If house dust mite allergen (Der p I) is an important cause of asthma, there should be a direct relationship between level of exposure to this allergen and asthma severity. To examine this, we studied six large random samples of children in different regions of New South Wales, Australia. We measured recent wheeze by questionnaire, airway hyperresponsiveness (AHR) by histamine inhalation test and sensitization to house dust mites by skin prick tests. Current asthma was defined as the presence of recent wheeze and AHR. We measured Der p I levels in the beds of approximately 80 children in each region. In regions where Der p I levels were high, more children were sensitized to house dust mites, and these children had significantly more AHR and recent wheeze. After adjusting for sensitization to other allergens, we found that the risk of house dust mite-sensitized children having current asthma doubled with every doubling of Der p I level. There was a modest correlation between AHR and Der p I exposure in individuals (r = 0.23, p < 0.03). These data suggest that house dust mite allergens are an important cause of childhood asthma and that reducing exposure to these allergens could have a large public health benefit in terms of asthma prevention.

Rapid reviews have the potential to overcome a key barrier to the use of research evidence in decision making, namely that of the lack of timely and relevant research. This rapid review of systematic reviews and primary studies sought to answer the question: What are the best methodologies to enable a rapid review of research evidence for evidence-informed decision making in health policy and practice? This rapid review utilised systematic review methods and was conducted according to a pre-defined protocol including clear inclusion criteria (PROSPERO registration: CRD42015015998). A comprehensive search strategy was used, including published and grey literature, written in English, French, Portuguese or Spanish, from 2004 onwards. Eleven databases and two websites were searched. Two review authors independently applied the eligibility criteria. Data extraction was done by one reviewer and checked by a second. The methodological quality of included studies was assessed independently by two reviewers. A narrative summary of the results is presented. Five systematic reviews and one randomised controlled trial (RCT) that investigated methodologies for rapid reviews met the inclusion criteria. None of the systematic reviews were of sufficient quality to allow firm conclusions to be made. Thus, the findings need to be treated with caution. There is no agreed definition of rapid reviews in the literature and no agreed methodology for conducting rapid reviews. While a wide range of ‘shortcuts’ are used to make rapid reviews faster than a full systematic review, the included studies found little empirical evidence of their impact on the conclusions of either rapid or systematic reviews. There is some evidence from the included RCT (that had a low risk of bias) that rapid reviews may improve clarity and accessibility of research evidence for decision makers. Greater care needs to be taken in improving the transparency of the methods used in rapid review products. There is no evidence available to suggest that rapid reviews should not be done or that they are misleading in any way. We offer an improved definition of rapid reviews to guide future research as well as clearer guidance for policy and practice.

Introduction Antidepressants introduced since 1990, especially selective serotonin reuptake inhibitors and venlafaxine, have been used increasingly as first line treatment for depression in children.1 2 The safety of prescribingantidepressants to children (including adolescents) has been the subject of increasing concern in the community and the medical profession, leading to recommendations against their use from government and industry (box 1). In this paper, we review the published literature on the efficacy and safety of newer antidepressants in children. References ↵ Chan RTW, Rey JM, Hazell PL . Clinical practice guidelines for depression in young people: are the treatment recommendations outdated? Med J Aust 2002; 177: 448–51. ↵ Safer DJ, Zito JM, dosReis S . Concomitant psychotropic medication for youths. Am J Psychiatry 2003; 160: 438. ↵ Keller MB, Ryan ND, Strober M, Klein RG, Kutcher SP, Birmaher B, et al . Efficacy of paroxetine in the treatment of adolescent major depression: a randomized, controlled trial. J Am Acad Child Adolesc Psychiatry 2001; 40: 762–72. ↵ Jureidini J, Tonkin A . Paroxetine in major depression (letter). J Am Acad Child Adolesc Psychiatry 2003; 42: 514. ↵ Simeon JG, Dinicola VF, Ferguson HB, Copping W . Adolescent depression: a placebo-controlled fluoxetine treatment study and follow-up. Prog Neuropsychopharmacol Biol Psychiatry 1990; 14: 791–5. ↵ Mandoki MW, Tapia MR, Tapia MA, Sumner GS, Parker JL . Venlafaxine in the treatment of children and adolescents with major depression. Psychopharmacol Bull 1997; 33: 149–54. ↵ Emslie GJ, Rush AJ, Weinberg WA, Kowatch RA, Hughes CW, Carmody T, et al . A double-blind, randomized, placebo-controlled trial of fluoxetine in children and adolescents with depression. Arch Gen Psychiatry 1997; 54: 1031–7. ↵ Emslie GJ, Heiligenstein JH, Wagner KD, Hoog SL, Ernest DE, Brown E, et al . Fluoxetine for acute treatment of depression in children and adolescents: a placebo-controlled, randomized clinical trial. J Am Acad Child Adolesc Psychiatry 2002; 41: 1205–15. ↵ Wagner KD, Ambrosini P, Rynn M, Wohlberg C, Yang R, Greenbaum MS, et al . Efficacy of sertraline in the treatment of children and adolescents with major depressive disorder: two randomized controlled trials. JAMA 2003; 290: 1033–41. ↵ Braconnier A, Le Coent R, Cohen D . Paroxetine versus clomipramine in adolescents with severe major depression: a double-blind, randomized, multicenter trial. J Am Acad Child Adolesc Psychiatry 2003; 42: 22–9. ↵ FDA Center for Drug Evaluation and Research . Background on suicidality associated with antidepressant drug treatment (memorandum). www.fda.gov/ohrms/dockets/ac/04/briefing/4006B1_03_Background%20Memo%2001–05-04.htm (accessed 17 Feb 2004). ↵ King RA, Riddle MA, Chappell PB, Hardin MT, Anderson GM, Lombroso P, et al . Emergence of self-destructive phenomena in children and adolescents during fluoxetine treatment. J Am Acad Child Adolesc Psychiatry 1991; 30: 179–86. ↵ Herxheimer A, Mintzes B . Antidepressants and adverse effects in young patients: uncovering the evidence. CMAJ 2004; 170: 487–9. ↵ Kirsch I . St John's wort, conventional medication and placebo. Complement Ther Med 2003; 11: 193–5. ↵ Moncrieff J, Wessely S, Hardy R . Active placebo versus antidepressants for depression. Cochrane Database Syst Rev 2004;(1): CD003012 ↵ Hughes CW, Emslie G, Kowatch R, Weinberg W, Rintelman J, Rush J . Clinician, parent, and child prediction of medication or placebo in double-blind depression study. Neuropsychopharmacol 2000; 23: 591–4. ↵ Quitkin FM . Placebos, drug effects, and study design: a clinician's guide. Am J Psychiatry 1999; 156: 829–36. ↵ Swartzman LC, Burkell J . Expectations and the placebo effect in clinical drug trials: why we should not turn a blind eye to unblinding, and other cautionary notes. Clin Pharmacol Ther 1998; 64: 1–7. ↵ Varley CK . Psychopharmacological treatment of major depressive disorder in children and adolescents. JAMA 2003; 290: 1091–3. ↵ Keller MB, Ryan ND, Strober M, Weller EB, McCafferty JP, Hagino OR, et al . Paroxetine in major depression (letter). J Am Acad Child Adolesc Psychiatry 2003; 42: 515–6. ↵ FDA Center for Drug Evaluation and Research . Statistical review of Prozac for pediatric OCD and depression. www.fda.gov/cder/foi/nda/2003/18936S064_Prozac%20Pulvules_statr.pdf (accessed 17 Feb 2004). ↵ Committee on Safety of Medicines . Selective serotonin reuptake inhibitors (SSRIs)—overview of regulatory status and CSM advice relating to major depressive disorder (MDD) in children and adolescents: summary of clinical trials. medicines.mhra.gov.uk/ourwork/monitorsafequalmed/safetymessages/ssrioverviewclintrialdata_101203.htm (accessed 18 Feb 2004). ↵ Harrington R, Whittaker J, Shoebridge P, Campbell F . Systematic review of efficacy of cognitive behaviour therapies in childhood and adolescent depressive disorder. BMJ 1998; 316: 1559–63. ↵ Lasser KE, Allen PD, Woolhandler SJ, Himmelstein DU, Wolfe SM, Bor DH . Timing of new black box warnings and withdrawals for prescription medications. JAMA 2002; 287: 2215–20.

Research from JAMA Psychiatry — The Burden of Major Depression Avoidable by Longer-term Treatment Strategies

To conduct a systematic review to estimate the prevalence of asymptomatic Zika virus infection in the general population and in specific population groups. We searched PubMed®, Embase® and LILACS online databases from inception to 26 January 2018. We included observational epidemiological studies where laboratory testing was used to confirm positive exposure of participants to Zika virus and in which Zika virus symptom status was also recorded. We excluded studies in which having symptoms of Zika virus was a criterion for inclusion. The main outcome assessed was percentage of all Zika virus-positive participants who were asymptomatic. We used a quality-effects approach and the double arcsine transformation for the meta-analysis. We assessed 753 studies for inclusion, of which 23 were included in the meta-analysis, totalling 11 305 Zika virus-positive participants. The high degree of heterogeneity in the studies (I2 = 99%) suggests that the pooled prevalence of asymptomatic Zika virus-positive participants was probably not a robust estimate. Analysis based on subgroups of the population (general population, returned travellers, blood donors, adults with Guillain-Barré syndrome, pregnant women and babies with microcephaly) was not able to explain the heterogeneity. Funnel and Doi plots showed major asymmetry, suggesting selection bias or true heterogeneity. Better-quality research is needed, using standardized methods, to determine the true prevalence of asymptomatic Zika virus and whether it varies between populations or over time.

Objective: To report on a new modelling approach developed for the assessing cost-effectiveness in obesity (ACE-Obesity) project and the likely population health benefit and strength of evidence for 13 potential obesity prevention interventions in children and adolescents in Australia. Methods: We used the best available evidence, including evidence from non-traditional epidemiological study designs, to determine the health benefits as body mass index (BMI) units saved and disability-adjusted life years (DALYs) saved. We developed new methods to model the impact of behaviours on BMI post-intervention where this was not measured and the impacts on DALYs over the child's lifetime (on the assumption that changes in BMI were maintained into adulthood). A working group of stakeholders provided input into decisions on the selection of interventions, the assumptions for modelling and the strength of the evidence. Results: The likely health benefit varied considerably, as did the strength of the evidence from which that health benefit was calculated. The greatest health benefit is likely to be achieved by the ‘Reduction of TV advertising of high fat and/or high sugar foods and drinks to children’, ‘Laparoscopic adjustable gastric banding’ and the ‘multi-faceted school-based programme with an active physical education component’ interventions. Conclusions: The use of consistent methods and common health outcome measures enables valid comparison of the potential impact of interventions, but comparisons must take into account the strength of the evidence used. Other considerations, including cost-effectiveness and acceptability to stakeholders, will be presented in future ACE-Obesity papers. Information gaps identified include the need for new and more effective initiatives for the prevention of overweight and obesity and for better evaluations of public health interventions.