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Recent eLetters

Displaying 11-20 letters out of 290 published

  1. Re:Foetal growth restriction, induction of labour and reduced still birth rate at term

    Thanks to Lionel Carbillon, Claire de la Hosseraye & Arsene Mekinian for their interest in and comments to our paper on stillbirth reduction in Denmark with a more proactive induction practice.

    No doubt, that the improved ultrasound monitoring of pregnancies at term is expected to have decreased the stillbirth rates all over the industrialised world. It is also true, that the stillbirth rates may be higher in women with preeclampsia and intrauterine growth restriction.

    The number of deaths after 37 weeks associated with IUGR was around 6 per year without any consistent trend during the study period. The adjusted hazard ratio of stillbirth among women with IUGR was 1.85 (1.4- 2.5). And the mean gestational age at delivery among women with IUGR was stable during the study period (39 weeks +/- 1 day). Thus, IUGR had a relatively little share of the total number of fetal deaths from 37 weeks, and did not play any confounding role on the influence of inductions.

    The number of women with preeclampsia (or more correctly with a diagnosis of preeclampsia) increased through the study period, but stillbirths in women with preeclampsia were slightly decreasing from 6 to 4 deaths per year. The HR of stillbirths among women with preeclampsia was not significantly elevated. The average gestational age at delivery among women with preeclampsia was (surprisingly) stable through the study period; 39 + 1-2. The confounding influence from preeclampsia on the influence of induction was not significant.

    Our point was and still is that the more intensive surveillance of women with IUGR or preeclampsia did not differ from our neighbour countries. While the stillbirth rates have been rather stable in these countries, our stillbirth rates were substantially reduced. Therefore, we don't think that these two conditions or the handling of them, can explain the substantial reduction in stillbirths in Denmark, especially not the decrease after 40 weeks, at which time the majority of women with these two conditions have delivered. Earlier induction in women having passed 40 weeks is certainly not the only contributing factor for the decrease in stillbirths in Denmark. We already had a low rate 10 years ago, but have experienced a further substantial reduction with the new induction practice, a reduction not seen in other countries. Thus, we still think that the more proactive induction practice has the main responsibility for this recent decrease.

    Conflict of Interest:

    See original paper.

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  2. Infections in rheumatoid arthritis - roles for herpes viruses

    This is a fascinating study into infections during onset and progress of RA.

    I have recently been investigating potential roles for herpes viruses, especially cytomegalovirus (CMV), in a series of infectious-like outbreaks seen within the UK over many years. These outbreaks lead to increased deaths and hospital admission for a range of medical conditions which include allergy[1-9]. There are several areas of potential cross- over with this study.

    Firstly, a review of the role of CMV in autoimmune diseases has suggested that this immune modulating virus may act to exacerbate symptoms [10].

    CMV has also been circumstantially implicated in a range of respiratory symptoms which appear to be associated with the outbreaks seen in the UK [11] and noted in this study.

    Hence would it be possible for the authors to re-evaluate their data to see if the infectious episodes cluster in time around 2002, 2007 and 2012 (not included in the study which is however presumably on-going) - or at least roughly five years apart? My own studies indicate that the 2012 outbreak can be seen in over 9 European countries (unpublished) and Russia is unlikely to be an exception.

    High fever of uncertain origin (as reported in the study) is one potential red flag for an active CMV infection.

    The study may well be too small, but could the authors also look and see if there is a disproportionate incidence of appendicitis, since the outbreaks in the UK also appear to be in some way linked to surges in the incidence of appendicitis [12].

    References

    1. Jones R (2013) Could cytomegalovirus be causing widespread outbreaks of chronic poor health. In Hypotheses in Clinical Medicine, pp 37-79, Eds M. Shoja, et al. New York: Nova Science Publishers Inc. Available from: http://www.hcaf.biz/2013/CMV_Read.pdf

    2. Jones R (2013) Recurring outbreaks of a subtle condition leading to hospitalization and death. Epidemiology: Open access 4(3): 137.

    3. Jones R (2013) Do recurring outbreaks of a type of infectious immune impairment trigger cyclic changes in the gender ratio at birth? Biomedicine International 4(1): 26-39.

    4. Jones R (2013) A recurring series of infectious-like events leading to excess deaths, emergency department attendances and medical admissions in Scotland. Biomedicine International 4(2): 72-86.

    5. Jones R, Goldeck D (2014) Unexpected and unexplained increase in death due to neurological disorders in 2012 in England and Wales: Is cytomegalovirus implicated? Medical Hypotheses 83(1): 25-31.

    6. Jones R (2014) Unexpected single-year-of-age changes in the elderly mortality rate in 2012 in England and Wales. British Journal of Medicine and Medical Research 4(16): 3196-3207.

    7. Jones R (2014) Infectious-like Spread of an Agent Leading to Increased Medical Admissions and Deaths in Wigan (England), during 2011 and 2012. British Journal of Medicine and Medical Research 4(28): 4723- 4741.

    8. Jones R (2014) Trends in admission for allergy. British Journal of Healthcare Management 20(7): 350-351.

    9. Jones R (2014) Infectious-like spread of an agent leading to increased medical hospital admission in the North East Essex area of the East of England. Biomedicine International 5(1): in press

    10. Jones R (2014) Roles for cytomegalovirus in infection, inflammation and autoimmunity. In Infection and Autoimmunity, 2nd Edition, Eds: N Rose, et al. Elsevier: Amsterdam. (in press)

    11. Jones R (2014) A Study of an Unexplained and Large Increase in Respiratory Deaths in England and Wales: Is the Pattern of Diagnoses Consistent with the Potential Involvement of Cytomegalovirus? British Journal of Medicine and Medical Research 4(33): 5179-5192.

    12. Jones R (2014) An unexpected increase in adult appendicitis in England (2000/01 to 2012/13): Could cytomegalovirus (CMV) be a risk factor? British Journal of Medicine and Medical Research (in press)

    Conflict of Interest:

    None declared

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  3. Re:Re:Reply to "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention"

    A call for humility on the Reduction in stillbirths at term after new birth induction paradigm

    Hedegaard et al state in their recent article: Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention, that they 'see no reason why a similar, more proactive induction paradigm could not be implemented in other countries' (1). Their observational study design limits drawing conclusions about causality, and their overly optimistic interpretation of the data provide good reason to proceed with caution.

    Is stillbirth the best and only outcome measure?

    All interventions carry risks for mother and unborn. Although the authors mention risks associated with inductions they do not provide any data on maternal risk and only limited data on risk to the foetus.

    Hedegaard et al base their conclusion mainly on differences in stillbirth rates and deaths the first week. The overwhelming importance to parents is whether they can celebrate future birthdays with their healthy child or not, not that they only reached full term with a live foetus. Neo -, peri- or infant mortality rates provides essential information to monitor delayed complications of induction these measures is however not used in this article. According to the official published Danish statistics on birth outcome there has not been any significant change from 2009-12 in the overall perinatal mortality (2,3).

    What is the best way to make conclusions about causality from observational data?

    When reviewing observational data, the conclusions can radically change based on broadening the time frame, or by excluding or including "anomalous" data points.

    We planned to add figure 1. here, however the BMJ comment system does not allow us to upload pictures. You can access the relevant figures here: http://figshare.com/articles/A_call_for_humility_on_the_Reduction_in_stillbirths_at_term_after_new_birth_induction_paradigm/1157865

    Figure 1. contains crude data from the Medical Birth Register (including all Danish birth from 1996-2013 from 37+0 weeks and onwards). The red curve illustrates stillbirth rates. The authors highlight that: 'The fall [in stillbirth] was steepest from 2009-2010 to 2011-2012' and they link the steep decrease to the change in the 2009 guidelines about induction of labour. However, the rate of stillbirths actually increased in 2010. The authors' selective reporting of annual data does not help explain the trends and variations in incidences, and it paves the way for a conclusion that is unfounded. One might even notice a slight increase in stillbirth in 2013 which is after the study period (4).

    Stillbirth is the one side of the equation on the other side is inductions; let's now take a look at this (Figure 2).

    Figure 2. Induction rates 1997-2023 in %. You can access it here: http://figshare.com/articles/A_call_for_humility_on_the_Reduction_in_stillbirths_at_term_after_new_birth_induction_paradigm/1157865

    Figure 2. shows a rather steep increase in number of inductions 1997- 2001, a stable period 2002-2007, and a steep increase 2008 -2013. However, the stillbirth rate appears to decline continuously over time and if we overlay the two figures, it does not mirror the change pattern in induction rates. Hedegaard et al. utilize a narrow time frame between the years 2009-12 to support an argument in favour of early induction.

    However one peak or decrease in the dataset of an observational study is not sufficient to draw strong conclusions. The Cochrane handbook recommends that studies like Hedegaard et al. which utilize a single intervention or studies which do not clearly define a period of time course through which the intervention was carried out should adhere to an additional level of scrutiny. In particular, The Cochrane Collaboration recommends at least three data points prior to and three after the intervention, in order to strengthen conclusions from these weaker study designs. Reviewing Hedegaard et al with this in mind, it is unclear if the authors are utilizing one or two interventions (the guidelines or inductions). And because the intervention itself is unclear it is difficult to determine the time course through which the intervention was carried out.

    Does the data support induction in gestational week 41 +3 to reduce stillbirths?

    We acknowledge, as we mentioned earlier, the decrease in stillbirth throughout the study period. We are however not convinced that 'the striking decreases in risk of late foetal deaths is likely primarily to be due to the earlier and increased induction rates' (our emphasis). Numerous additional factors are still not accounted for by the authors. Others rightfully highlighted that the study did not control for a range of relevant factors, such as birth defects, IUGR, and socio-economic status to name only a few. Also, the presented data shows that the stillbirth decreased in all gestational weeks after 37 weeks. This decrease in stillbirth in week 37+0-6 weeks is curious, especially if we are supposed to conclude that induction accounts for the decrease in stillbirth from 37 weeks. It has not been common practice in Denmark to induce in the 37+0-6 gestational week except in rare cases, and this decrease suggests that factors other than induction of labour, such as improved surveillance, could significantly contribute.

    This study raises many methodological questions, we have pointed to a few of them. We believe that the conclusions drawn from this study are too far reaching.

    Will the correct intervention please step forward?

    Hedegaard et al suggests that other countries should implement a proactive induction regime including early induction of labour for low risk women. We suggest a more humble approach that acknowledges multiple factors interacting in this significant decrease in stillbirths beyond the 37. gestational week over the last decades. Also we have significant concerns about unleashing a technology intensive solution, such as induction of labour, especially on women with normal and uncomplicated deliveries. We see no reason why this more proactive induction paradigm should be exported to other countries as the authors do not present data that support such a strong conclusion.

    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) Sundhedsstyrelsen. F?dselsstatistikken. 2011; tabel 2.2. http://sun3) dhedsstyrelsen.dk/publ/Publ2012/03mar/Foedselsstatistik2011.pdf Accessed August 26th

    3) Statens Seruminstitut. F?dselsstatistik tal og analyser. 2012; table 2.2. http://www.ssi.dk/~/media/Indhold/DK%20- %20dansk/Sundhedsdata%20og%20it/NSF/Registre/Fodselsregisteret/f%C3%B8dselsstatistikken2012_vers%204.ashx. Accessed August 26th

    4) Statens Serum Institut. The online Medical Birth Registry. http://www.ssi.dk/Sundhedsdataogit/Sundhedsvaesenet%20i%20tal/Specifikke%20omraader/Fodsler%20og%20aborter/Fodsler%20og%20komplikationer.aspx Accessed August 26th

    Conflict of Interest:

    None declared

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  4. Reply to "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention"

    Thank you to the authors for considering my comments to their recent publication.

    I agree with the authors that in real life we often have to rely on observational studies. Therefore we must allow us self to discuss the limitations of our analysis to avoid to draw biased conclusions.

    Causal inference in non-experimental studies typically requires; that no unobserved factors confound the relationship between the exposure and the outcome. Violations of this assumption will lead to biased estimation of causal effects.(1)

    Socio-economic status is one of the most recognized confounders in medical science and especially relevant when studying stillbirth. Moreover, confounding by treatment as a result of a better and a more intensive regime of ultrasonography in early and late pregnancy is hard to disallow.

    Comparing observational data for different countries with different induction and ultrasonography regimes for pregnant women is not a strong argument for causal effect.

    Considering both strengths and limitations in study design as well as relevant confounding factors is not normally addressed as being puritan but considered as timely in scientific practice.

    1. Editorial. Associations are not effects. Am J Epidemiol. 1991;133:101-102.

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  5. Correction

    We would like to make a minor correction to the discussion section of our paper. The quotation from Atroshi et al, regarding false positive/negative nerve conduction studies in CTS should read "30% false negative and 18% false-positive"

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  6. Correction to AAFP title in "Current and future use of point-of-care tests in primary care: an international survey in Australia, Belgium, The Netherlands, the UK and the USA"

    We wish to make a notation to this article. In all instances "American Academy of Family Practitioners" should read "American Academy of Family Physicians."

    Thank you

    Conflict of Interest:

    None declared

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  7. 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

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  8. Reply to "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention"

    Dear Sirs,

    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:

    None declared

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  9. 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.

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  10. 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:13738062354@163.com 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:mayuefengbj@163.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:zmhzjzk@163.com

    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: zmhzjzk@163.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.

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    None declared

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