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Recent eLetters

Displaying 1-10 letters out of 1372 published

  1. Context matters in children's experiences of napping and night-time sleep

    Given the media headline in response to this paper--that "Daytime naps 'should stop at the age of two'" (http://www.dailymail.co.uk/health/article-2957907/Daytime-naps-stop-age- two.html)--we would like to emphasise that napping can be an effective strategy for children to achieve sufficient amounts of sleep. This is particularly important when children experience inconsistent nighttime sleep arrangements, in which they are unable to achieve recommended amounts of sleep at nighttime alone; and for children from more socio- economically deprived backgrounds, who are already at a health disadvantage.

    In interviewing parents of over 80 three-year-old children about their child's sleep, we were struck by the many households in which sleep hygiene behaviours were not, and probably could not, be implemented, for reasons including household crowding, irregular schedules, fluctuating sleep environment, lack of parental knowledge, support or motivation. 21% of children did not have a regular bedtime implemented by their parents on all or most nights, and 23% did not fall asleep in their own bed each night with some children sleeping in multiple households every week (e.g. mother's home, father's home, grandparents' homes)1. These children, more commonly from socio-economically deprived areas, had significantly shorter nighttime sleep: but not shorter sleep over 24 hours. This suggests that napping compensates for shorter nighttime sleep in some children without 'healthy' nighttime sleep behaviours, preventing these children from experiencing insufficient sleep duration.

    There is a lack of high quality evidence on whether consolidated nighttime sleep versus combined nighttime sleep and daytime napping is better for health. Furthermore, as the authors point out, there is insufficient evidence to conclude whether napping results in delayed nighttime sleep onset and shorter nighttime sleep, or whether short nighttime sleep results in daytime napping (we suspect both are at play in different groups of children, depending on their home environment).

    Given the lack of high quality evidence, discouraging naps in those children with corresponding shorter nighttime sleep duration could unnecessarily penalise children who rely on daytime napping to achieve sufficient sleep amounts. In the context of crowded, perhaps chaotic, households, preventing naps where nighttime sleep is unlikely to be improved would lead to a reduction in 24 hour sleep duration, thereby negatively impacting health and development and increasing health-related inequalities.

    It should not be assumed that one approach fits all children. Blanket recommendations about the suitability of napping might increase inequalities in outcomes. Children's sleep behaviours and sleep environments are diverse. For some, regular and early bedtimes, in a quiet, dark room, enable them to achieve sufficient sleep through nighttime sleep alone. However others operating under more constrained contexts exhibit different strategies, including irregular, later bedtimes combined with napping, to achieve similar sleep amounts over 24 hours. Until there is good evidence that there are negative consequences to this second strategy, and that preventing napping will not result in decreased, insufficient sleep for some children, then napping should not be dismissed.

    1Jones CHD & Ball H (2014) Exploring socioeconomic differences in bedtime behaviours and sleep duration in English preschool children. Infant and Child Development, DOI: 10.1002/icd.1848

    Conflict of Interest:

    We are the authors of one of the papers included in this systematic review.

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  2. Re:Environmental tobacco smoke and effect on children

    Dear Editor,

    We thank Dr Williamson and Dr Odeka for their nice comments.

    Indeed, starting point of our research was my concern of chronically sick children exposed to parental smoking and developing asthma. Moreover, these children often seek for professional immunological care, while the explanation for their sickness is rather different from expectations of their parents.

    In fact, the parents in our practice, admit to smoke only "on the balcony" or "under the kitchen hood" and therefore we felt obliged to provide more scientific arguments to explain detrimental effects of ETS exposure in children (including recurrent bronchitis, chronic cough and eventually atopic dermatitis or asthma).

    We are happy to read, that our report will support your everyday pediatric practice. We also do believe, that our article will influence current legislation procedures aiming at limiting passive smoking of conventional cigarettes in children.

    We allow ourselves to take this opportunity and to suggest, that presumably electronic nicotine delivery systems (ENDS) may offer an interesting alternative to nicotine-addicted parents of children with chronic respiratory conditions. Probably ENDS may soon be offered also in the routine pediatric work. The studies are ongoing...

    Conflict of Interest:

    None declared

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  3. Positioning Early Child Development in the Post-2015 Agenda

    The Archives of Disease in Childhood series on the progress achieved towards attaining the Millennium Development Goals (MDG) draws attention to significant progress globally. Requejo and Bhutta [1] report the progress for MDG 4 (reduce by two-thirds, between 1990 and 2015, the under -five mortality rate). The number of child deaths has been reduced by half to around 6.3 million. Keeping attention on child survival is necessary if we are to end the preventable deaths of 17, 000 children who still die each day; however, a sole focus on survival ignores the reality of the quality of life for the children who survive. More than 200 million children under 5 years of age are at risk of not reaching their full developmental potential [2]. These children are largely concentrated in the same countries with poor survival rates as the risks for survival and development are largely the same, namely malnutrition, poverty, disease, neglect and a lack of learning opportunities.

    The long term impact of adversity in early childhood includes lower educational attainment and economic productivity, poorer health outcomes, increased risks of chronic conditions such as obesity and cardiovascular diseases, and increased risks of mental health problems and violence[3-4]. Mechanisms underlying many of these poor life outcomes operate through compromised early brain development. Interventions in early life that protect and promote cognitive and social-emotional functioning are as critical as efforts to protect and promote survival and physical health. Interventions to mitigate risks such as malnutrition and preventable illnesses improve children's health, growth and development, but alone they do not enable children to catch up to cognitive levels of healthy nourished children.

    Children also require stable, nurturing and responsive care, opportunities to learn, and safe and healthy environments. Without strategies to address both the survival and development of children, the lost potential and long term costs to individuals and society remain high. The 2014 special series in the 'Annals of the New York Academy of Sciences' on child development and nutrition reported that low cost interventions to promote early learning, care and development are effective, including when integrated with health and nutrition services. Since then, important evidence has emerged about the long-term effects of care for development intervention on educational attainment and long-term productivity[5].

    Inequalities between children precede birth and grow wider in environments that fail to support their development. Interventions in early childhood have the potential to reduce these inequalities. Early child development (ECD) programmes for young children and families are among the most promising approaches to alleviating poverty and achieving social and economic equity. The UN Secretary General synthesis report on the post-2015 agenda 'The Road to Dignity by 2030: Ending Poverty, Transforming All Lives and Protecting the Planet' (Documents\post-- 2015\synthesis report\N1467001.pdf) presents a transformational approach that builds around 6 elements that will help us deliver on the Sustainable Development Goals. ECD is part of this new agenda as a clear strategy for investment in 'People.' The acknowledgement of ECD in a global development framework recognizes the early years as the foundation for human development and life-long learning.

    The child health community has an obligation to ensure that all children survive and thrive. Efforts to reduce mortality and improve health must be accompanied by investments to promote children's optimal social-emotional, cognitive and linguistic development as a foundation for a sustainable development.

    The authors alone are responsible for the views expressed in this publication and they do not necessarily represent the decisions or the stated policies of WHO or of UNICEF.

    1.Requejo JH, Bhutta ZA (2015). The post-2015 agenda: staying the course in maternal and child survival. Archives Disease in Childhood; 100 (Suppl 1):s76-s81.

    2.Grantham-McGregor SM Grantham-McGregor SM, Cheung Y, Cueto S, Glewwe P, Richter L, Strupp B. (2007). Developmental potential in the first 5 years for children in developing countries. Lancet; 369:60-70.

    3.Walker SP, Chang SM, Vera-Hernandez M, Grantham-McGregor S (2011). Early childhood stimulation benefits adult competence and reduces violent behavior. Pediatrics; 127(5):849-57.

    4.Campbell F, Conti G, Heckman JJ, Moon SH, Pinto R, Pungello E, et al (2014). Early childhood investments substantially boost adult health. Science; 343(6178):1478-85.

    5.Gertler P, Heckman J, Pinto R, Zanolini A, Vermeersch C, Walker S, Change SM, Grantham-McGregor S (2014). Labor market returns to an early childhood stimulation intervention in Jamaica. Science, 344; 998-1001

    Conflict of Interest:

    None declared

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  4. Is there really any good evidence that rickets is associated with prolonged breast feeding?

    I enjoyed this review article and found it helpful to allow me to understand how both vitamin D and calcium deficiency could both produce the same clinical picture. However I was saddened to again see it asserted that a risk factor for vitamin D defiency rickets is "prolonged breast-feeding". There is no doubt that there have been many case series showing that children presenting with rickets are predominantly breastfed. I expect that all the children had arms and legs, but that is not given as a risk factor. Breast feeding is the normal physiological state and around 80% of UK children are now at least initially breast fed. These case series also show that the majority of cases are found in dark skinned mothers who are generally much more likely to breast feed and who, if investigated, are commonly themselves vitamin D deficient (1,2). In my personal experience children presenting with rickets have also had highly limited diets. Few case reports refer to dietary intake, but one that did, found that solid feeding in cases was both delayed and inadequate(3). WHO recommend continuing to feed for at least 12 months, so when does breast feeding become prolonged? I suspect that what authors mean is that the children are subsisting largely or solely on breast milk beyond the age of 6 months, when complimentary solids are needed. Although we all pay lip service to the importance of breast feeding, it remains always under threat from the combined forces of convention - services that are not yet used to the idea of breast feeding - and commercial influences. It is of note that Danone, a major manufacturer of formula milk have been actively promoting the issue of vitamin D (see http://www.theguardian.com/healthcare-network/2014/apr/02/action-needed-on -vitamin-d). It seems clear that they at least understand that regularly linking rickets to breast feeding will increase their sales of formula milk. 1.Agarwal N, Faridi MM, Aggarwal A, Singh O. Vitamin D Status of term exclusively breastfed infants and their mothers from India. Acta Paediatr. 2010;99(11):1671-1674. 2.Madar AA, Stene LC, Meyer HE. Vitamin D status among immigrant mothers from Pakistan, Turkey and Somalia and their infants attending child health clinics in Norway. Br J Nutr. 2009;101(7):1052-1058. 3.Majid Molla A, Badawi MH, al-Yaish S, Sharma P, el-Salam RS, Molla AM. Risk factors for nutritional rickets among children in Kuwait. Pediatrics international : official journal of the Japan Pediatric Society. 2000;42(3):280-284.

    Conflict of Interest:

    I take great pains to avoid any sponsorship or involvement with manufacturers of formula milk, but find it hard to completely escape their long reach.

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  5. Next generation sequencing should be the first line of investigation in non syndromic deafness in people of African descent

    In response to Parker and Bitner-Glindzicz's review article on Genetic investigations in childhood deafness,1 we will like to contribute to this topic with some data, that strongly question the clinical utility of GJB2 and GJB6 testing in non-syndromic hearing loss in people of African descent.

    Indeed, we investigated GJB2 genes in 205 patients affected with sensorineural non-syndromic hearing loss from Cameroonian2 and South African of Xhosa ancestry.3 Subsequently, 100 patients that do not presented any mutation in GJB2 gene, were further investigated for mutation in GJB6.3 In addition to the Sanger sequencing of the coding regions of GJB2 and GJB6,3,4 detection of the most frequent deletion in European and Asian patients, del(GJB6-D13S1830), was also investigated.4

    We did not found in the GJB2 gene, pathogenic variants that could explain the hearing loss in any of the 205 patients from Cameroon and South Africa.3 When comparing control Cameroonian and South African GJB2 sequences data with those extracted from the 1000 Genomes Project, there was a low level of variance amongst population groups,3 supporting the hypothesis that the prevalence of mutations in GJB2 amongst European and Asian populations affected by non-syndromic hearing loss, is due to a founder effects,5 arising after their migration out of Africa. Interestingly, in syndromic hearing loss involving GJB2 gene, the nature and frequency of mutations are likely not to be population specific; we reported in two unrelated Cameroonian individuals affected with sporadic Keratitis-Ichthyosis-Deafness (KID) syndrome, heterozygous p.Asp50Asn mutation in GJB2, in both cases;6 p.Asp50As is the most frequent mutation in KID syndrome in various World populations. The low frequency of mutation in GJB2 in non-syndromic hearing loss has been also reported in patients from Soudan and Kenya,7 Nigeria,8 in other group of South African of African descent,9 and other group of Cameroonian patients.10 The exception to this low prevalence of GJB2 mutations in African patients with non-syndromic deafness, is a specific mutation, p.R143W (c.427C>T), occurring at a high rate in the Ghanaian population from Adamarobe village.11 This could be also attributed to a founder effect, since p.R143W (c.427C>T) has not been reported in other sub-Saharan Africans, but in few African Americans,12 whose ancestors were probably brought from Ghana during the slave trade.

    The study have shown that, there was no coding region variation in GJB6 associated with non-syndromic deafness among Cameroonian and Xhosa South African patients, nor GJB6-D13S1830 deletion.4 Equally, no GJB6- D13S1830 deletion was reported in patients with non-syndromic hearing loss in Nigeria,8 in another group of patients from South Africa,9 nor in African Americans and Caribbean.12

    In summary, available data do not provide enough evidence to routinely investigate GJB2 and GJB6 in clinical practice in patients of sub-Saharan African ancestry with non-syndromic hearing loss. Massively parallel sequencing should be the best approach forward, and possibly the fist line of investigation to uncover the genetic aetiology of non- syndromic hearing loss among people of African descent.

    Acknowledgements The research was funded by the University of Yaounde for clinical phenotyping and DNA extraction and the National Health Laboratory Services (NHLS), South Africa for recruitment of South African samples and molecular analysis.

    Reference 1.Parker M, Bitner-Glindzicz M. Genetic investigations in childhood deafness. Arch Dis Child 2014, doi: 10.1136/archdischild-2014-306099. [Epub ahead of print] 2.Wonkam A, Noubiap JJ, Djomou F, Fieggen K, Njock R, Toure GB. Aetiology of childhood hearing loss in Cameroon (sub-Saharan Africa). Eur J Med Genet 2013;56:20-5. 3.Bosch J, Noubiap JJ, Dandara C, et al.Sequencing of GJB2 in Cameroonians and Black South Africans and comparison to 1000 Genomes Project Data Support Need to Revise Strategy for Discovery of Nonsyndromic Deafness Genes in Africans. OMICS. 2014 Aug 27. [Epub ahead of print] 4.Bosch J, Lebeko K, Nziale JJ, Dandara C, Makubalo N, Wonkam A. In search of genetic markers for nonsyndromic deafness in Africa: a study in Cameroonians and Black South Africans with the GJB6 and GJA1 candidate genes. OMICS 2014;18:481-5. 5.Dzhemileva LU, Barashkov NA, Posukh OL, et al.Carrier frequency of GJB2 gene mutations c.35delG, c.235delC and c.167delT among the populations of Eurasia. J Hum Genet 2010;55:749-54. 6.Wonkam A, Noubiap JJ, Bosch J, Dandara C, Toure GB. Heterozygous p.Asp50Asn mutation in the GJB2 gene in two Cameroonian patients with keratitis-ichthyosis-deafness (KID) syndrome. BMC Med Genet 2013;14:81. 7.Gasmelseed NM, Schmidt M, Magzoub MM, et al. Low frequency of deafness- associated GJB2 variants in Kenya and Sudan and novel GJB2 variants. Hum Mutat 2004;23:206-7. 8.Lasisi AO, Bademci G, Foster J 2nd, Blanton S, Tekin M. Common genes for non-syndromic deafness are uncommon in sub-Saharan Africa: A report from Nigeria. Int J Pediatr Otorhinolaryngol 2014;78:1870-3. 9.Kabahuma RI, Ouyang X, Du LL, Yan D, Hutchin T, Ramsay M, Penn C, Liu XZ. Absence of GJB2 gene mutations, the GJB6 deletion (GJB6-D13S1830) and four common mitochondrial mutations in nonsyndromic genetic hearing loss in a South African population. Int J Pediatr Otorhinolaryngol 2011;75:611- 7. 10.Trotta L, Iacona E, Primignani P, et al.GJB2 and MTRNR1 contributions in children with hearing impairment from Northern Cameroon. Int J Audiol. 2011;50:133-8. 11.Hamelmann C, Amedofu GK, Albrecht K, et al. Pattern of connexin 26 (GJB2) mutations causing sensorineural hearing impairment in Ghana. Hum Mutat 2001;18:84-5. 12.Samanich J, Lowes C, Burk R, et al. Mutations in GJB2, GJB6, and mitochondrial DNA are rare in African American and Caribbean Hispanic individuals with hearing impairment. Am J Med Genet A 2007;143A:830-8.

    Conflict of Interest:

    None declared

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  6. Using time and serial measurements to improve diagnostic strategies in febrile children

    Response to: 1 Segal I, Ehrlichman M, Urbach J, Bar-Meir M. Use of time from fever onset improves the diagnostic accuracy of C-reactive protein in identifying bacterial infections. Arch Dis Child. Nov 2014;99(11):974-978.

    We thank Segal et al. for their work and congratulate them with this interesting paper. The diagnostic value of CRP as reported by Segal et al. is very much in line with earlier work, and in keeping with the cut-off points of <20 mg/L for ruling out serious bacterial infections, and >80 mg/L for ruling in serious bacterial infections that were suggested in the meta-analysis by van den Bruel et al.2 Although the authors stated that time could be a valuable differentiating variable for interpreting the diagnostic value of CRP, their results also showed that duration in itself was not a significant predictor in multivariable analysis. This is similar to results we presented recently, showing no differentiating effect for duration of fever in a general population of febrile children, and in particular that duration of fever was not useful for deciding on using either CRP or procalcitonin (PCT) in the evaluation of febrile children.3 In our opinion the most important message of the study is that the diagnostic value of CRP increased over time. Notably, in this study children without SBI who had an early increase of CRP had early stabilization of CRP at relatively low levels, whereas CRP levels in children with SBI continued to rise and reach higher threshold values. Likewise, we found that the diagnostic value of CRP in children with a fever lasting >24 hours was better than in children with a short duration of fever.3 Others already showed an effect of using serial measurements of biomarkers on the duration of antibiotic prescribing in an outpatient setting.4 As a next step, longitudinal diagnostic strategies in the emergency department should be explored. The findings of Segal et al. support the potential use of serial measurements and of time dependent thresholds of biomarkers such as CRP and PCT at the emergency department. Taken altogether, the current cross-sectional approach of diagnostic research in febrile children may need to be replaced by a more longitudinal approach.

    references:

    1. Segal I, Ehrlichman M, Urbach J, Bar-Meir M. Use of time from fever onset improves the diagnostic accuracy of C-reactive protein in identifying bacterial infections. Arch Dis Child. Nov 2014;99(11):974-978.

    2. Van den Bruel A, Thompson MJ, Haj-Hassan T, et al. Diagnostic value of laboratory tests in identifying serious infections in febrile children: systematic review. BMJ. 2011;342:d3082.

    3. Nijman RG, Moll HA, Smit FJ, et al. C-Reactive Protein, Procalcitonin, and the Lab-Score for Detecting Serious Bacterial Infections in Febrile Children at the Emergency Department: A Prospective Observational Study. Pediatr Infect Dis J. Aug 4 2014.

    4. Baer G, Baumann P, Buettcher M, et al. Procalcitonin guidance to reduce antibiotic treatment of lower respiratory tract infection in children and adolescents (ProPAED): a randomized controlled trial. PLoS One. 2013;8(8):e68419.

    Conflict of Interest:

    None declared

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  7. Peanut anaphylaxis diagnosis

    The peanut allergy (PA) prevalence is about 1-2% in children. PA may account also for severe food allergy, such as anaphylaxis (1). The severity of reactions may depend on the type of allergen component sensitization. In this regard, at least 11 peanut allergen proteins have been identified and characterized. Ara h 1, 2, and 3 are the major peanut allergens and belong to the seed storage proteins family (Ara h 1 is a vicilin, Ara h 2 is a conglutin, Ara h 3 is a glycinin) (2). A very recent review pointed out the diagnostic work-up, underlining the importance of a correct diagnosis (3). We recently reported that comparing 2 groups of children with anaphylaxis to peanut (14 subjects) or peanut allergy (15 ones) a different immunological profile may be defined. Indeed, allergen-specific IgE levels to raw peanut were significantly higher in the anaphylaxis group (p=0.0044). Sensitization to either Ara h 2 or Ara h 3 was more frequently detected in the group of children with anaphylaxis than in those with PA (p = 0.0209 and p = 0.0007, respectively). Raw peanut cut-off > 2.1 kUA/L, Ara h 1 cut-off > 1 ISU, Ara h 2 cut-off > 4.7 ISU, and positivity for Ara h 3 had fair reliability to predict anaphylaxis. Therefore, we concluded that children with peanut anaphylaxis have higher IgE levels to raw peanut, Ara h 2, and Ara h 3 than children with less severe peanut allergy. Thus, molecular-based allergy diagnostics may improve the work-up pathway and provides fruitful information for prognosis and management. We suggest that all children with suspected anaphylactic reaction and possibly in all children with PA molecular diagnostic should be performed to define the allergen molecule profile involved.

    References 1) Tariq SM, Stevens M, Matthews S, Ridout S, Twiselton R, Hide DW. Cohort study of peanut and tree nut sensitisation by age of 4 years. BMJ 1996;313:514-7 2) Meyling FHJ, et al. The diagnostic value of specific IgE to Ara h 2 to predict peanut allergy in children is comparable to a validated and updated diagnostic prediction model. J Allergy Clin Immunol 2013;131:157- 63 3) Anagnostou K, Clark A. The management of peanut allergy. Arch Dis Child 2015;100:68-72 4) Ciprandi G, Pistorio A, Silvestri M, Rossi GA, Tosca MA.Peanut anaphylaxis: the usefulness of molecular-base allergy diagnostics. Allergy 2015;70:129-30

    Conflict of Interest:

    None declared

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  8. Environmental tobacco smoke and effect on children

    Dr Editor, We read with interest the publication by Feleszko Ruszczynski M, Jaworska J et al on the effect of Environmental tobacco smoke exposure and risk of allergic sensitisation in children.

    As a trainer and my Paediatric ST3 in the North West deanery we write to thank you for the article referenced above. we found it very interesting read indeed and it has really enhanced the understanding of the risks of environmental tobacco smoke.

    It is interesting to note that when assessing patients with asthma and other atopic conditions that parents are reluctant to admit to tobacco smoking, and if they did it is usually "I only smoke outside" or "only when he's gone to bed," and more recently (following recent legislation) "I never smoke in the car." Parents are often informed of the negative effects on their child's health, as well as on their own health. With this information it is important to now start to inform them of recent articles which are providing us with the evidence to support this. we belief that our practice and the best outcome for the patients will continue to be enhanced. We therefore have to thank you for providing this useful information.

    Reference

    Feleszko W, Ruszczynski M, Jaworska J et al. Environmental tobacco smoke exposure and risk of allergic sensitisation in children: a systematic review and meta-analysis Arch dis child Nov 2014: 985-992

    Conflict of Interest:

    None declared

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  9. Making the most of measles vaccination

    We thank Bustreo, Okwo-Bele, and Kamara for a comprehensive overview of the impressive achievements by the Global Alliance for Vaccines and Immunization on reducing child mortality world wide by providing vaccines[1]. With regard to measles vaccine, the authors note that child mortality in Niger was almost halved from 1998 to 2009, and measles vaccination contributed to this achievement. They refer to a Lives Saved Tool[2]-based estimate of 5% of the lives saved due to measles vaccines[3]. They add that "This impact is in addition to the non-specific effects (vaccines acting independently of other vaccines) of measles vaccination, which when provided with vitamin A or followed by DTP3 vaccination within a specified administration schedule can contribute to further mortality reduction from diseases other than measles".

    We agree that the remarkable reductions in child morality can also be attributed to the non-specific effects of measles vaccine - effects, which are not yet incorporated into the cause specific-child survival projections. These non-specific effects of vaccines may indeed be modified by other interventions such as vitamin A and other vaccines. However, we find it important to point out that measles vaccine provided with vitamin A or followed by DTP3 may not be the best combinations.

    First, vitamin A seems to enhance NSE of vaccines[4]. However, the effect of measles vaccine provided together with vitamin A on overall mortality has only been the subject of one placebo-controlled randomised trial, and that trial showed that while measles vaccine provided with vitamin A may be very beneficial for females (mortality rate ratio (MMR) 0.45 [95% confidence interval (CI): 0.24-0.87]), it had the opposite effect in males (MMR 1.92 [95% CI: 0.98-3.75], p-value for same effect in females and males = 0.003)[5]. Hence, while girls may benefit from the combined treatment, males may be harmed.

    Second, with respect to measles vaccination followed by DTP, this sequence has been associated with an increase in overall mortality among girls in spite of the disease-specific effects[6]. In contrast, DTP followed by measles vaccine seems much more beneficial - e.g. in a recent trial, compared with having DTP3 as the most recent vaccination, providing measles vaccination at 4.5 months of age shortly after DTP3 was associated with strong reductions in overall mortality until the children received the usual measles vaccine at nine months of age[7]. The sequence of vaccination has important implications for overall mortality: In a situation with herd immunity to pertussis, available evidence suggest that a policy of not providing DTP after measles vaccine would be associated with a 2-fold reduction in overall mortality for girls compared with situations where measles vaccination was followed by DTP[6].

    Hence, to make the most of the beneficial non-specific effects of measles vaccine, it should be given after DTP3 and it should not be followed by DTP vaccination.

    References

    1 Bustreo F, Okwo-Bele J-M, Kamara L. World Health Organization perspectives on the contribution of the Global Alliance for Vaccines and Immunization on reducing child mortality. Arch Dis Child 2015;100 Suppl 1:S34-7. doi:10.1136/archdischild-2013-305693

    2 Fox MJ, Martorell R, van den Broek N, et al. Assumptions and methods in the Lives Saved Tool (LiST). Introduction. BMC Public Health 2011;11 Suppl 3:I1. doi:10.1186/1471-2458-11-S3-I1

    3 Amouzou A, Habi O, Bensa?d K, et al. Reduction in child mortality in Niger: a Countdown to 2015 country case study. Lancet 2012;380:1169-78. doi:10.1016/S0140-6736(12)61376-2

    4 Jensen KJ, Ndure J, Plebanski M, et al. Heterologous and sex differential effects of administering vitamin A supplementation with vaccines. Trans R Soc Trop Med Hyg 2015;109:36-45. doi:10.1093/trstmh/tru184

    5 Fisker AB, Bale C, Rodrigues A, et al. High-dose vitamin A with vaccination after 6 months of age: a randomized trial. Pediatrics 2014;134:e739-48. doi:10.1542/peds.2014-0550

    6 Aaby P, Benn C, Nielsen J, et al. Testing the hypothesis that diphtheria-tetanus-pertussis vaccine has negative non-specific and sex- differential effects on child survival in high-mortality countries. BMJ Open 2012;2. doi:10.1136/bmjopen-2011-000707

    7 Aaby P, Aaby P, Martins CL, et al. Non-specific effects of standard measles vaccine at 4.5 and 9 months of age on childhood mortality: randomised controlled trial. BMJ 2010;341:c6495.

    Conflict of Interest:

    None declared

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  10. Use of Carbamazepine in the Treatment of Childhood Rolandic Epilepsy

    Authors Maria Moran1, Nikolina Docheva2, William Whitehouse 1,2 1. Nottingham Children's Hospital, 2. University of Nottingham

    We were interested to read the article by Mellish et al.(1) which reports preference for carbamazepine first line for UK paediatricians treating Benign Rolandic Epilepsy (also known as Benign Epilepsy with Centrotemporal Spikes), perhaps better called Childhood Rolandic Epilepsy (CRE), an archetypal Genetic Focal Epilepsy (GFE). As described in their article, and in NICE guidance, carbamazepine may worsen seizures in a significant minority of children with CRE which perhaps makes it a questionable first-line choice. We have had local experience of a few cases evolving into Atypical Benign Partial Epilepsy of Childhood (ABPEC or pseudo-Lennox syndrome) temporarily while on carbamazepine.

    A systematic literature search revealed case reports describing onset of new atonic/absence seizures and continuous spike and wave discharges in sleep on EEG (2,3). A worsening of epileptic negative myoclonus has also been described (4,5). In a retrospective study of 98 cases of CRE, Corda et al describe 40 patients who received carbamazepine (35 as monotherapy) (6). Only 2 experienced deterioration in seizures (5%; 95% CI -1.7% to 11.7%).

    In a recent local retrospective clinical audit, epilepsies worsened on carbamazepine in 8/44 (18%), and on sodium valproate in 5/40 (13%). However only 4 (9%) on carbamazepine had a GFE.

    It seems that carbamazepine can aggravate CRE but this is perhaps not specific to CRE, or even any GFE, nor frequent enough to caution this practice. However prescribers do need to be aware of this property, and must be prepared to withdraw carbamazepine promptly if seizures worsen.

    This question would be best resolved by including carbamazepine in a multicentre prospective trial of treatment na?ve children with GFE (including CRE) with EEG and clinical outcome assessments designed not only to ascertain clinical effectiveness but also worsening of the epilepsy and EEG.

    References 1. Mellish L, Dunkley C, Ferrie C, Pal D. Antiepileptic drug treatment of rolandic epilepsy and Panayiotopoulos syndrome: clinical practice survey and clinical trial feasibility Arch Dis Child 2015;100:1 62-6

    2. Lerman P. Seizures induced or aggravated by anticonvulsants. Epilepsia 1986:27:706-10

    3. Nanba Y, Maegaki Y. Epileptic negative myoclonus induced by carbamazepine in a child with BECTS. Pediatr Neurol 1999;21(3):664-7

    4. Parmeggiani L, Seri S, Bonanni P, Guerrini R. Electrophysiological characterization of spontaneous and carbamazepine-induced epileptic negative myoclonus in benign childhood epilepsy with centro-temporal spikes. Clin Neurophysiol. 2004;115(1):50-8

    5. Corda D, Gelisse P, Genton P, Dravet C, Baldy-Moulinier M. Incidence of drug-induced aggravation in benign epilepsy with centrotemporal spikes. Epilepsia 2001; 42(6):754-759.

    Conflict of Interest:

    None declared

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