounting for what we considered to be the most important confounders for the observed decline. Many risk factors exist for stillbirths, but only a fraction of these are confounders, which in addition to being risk factors of stillbirths also should be associated with the secular change in induction practice. Thus intrauterine growth restriction and preeclampsia are certainly risk factors of stillbirth, but had no confounding influence in our study when we tested for it, probably due the almost constant prevalence of these conditions through the study period.
The increasing proportion of adipose delivering women, higher maternal age, fewer post term twin deliveries and the reduced fraction of smokers, on the other hand, were all confounders and adjusted for.
It was not possible to adjust for number of ultrasound examinations, and it is true, that the surveillance of post term pregnancies has improved by time. Our point was, however, that this improvement has also been implemented in our neighbour countries, without a similar reduction in stillbirths.
We did not only mention the many circumstances which contributed to the decline in stillbirths, but also attempted to quantify the contribution of each of these factors. Thus the detection and abortion of foetuses with malformations was quantified, the contribution of the decline in smokers was quantified, and the small influence of the slightly increasing body mass index and age of delivering women were quantified.
The significance (influence) of twin pregnancies for stillbirths declined by time, due to more consequent and earlier induction of twin deliveries by time. The same applies to pregnancies in women beyond 40 years and in women with high body mass index, which have been selectively induced even earlier in accordance with the new guidelines. Our data confirmed that these circumstances had a profound declining influence on stillbirth rates. So, we still think our data support our conclusion, which never was that earlier induction was the only contributing factor, but according to our analysis was the most important contributing factor of all the investigated circumstances for the dramatic decline in stillbirths.
The significance (influence) of twin pregnancies for stillbirths declined by time, due to more consequent and earlier induction of twin deliveries by time. The same applies to pregnancies in women beyond 40 years and in women with high body mass index, which have been selectively induced even earlier in accordance with the new guidelines. Our data confirmed that these circumstances had a profound declining influence on stillbirth rates.
So, we still think our data support our conclusion, which never was that earlier induction was the only contributing factor, but according to our analysis was the most important contributing factor of all the investigated circumstances for the dramatic decline in stillbirths.
Conflict of Interest:
Declared in the primary publication
Reply to "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention"
I enjoyed reading the paper "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention" by Hedegaard et al with the encouraging message that the mortality rate for Danish newborns has declined to a historically low number.
The authors' conclusions seem, however, a bit too far-reaching when they claim that earlier induction has reduced the stillbirth rate and may be self-accountable for up to 15 % of the reduction of stillbirths. The study by Hedegaard et al. is an observational study and a causal relationship can therefore not be established. Moreover, the lack of adjustment for birth defect, intra uterine growth restriction (IUGR), medical diseases before and during pregnancy, ultrasound scans, and socio- economic status in analysis may introduce to bias in the risk estimates due to residual confounding.
The continuing decline in stillbirths in the study period is probably a result of several concurrent interventions. In particular, the comprehensive surveillance program introduced during the year 2011 may relevant. A total of 17 of the 24 Danish maternity wards implemented routine antenatal surveillance of pregnancies that exceeded 41 weeks of gestation. This practice included ultrasound monitoring of foetal well- being as well as cardiotocography and clinical examinations at each visit after 41 weeks of gestation (the visits are normally scheduled at gestational age 41+3 and 41+5). This surveillance program is not mentioned by Hedegaard et al.
The present study provide clear and solid evidence that the stillbirth rate in Denmark have declined during the study period from 2000 - 2012 but provides little data to support the authors conclusion that earlier induction is a major explanation for the decline in stillbirths.
Conflict of Interest:
Foetal growth restriction, induction of labour and reduced still birth rate at term
We read with great interest the recently published National cohort study of Hedegaard et al (1). The authors rightly indicate in their introduction that women with foetal growth restriction or preeclampsia are at high risk for stillbirth, and that in these women induction before term is often recommended; these authors also stress that since 2009, Denmark has had a more proactive policy including early intervention in women with preeclampsia. However, no data are given in the article about the rates of preeclampsia, small for gestational age babies, or foetal growth restriction, although, as stated by the authors, the increased quality of screening for ultrasound foetal growth and Doppler during the last decade may have improved the monitoring of foetuses in utero, making it easier to detect foetal growth restricted foetuses and to induce labour to avoid foetal death or preeclampsia. Without these data, it is difficult to agree with Hedegaard et al that "these circumstances are probably of minor importance for the decrease in stillbirths" from the comparison of Danish figures with the whole proportion of deliveries after 42 weeks in Sweden, or the whole stillbirth rate after 37 gestational weeks in Norway. Indeed, using the ReCoDe ("relevant condition at death") classification for stillbirth, Gardosi et al confirmed that the most common cause of foetal death was precisely foetal growth restriction (43.0%) in West Midlands region of the UK (2) as it is observed worldwide (3), and the incidence of this condition is probably similar in Denmark. This significant contribution of foetal growth restriction (and possibly associated preeclampsia in cases of defective placentation) is all the more plausible that in the Disproportionate Intrauterine Growth Intervention Trial At Term (DIGITAT) study (3) comparing the effect of induction of labour with a policy of expectant monitoring for intrauterine growth restriction near term in the Netherlands, even in the "expectant monitoring group" labour had to be induced in as high as 50% of the patients at gestational age 277 (269-283) days [versus 95.6% at gestational age 266 (261-271) days in the "Induction of labour group"]. Furthermore, taking into account the possible impact of the message delivered by Hedegaard et al's article in daily practice, the historical design (and not true intervention design) of this study, with the inherent limitations, should have been clearly specified in the clinical message.
1.Hedegaard M, Lidegaard O, Skovlund CW, M?rch LS, Hedegaard M. Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention. BMJ Open. 2014;4:e005785. 2.Gardosi J, Kady SM, McGeown P, Francis A, Tonks A. Classification of stillbirth by relevant condition at death (ReCoDe): population based cohort study. BMJ. 2005;331(7525):1113-7. 3.Lawn JE, Blencowe H, Oza S et al and Lancet Every Newborn Study Group. Every Newborn: progress, priorities, and potential beyond survival. Lancet. 2014;384(9938):189-205. 4.Boers KE, Vijgen SM, Bijlenga D et al. Induction versus expectant monitoring for intrauterine growth restriction at term: randomised equivalence trial (DIGITAT). BMJ. 2010;341:c7087.
Conflict of Interest:
Red cell distribution width?A novel predictor of mortality in acute pancreatitis
Title page Title:Red cell distribution width:A novel predictor of mortality in acute pancreatitis Authors: 1. Libing Jiang, BM Department of Emergency Medicine, Second Affiliated Hospital, School of Medicine?Institute of emergency Medicine, Zhejiang University, Hangzhou, China. Email:firstname.lastname@example.org 2. Yuefeng Ma, PhD, MD, chief physician Department of Emergency Medicine, Second Affiliated Hospital, School of Medicine?Institute of emergency Medicine, Zhejiang University, Hangzhou, China. Email:email@example.com 3.Mao Zhang, PhD, MD, chief physician Department of Emergency Medicine, Second Affiliated Hospital, School of Medicine?Institute of emergency Medicine, Zhejiang University, Hangzhou, China. Email:firstname.lastname@example.org
Corresponding author: Mao Zhang PhD, MD Complete postal address or affiliations: Emergency Medicine Research Institute of Zhejiang University; Emergency Medicine Center, Second Hospital Affiliated to Medical College, Zhejiang University, 88# Jie Fang road, Shang Cheng district, Hangzhou, China. Postcode: 310009 Tel.:+86571-87783921. E-mail address: email@example.com Keywords: red cell distribution width, acute pancreatitis
Word count: 625
To the Editor, We have read with great interest the recently published article titled "Association between red cell distribution width and acute pancreatitis: a cross-sectional study" by Yao et al. 1 In that very well-presented article, the authors aimed to investigate whether red cell distribution width (RDW) was a predictor of mortality in patients with acute pancreatitis (AP). They concluded that RDW measured on emergency department (ED) admission was significantly associated with 90-day mortality in patients with AP. We would like to thank Yao et al 1 for their comprehensive contribution. RDW is a quantitative measure of anisocytosis, any processes result in the release of immature erythrocytethe or increased destruction of red blood cell (RBC) will cause the increase of RDW.2 RDW is traditionally used for the differential diagnosis of anemia (especially iron-deficiency anemia). 2 However, it has been reported recently RDW is an independent predictor of mortality in various conditions, including chronic and acute heart failure, acute dyspnea, acute pancreatitis, severe sepsis and septic shock, trauma, acute pulmonary embolism, and even community-dwelling older adults. 3-8 Whereas, RDW is an index affected by many factors such as anemia, renal dysfunction or hepatic dysfunction, thyroid disease, transfusion, acute or chronic inflammation, neurohumoural activation, malnutrition (i.e. iron, vitamin B12 and folic acid), ethnicity, bone marrow depression, and use of some medications ( i.e. erythropoietin use and antibiotic use). 2, 5 However, in the present study, the authors did not describe these conditions in detail and also did not exclude relevant diseases in their exclusion criteria. We believe it would be better if the authors elaborated on the above mentioned RDW affecting factors in more detail. In addition, there are several other questions about this article. Firstly, the time elapsed between blood sampling and RDW measuring was not clearly defined, because the length of this interval may significantly alter RDW levels.2 Secondly, this was a small sample size study, and only 8 non-survivors were included, we deduced that there is no enough statistical power to reach this conclusion and this will increase the probability of type I error. Meanwhile, in this study, multi-variate regression analysis was not used to adjust other confounding factors, therefore, we don't know whether the RDW - mortality association in patients with AP is independent of other covariates. Thirdly, the reasons why survivors of patients with AP had lower RDW than the healthy participants appear to be most of these patients suffered from mild AP, not only what the authors said in their article. Fourthly, according to the data in the original report, positive likelihood ratio and negative likelihood ratio of RDW to predict mortality should be 7.35 and 0.28, rather than 7.35% and 0.28%. Fifthly, another major limitation of the study by Yao et al1 is that no comparison of RDW and APACHE? and Ranson scores has been made. Therefore, it still remains unclear whether the discriminative power of RDW is better than both APACHE?and Ranson scores. Moreover, we would like to know whether addition of RDW in the classical prognostic model (such as APACHE?) may improve prognostic accuracy. All these questions might be answered by further investigation. In addition to RDW, many other biomarkers has also been shown to have an independent association with mortality, such as neutrophil lymphocyte ratio, uric acid, tumor necrosis factor-like weak inducer of apoptosis (TWEAK), serum creatine. Therefore, whether the combination of these indices may improve prognostic accuracy? In conclusion the study by Yao et al1 will lead to further studies regarding the association between RDW and mortality or other adverse outcomes in patients with AP. However, one should keep in mind that RDW should be evaluated together with other prognostic or inflammatory markers. Only in this way, can we obtain exact information from these predictors.
Reference 1. Yao J, Lv G. Association between red cell distribution width and acute pancreatitis: a cross-sectional study. BMJ open 2014;4:e004721. 2. Karagoz E, Tanoglu A. Red Blood cell distribution width: an emerging diagnostic factor of acute appendicitis? World journal of emergency surgery : WJES 2013;8:54. 3. N. Hong, J. Oh, S. M. Kang, et al. Red blood cell distribution width predicts early mortality in patients with acute dyspnea. Clin Chim Acta 2012; 413: 992-7. 4. K. Senol, B. Saylam, F. Kocaay, et al. Red cell distribution width as a predictor of mortality in acute pancreatitis. Am J Emerg Med 2013; 31: 687 -9. 5. C. H. Kim, J. T. Park, E. J. Kim, et al. An increase in red blood cell distribution width from baseline predicts mortality in patients with severe sepsis or septic shock. Crit Care 2013; 17: R282. 6. S. Majercik, J. Fox, S. Knight, et al. Red cell distribution width is predictive of mortality in trauma patients. J Trauma Acute Care Surg 2013; 74: 1021-6. 7. H. S. Sen, O. Abakay, A. C. Tanrikulu, et al. Is a complete blood cell count useful in determining the prognosis of pulmonary embolism? Wien Klin Wochenschr 2014; 126: 347-354. 8. G. M. Felker, L. A. Allen, S. J. Pocock, et al. Red cell distribution width as a novel prognostic marker in heart failure: data from the CHARM Program and the Duke Databank. J Am Coll Cardiol 2007; 50: 40-7.
Conflict of Interest:
Identify the hospitals by name, along with their charges
As a physician licensed in the state of California, where this study was conducted, I would like to see each hospital identified by name, and ranked by order of the prices they charge for each test. I request the authors of this study please issue a supplementary data table exposing the billing practices of each hospital by name. As a result of the Affordable Care Act, many patients now have high-deductible medical insurance, and are effectively cash-paying patients, and may fail to comply with my test orders if they are overcharged.
Conflict of Interest:
Recent -( 2014 ) J E out Break in West Bengal, India, Need for JE vaccination programme in West Bengal that must cover the target children and young adults up to 20 years adequately( 700 MILLIONS) nationwide who are at risk of JE
Recent -( 2014 ) J E out Break in West Bengal, India, Need for JE vaccination programme in West Bengal that must cover the target children and young adults up to 20 years adequately( 700 MILLIONS) nationwide who are at risk of JE & there is need for investigation on the circulating strains of JE cases, in state of West Bengal .
Authors By Professor Pranab kumar Bhttacharya MD(Cal.Univ.( FIC path(India) Professor and Head Department of Pathology [in charge, of DCP course of WBUHS & DLT course, Member of Board of studies for Pathology(UG/PG/ Doctoral) & Member Secretary( For DCP) of Board of studies of West Bengal university of Health sciences(WBUHS) , DD36 sector-1, Salt lake, Kolkata, W.B, India; In-charge of DLT of STM, Kolkata, W.B Indiia ] Dept. of Pathology, 2nd floor; Room No 10 CCalcutta School of Tropical Medicine108 C.R. Avenue, Kolkata-700073; West Bengal; India E mail firstname.lastname@example.org Telephone no- 91 9231510535
2] Professor Sougata Ghosh MD( Cal.Univ) Professor and Head Department of Microbiology; Medical College Kolkata
Fever with altered sensorium and/or seizure is known as acute encephalitis syndrome(AES). Encephalitis may be caused by several viruses , bacterial and fungal infections parasites, spirochetes. More than 100 different pathogens are recognized as causative agents of AES are JEV, MVEV , West Nile virus, St. Louis encephalitis virus, Ebola Virus, herpes simplex, varicella-zoster, Epstein barr virus, mumps, measles, enteroviruses, influenza, adeno virus, echo virus, mycoplasma pneumonia the frequent pathogens. Bacterial, fungal, parasitic (like cerebral malaria) and some viral encephalitides (like Herpes simplex, Varicella- zoster) have however specific treatment. The majority of cases of viral AES (~90%) have no specific treatment (AESn). Japanese encephalitis(JE), is an encephalitis, caused by JEV- a mosquito-borne flavivirus infection , is prevalent in the regions like West Bengal; Manipur, Assam and in other south Indian states than other forms of Encephalities . JE occurring with an estimated 30,000 to 50,000 of cases and 15,000 deaths annually [3-5]. About 20% to 30% of JE cases lead to death, and 30-50% result in permanent neuropsychiatric squeal [5, 6]. Malnourished, poor economic class children and young adults are main victims of the disease [7, ] though adults in west Bengal states are also affected in 2014 . In India, nearly all states reported JE cases except that of Jammu & Kashmir, Himachal Pradesh, and Uttaranchal [8 ]. . In West Bengal, the first major outbreaks of JE occurred in the districts of Bankura and Burdwan in 1973, where about 700 cases and 300 deaths occurred. From 1978 to 2007, 103 389 cases and 33 729 deaths due to JEV infection were recorded from various parts of India. Every year, 1 500-4 000 cases are reported from this country. JE - is major public health problems world wide and is thus low endemic areas with seasonal distribution in China( higher Incidence Stratum is 3.3 at risk are 1026 millions populations in all age groups) , the Russian Federation's south-east, Australia and South and South-East Asia like India, Pakistan, Bangladesh, and Singapore( Lower incidence Stratum is .003 in all age groups at risk covering 89.5 millions populations ) . In India alone, 375 million population now at risk of developing AES. 70% to 75% of disease burden are in Uttar Pradesh of India.
In temperate areas of Asian countries , J E V transmitted during warm seasons, when large epidemics occur. In tropics and subtropics, transmission occur year-round but often intensifies during rainy seasons and pre-harvest period in rice-cultivating regions. JE is transmitted to humans through bites from infected mosquitoes of Culex species (mainly Culex tritaeniorhynchus). Humans, once infected, do not develop sufficient viraemia to infect feeding mosquitoes. The virus exists in transmission cycle between mosquitoes, pigs and/or water birds (enzootic cycle). The disease is predominantly found in rural and peri-urban settings, where humans live in closer proximity to these vertebrate hosts. Outbreaks of AES and JE are common every year in India, especially during the monsoon season, and claim hundreds of lives. Indian states that reported AESn cases were Andhra Pradesh, Assam, Bihar, Delhi, Goa, Haryana, Jharkhand, Kerala, Karnataka, Maharashtra, Manipur, Nagaland, Punjab, Tamil Nadu, Uttar Pradesh, Uttarakhand and West Bengal. States of India that did not report AESn were Arunachal Pradesh, Chhattisgarh, Gujarat, Himachal Pradesh, Jammu and Kashmir, Madhya Pradesh, Meghalaya, Mizoram, Odisha, Rajasthan, Sikkim and Tripura. But this year, major outbreaks - usually most prevalent in the northern states of Uttar Pradesh , Bihar(2013 &14) & have spread to regions such as West Bengal and in Assam. JE is not at all a contagious disease and does not spread from man to man unless there is an intermediate hosts like Pigs or water living birds. In West Bengal in 2014 , major outbreak occurred in North Bengal & toll from the disease in north Bengal only rose to 121 up to august 2nd and four new cases have also been reported in the state in August 04th 2014. Taking into account the death of 20 persons from other states in north Bengal due to possibly other Encephalitis, the death toll was 141 since January this year 2014. Death are reported from areas like Malda, Balurghat, Kranti near Maynaguri, North Bengal Medical College and Hospital (NBMCH), Birbhum, Bardwan, Bankra districts
In Assam state more than 100 people died of JE and AES so far, and over 24 districts have been affected by JE. The disease had severely affected Barpeta, Nagaon, Baksa, Darrang, Sonitpur, Nalbari and Bongaigaon where such cases were not many in the previous years. Diagnosis- Individuals who live in or had travelled to a JE-endemic area and experience encephalitis are considered a suspected JE case. Patients with JE present vivid signs of AES. JE cases are found highest amongst the children and young adults (2 -20 years). Children up to 10 years of age are most vulnerable group for JE due to either absence or low protective immunity against the virus in them However, in areas where JEV is recently introduced, adults are also getting the infection . Most common presenting symptoms are moderate to high grade fever , altered sensorium , seizures (82%), headache , and vomitings . Signs of meningeal irritation usually present in 55-60% of cases. Around 50% of JE patients undegoes in Glasgow comma scale (GCS) 3 to 8. All JE patients present to any hospital between 1 to 12 days from the onset of illness. The CSF WBC counts usually ranges from 2.0/mm3 to 520.0/mm3 Elevated levels of WBC (>5/mm3) found in 80% patients and predominantly lymphocyte. The mean CSF protein and glucose level usually 57.0 ? 27?mg/dL and 45.0 ? 12 mg/dL, . Of these 50% shows elevated (>40?mg/dL) level of protein. To confirm JE infection, to rule out other causes of encephalitis requires a laboratory testing of serum or, preferentially CSF by ELISA orby RT PCR. The kits available are Japanese Encephalitis-Dengue IgM Combo ELISA (Panbio Diagnostics, Australia) and JEV-CheX IgM capture ELISA (XCyton Diagnostics Limited, India). or JEV-CheX IgM capture ELISA (XCyton Diagnostics Limited, India). The average duration of illness is usually 5.4 days. Mortality rate from JE is more (49%) in children when admitted less than 7 days from the onset of illness. The mortality was significantly more in patients with GCS between 3 to 8 . Presences of meningeal signs are not found to be associated with fatal outcome. Similarly, no significant association is observed between high cell counts, elevated level of protein in CSF, and children fatality. As there is no specific treatment for Japanese encephalitis, supportive care in a medical facility is important to reduce the risk of death or Post JE neurological disability. The disease is preventable by proven effective vaccines - "Jenvac"(1), - Indian first indigenously developed vaccine for Japanese encephalitis jointly developed in 2013 by scientists at the Indian Council of Medical Research (ICMR), National Institute of Virology (NIV) and Bharat Biotech International Ltd. The Japanese encephalitis vaccine candidate strain (821564 XZ), used for making this Indian vaccine, Jenvac was isolated from the blood sample collected from a patient admitted to a government hospital in Kolar, Karnataka, in 1981.
There is another vaccine developed in China .The vaccine, manufactured in China, the attenuated SA 14-14-2 Japanese Encephalitis vaccine, needs to be given in one dose, can be used for infants, and is less expensive than other Japanese encephalitis vaccines. The imported Chinese vaccine costs around Rs.20 per dose while Jenvac is likely to be priced around Rs.70 per dose. In India, the Universal Immunization Programme targets 27 million infants and 30 million pregnant women every year against six vaccine-preventable diseases - tuberculosis, diphtheria, tetanus, pertussis, polio and measles - and the vaccination of pregnant women against tetanus. In some states, vaccines against hepatitis B and Japanese encephalitis are also included in the programme. However Indian Association of Paediatric Does not r outinely Recommend JE Vaccine(2) Factors which might have decreased JE 1] Improved environmental sanitation, proper health education and availability of more Infectious Disease doctors & Pathologists specialists might have resulted in early diagnosis and prevention of spread of AESn, JE & Dengue. 2] Improved communication and transport systems, methods of detection of treatable aetiologies and availability of multimedia teaching facilities might have supplemented the diagnostic efficiency of medical and nursing personnel resulting in early specific treatable diagnosis. 3] Although utmost care to be taken to report every case, there might be possibility that many cases of AESn might have died before being seen by any doctor, thereby reducing the number of cases of AESn. Part of the low IR might have been due to lack of staff or timely diagnostic facilities for making a diagnosis before the death of patient or lack of awareness among doctors that they have to report AESn cases. 4] JE vaccination with live attenuated china vaccine (SA-14-14-2) (genotype III) must be included in routine immunization programme as per National Immunization Schedule (NIS). vaccination programme must cover the target children adequately 700 MILLION children nationwide are at risk ; . Due to the widespread use of JE vaccine, JE cases has been declined in China, Korea, and Japan. The targeted age group for this vaccination should be below 20 years age. However there remains possibilities of the change in genotype of the circulating strains and that to be excluded in West Bengal. 5] dedicated hospital beds for encephalitis patients in affected districts. 6] investigation on the circulating strains are essentially required to find out the reasons of increasing tendency of JE cases in this state.
References-: 1]http://www.livemint.com/Industry/NVyjUE8DUW3phpiHFmIA2H/India-launches- first-indigenous-vaccineforJapanese-encepha.html?utm_source=copy 2] http://www.iapindia.org/IMM%20Schedule.pdf
3] R. Potula, S. Badrinath, and S. Srinivasan, "Japanese encephalitis in and around Pondicherry, south India: a clinical appraisal and prognostic indicators for the outcome," Journal of Tropical Pediatrics, vol. 49, no. 1, pp. 48-53, 2003. View at Publisher * View at Google Scholar * View at Scopus
4] Center for Disease Control and Prevention (CDC), "Question and answer about Japanese Encephalitis," March 2013, http://www.cdc.gov/japaneseencephalitis/qa/index.html.
5] World Health Organization (WHO), "Immunization, vaccines and biological," March 2013,http://www.who.int/immunization/topics/japanese_encephalitis/en/index.html.
6] World Health Organization, "Japanese encephalitis vaccines," The Weekly Epidemiological Record, vol. 81, pp. 331-340, 2006. 7] D. W. Vaughn and C. H. Hoke Jr., "The epidemiology of Japanese encephalitis: prospects for prevention," Epidemiologic Reviews, vol. 14, pp. 197-221, 1992. View at Scopus
8] A. Henderson, C. J. Leake, and D. S. Burke, "Japanese encephalitis in Nepal," The Lancet, vol. 2, no. 8363, pp. 1359-1360, 1983. View at Scopus
9] Banerjee K, Sengupta SN, Dandawate CN, Tongaonkar SS, Gupta NP. Virological and serological investigations of an epidemic of encephalitis which occurred at Bankura district, West Bengal. Indian J Med Res 1976; 64: 121-130.
 D utta K, Rangarajan PN, Vrati S, Basu A. Japanese encephalitis: pathogenesis, prophylactics and therapeutics. Curr Sci 2010; 98 (3): 326- 334
Acknowledgement-: Miss Upasana Bhattacharya Student Daughter of Professor Pranab kumar Bhattacharya; Mr Rupak Bhattacharya, Mr Ritwik Bhattacharya; Miss Rupsa Bhattacharya of 7/51 Purbapalli; Po-Sodepur Dist 24 Pargnas(north) West Bengal, Kolkata-700110, India; Miss Oindrila Mukherjee, Mrs Dalia Mukherjee and Mr Debasis Mukherjee of Swamiji Nagar; South Habra , North 24 Pargnas West Bengal India
Copy Right-: Copy Right of the article belongs to Professor Dr Pranab kumar Bhattacharya and his first degree blood relatives only as per copy right act & Rules of IPR
Conflict of Interest:
BMJ Open 2014 4:e005172; doi:10.1136/bmjopen-2014-005172: Erratum in Acknowledgements statement
Thomas S, Fazakarley L, Thomas P, et al. Testing the feasibility and acceptability of using the Nintendo Wii in the home to increase activity levels, vitality and well-being in people with multiple sclerosis (Mii- vitaliSe): protocol for a pilot randomised controlled study. BMJ Open 2014 4:e005172; doi:10.1136/bmjopen-2014-005172.
In the above article please note the Acknowledgements statement should acknowledge Mrs Kelly Jones and not Mrs Kelly Saunders as originally published. Below is the correct version of the acknowledgement:
They also thank Mrs Jo Hickson and Mrs Kelly Jones for attending the PPI workshop, for providing invaluable feedback about draft Mii-vitaliSe materials and the physical assessment protocol and for agreeing to be members of the study steering group.
Conflict of Interest:
We read with interest the article regarding UK newspaper coverage of common cancers by Konfortion et al  and were pleased that this confirmed similar findings to our previous work . We had previously looked at the UK's print media coverage of the top ten most common cancers in 2009: this found similar discrepancies between the prevalence of disease and the number of articles about each cancer, with over representation of breast and prostate cancer and under representation of colorectal and lung cancer . We noted that coverage of breast and prostate cancer was influenced by the illness of Kylie Monogue and Mr Al- Megrahi (the Lockerbie bomber) in keeping with the work of Konfortion, et al. We agree that the 'human element' articles may be key to representation of cancer within the media, as shown by coverage of Kylie Minogue, Jade Goody and Patrick Swayze (breast, cervical and pancreatic cancer respectively), and we have referred to this phenomenon as the 'Swayze Shift' [3-5].
We believe that media coverage of disease is one of the most important sources of health information to the general population and greatly influences both public perception and awareness of disease [6-9]. Whilst cancer awareness months do improve awareness of disease, it is clear from Konfortion et althat this strategy may not result in increased media coverage. We believe that a policy of media advocacy - positive engagement with health journalists - may greatly improve the quality and accuracy of health information within media articles. We have also suggested that media articles could be linked with 'red flag' symptoms to improve awareness and encourage patients to present earlier ; we are pleased to see this occurring in a recent article by the BBC (British Broadcasting Corporation) that linked an article on pancreatic cancer to the associated presenting symptoms .
Yours Sincerely James Williamson and David Hocken
References 1: Konfortion J, Jack RH, Davies EA. Coverage of common cancer types in UK national newspapers: a content analysis. BMJ Open 2014;4:e004677 2: Williamson JML, Jones IH, Hocken DB. How does the media profile of cancer compare with prevalence? Annals of the Royal College of Surgeons of England 2011;93:9-12 3: Chapman S, McLeod K, Wakefield M, Holding S. Impact of celebrity illness on breast cancer screening: Kylie Minogue's breast cancer diagnosis. Med J Aust 2005; 183: 247-50. 4: Casey GM, Morris B, Burnell M, Parberry A, Singh N, Rosenthal AN. Celebrities and screening: a measurable impact on high-grade cervical neoplasia diagnosis from the 'Jade Goody effect' in the UK. Br J Cancer 2013;109:1192-7 5: Williamson JML, Hocken DB. Pancreatic cancer in the media: the Swayze shift. Annals of the Royal College of Surgeons of England 2010;92:537-8 6: The PLoS Medicine editors. False hopes, unwarranted fears: the trouble with medical news stories. PLoS Medicine 2008; 5: 681-3. 7: Williamson JML, Skinner CI, Hocken DB. Death and illness as depicted in the media. International journal of clinical practice 2011;65:547-551 8: Jones IH, Williamson JML, Hocken DB. How informative is the print media coverage of colorectal cancer? Colorectal Disease 2012;14:250-2 9: Williamson JML, Rink J, Hewin D. The portrayal of Bariatric Surgery in the UK print media. Obesity Surgery 2012;22:1690-1694 10: Mountjoy S. Pancreatic cancer 'missed 19 times by NHS'. BBC news website 7 July 2014. http://www.bbc.co.uk/news/uk-england-devon-28171117
Conflict of Interest:
Interaction of doctors with pharmaceutical companies
Dear Editor of the BMJ,
We read with interest the systematic review on 'Legislative, educational, policy and other interventions targeting physicians' interaction with pharmacetical companies' by Alkhaled and colleagues. In 2012, the Irish medical council provided ethical guidelines on the interaction of doctors with pharmaceutical companies. These guidelines stated that doctors should not accept gifts or hospitality, directly from pharmaceutical companies. In 2013, we surveyed 126 Irish doctors at our large university hospital to assess if they were following the medical council guidelines and to further assess their perception of the influence of pharmaceutical companies on their prescription choice using an online questionnaire. 99% (125/126) of respondents admitted to having received something (sandwich, pen, free dinner, educational trip) from a pharmaceutical company at some point in their career. Nine months after publication of the medical council guidelines on interaction with pharmaceutical companies, 35% (41/117) of doctors were unaware of the new guidelines. Of those who said that they were in accordance with the new guidelines, 89% (48/52) had received gifts or hospitality from a pharmaceutical company since the introduction of the guidelines. 58% (69/118) of respondents felt that pharmaceutical company involvement with health care workers created a professional conflict of interest, and half of respondents (56/105) would prefer if pharmaceutical company representatives did not contact them while they were at work. 81% (95/115) of respondents felt that hospitals should have policies on the interactions between doctors and pharmaceutical company representatives. Only 12% (14/120) of the doctors surveyed had been given guidance on interaction with pharmaceutical company representatives or interpretation of information provided by pharmaceutical companies while at university. 84% (97/116) would have liked to have had more guidance as an undergraduate student.
In our study many doctors were keen to have policies on interaction with pharmaceutical company representatives in place in their hospital. Junior doctors expressed a wish to have received guidance on interaction with pharmaceutical companies, their representatives and associated literature while at university. The three observational studies reviewed in the paper by Alkhaled and colleagues demonstrated that introduction of policies can have a positive effect on the interaction between doctors and pharmaceutical companies and subsequent prescribing. The majority of doctors in our study have expressed a wish for hospitals to implement policies on the presence of pharmaceutical company representatives on campus. Now is the time for change.
Kind regards, Dr Susan Byrne Dr Tudor Montaneau Dr Janice Redmond
Department of Neurology, St.James Hospital, James Street, Dublin 8, Ireland.
1. Alkhaled, L., et al., Legislative, educational, policy and other interventions targeting physicians' interaction with pharmaceutical companies: a systematic review. BMJ Open, 2014. 4(7): p. e004880.
Conflict of Interest:
Susan Byrne received 6,298 pens, 467 sandwiches, and a travel grant from pharmaeutical companies between 2005 and 2010. Susan Byrne has not received anything from pharmaceutical companies since 2011. Tudor Montaneau reports no conflicts of interest. Janice Redmond accepted research funding from Merck-Serono in 2009.
Addendum to 'Functionality and feedback: a protocol for a realist synthesis of the collation, interpretation and utilisation of PROMs data to improve patient care'. 2014-005601
The authors would like to add the following sentence to the 'Ethics and Dissemination': We will also submit a final report to the National Institute for Health Research (NIHR) that will be published in the NIHR journals library.
Conflict of Interest: