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• W1947887788 abstract "To estimate where intermittent preventive treatment (IPTp) using sulphadoxine–pyrimethamine (SP) could be withdrawn as an intervention due to declining malaria transmission intensity, or due to increasing prevalence of the Plasmodium falciparum dihydropteroate synthetase resistance mutation at codon 581G. We conducted a systematic review and meta-analysis of protection against the incidence of low birth weight (LBW) conferred by ≥2 doses of IPTp-SP. We matched these outcomes to a proxy measure of malaria incidence in women of the same studies, applied meta-regression models to these data and conducted sensitivity analysis of the 581G mutation. Variation in the protective effect of IPTp-SP against LBW could not be explained by malaria transmission intensity. Among primi- and secundigravidae, IPTp-SP protected against LBW where 581G was ≤10.1% [odds ratio (OR): 0.49; 95% confidence intervals (CI): 0.29, 0.81; P = <0.01] and 581G was >10.1% (OR = 0.73; 95% CI: 0.29, 1.81; P = 0.03). Random-effects models among multigravidae showed that IPTp-SP protects against LBW where 581G was ≤10.1% (OR = 0.56; 95% CI: 0.37, 0.86; P = 0.07), a finding of borderline statistical significance. No evidence of protection against LBW was observed where 581G was >10.1% (OR = 0.96; 95% CI: 0.70, 1.34; P = 0.47). There appears to be a prevalence of 581G above which IPTp-SP no longer protects against LBW. Pregnancy studies are urgently needed where 581G is >10.1% to define the specific prevalence threshold where new strategies should be deployed. Estimer là où le traitement préventif intermittent (TPI) utilisant la sulfadoxine-pyriméthamine (SP) pourrait être retiré comme intervention en raison de la baisse de l'intensité de la transmission du paludisme ou en raison de la prévalence croissante de la mutation de résistance au niveau du codon 581G de la dihydroptéroate synthétase de Plasmodium falciparum. Nous avons effectué une revue systématique et une méta-analyse de la protection contre l'incidence du faible poids de naissance (FPN) conférée par plus de 2 doses de TPI-SP. Nous avons croisé ces résultats à une mesure indirecte de l'incidence du paludisme chez les femmes des mêmes études, avons appliqué des modèles de méta-régression à ces données et effectué une analyse de sensibilité de la mutation 581G. La variation dans l'effet protecteur du TPI-SP contre le FPN ne pouvait pas être expliquée par l'intensité de la transmission du paludisme. Parmi les primi et secundi-pares, le TPI-SP protégeait contre le FPN là où le taux de 581G était ≤10,1% (Odds Ratio [OR]: 0,49; intervalles de confiance [IC] 95%: 0,29–0,81; P = <0,01) et là où 581G était >10,1% (OR = 0,73; IC95%: 0,29–1,81; P = 0,03). Les modèles à effets aléatoires sur les multipares ont montré que le TPI-SP protège contre le FPN là où le taux de 581G était ≤10,1% (OR = 0,56; IC à 95%: 0,37, 0,86; P = 0,07), une observation de signification statistique intermédiaire. Aucune preuve de la protection contre le FPN n'a été observée lorsque 581G était >10,1% (OR = 0,96; IC95%: 0,70–1,34; P = 0,47). Il semble exister une prévalence de 581G au-dessus de laquelle le TPI-SP ne protège plus contre le FPN. Des études sur les grossesses sont urgemment nécessaires là où le taux de 581G est >10,1% pour définir le seuil de prévalence spécifique où de nouvelles stratégies doivent être déployées. Evaluar si el tratamiento preventivo intermitente durante el embarazo utilizando sufadoxina-pirimetamina (IPTp-SP) podría retirarse como intervención, debido a la disminución en la intensidad de la transmisión de malaria, o al aumento en la prevalencia de mutación en el codón 581G de la dihidropteroato sintetasa de Plasmodium falciparum que genera resistencia. Hemos realizado una revisión sistemática y un meta-análisis de protección frente a la incidencia del bajo peso al nacer (BPN) conferida por ≥ 2 dosis de IPTp-SP. Estos resultados los hemos pareado con una medida proxy de la incidencia de malaria en mujeres de los mismos estudios, aplicamos modelos de meta-regresión a estos datos y llevamos a cabo un análisis de sensibilidad de la mutación 581G. La variación en el efecto protector del IPTp-SP frente al BPN no podía explicarse por la baja intensidad de transmisión de malaria. Entre primi grávidas y secundigrávidas, el IPTp-SP protegía frente al BPN en lugares en donde 581G era ≤10.1% (Razón de Momios [OR]: 0.49; 95% Intervalos de Confianza [IC]: 0.29, 0.81; P = <0.01) y 581G era >10.1% (OR = 0.73; IC95%: 0.29, 1.81; P = 0.03). Los modelos de efectos aleatorios entre multigrávidas mostraron que el IPTp-SP protegía frente al BPN en donde 581G era ≤10.1% (OR = 0.56; IC 95%: 0.37, 0.86; P = 0.07), un hallazgo en el límite de la significancia estadística. No se observó evidencia de protección frente al BPN en lugares en donde 581G era >10.1% (OR = 0.96; IC 95%: 0.70, 1.34; P = 0.47). Parece haber una prevalencia de 581G sobre la cual el IPTp-SP no protege frente al BPN. Se necesitan urgentemente estudios durante el embarazo en lugares en donde 581G es >10.1%, con el fin de definir el umbral de prevalencia específico en el que deberían implantarse nuevas estrategias. The World Health Organization (WHO) recommends the provision of intermittent preventive treatment (IPTp) using sulphadoxine–pyrimethamine (SP) at every scheduled antenatal care visit, from the second trimester until delivery, in areas of moderate (stable) to high transmission to protect pregnant women against the adverse consequences of malaria infection. Although sulphadoxine and pyrimethamine are synergistic and produce complimentary inhibition, several mutations are associated with decreased parasite sensitivity. Parasite resistance to SP is associated with mutation on the dihydrofolate reductase (Pfdhfr) and the dihydropteroate synthetase (Pfdhps) genes. Three Pfdhfr mutations, namely N51I, C59R and S108N, are commonly referred to as the triple mutation; Pfdhps mutations A437G and G540E are often described as the double mutation. Collectively, these constitute the quintuple mutations and compromise SP efficacy 1-3. The effectiveness of IPTp-SP to prevent low birth weight (LBW) decreases with increasing population prevalence of Pfdhps K540E mutation – a proxy for the quintuple Pfdhfr and Pfdhps mutant – although some beneficial effect on birth weight remains evident in areas where Pfdhps K540E is even above 90% 4. Importantly, however, IPTp-SP fails to inhibit parasite growth where the Pfdhps A581G mutation has emerged alongside the Pfdhfr and Pfdhps quintuple mutant to produce ‘sextuple’ mutant parasites 5. Thus, the population prevalence of 581G has assumed a central role in IPTp-SP policy discussions 6. With historic reductions in malaria transmission observed in some countries of sub-Saharan Africa over the past decade and increasing parasite resistance to SP during the same time period, two questions have come to the forefront related to IPTp-SP. Is there a level of malaria transmission intensity below which IPTp-SP no longer prevents LBW at the population level and can be withdrawn? Secondly, is there a prevalence threshold of 581G which renders falciparum parasites ‘super resistant’ to SP and above which IPTp-SP is no longer protective against LBW and can be withdrawn? To answer these questions, we delineated three objectives for this study. The first objective was to conduct a systematic review and meta-analysis of IPTp-SP studies that have reported the protective effect against LBW by gravidae. The second objective was to use meta-regression analysis to determine whether there was a level of malaria transmission intensity below which IPTp-SP no longer conferred protection against LBW at the population level. The third objective was to use sensitivity analysis among these same IPTp-SP studies to determine whether 581G prevalence appeared to affect LBW outcomes. These objectives could be achieved most directly with evidence from new, large, placebo-controlled randomised clinical trials conducted in endemic areas with narrowly different levels of low transmission or resistance. However, the use of placebo where IPTp-SP is policy, or the withholding of preventive treatment to create an unprotected comparison group, raises ethical concerns. Thus, analysis needs to be conducted using available data. This has its own set of challenges, particularly as it relates to our second objective. Maternal parasitaemia is highest between gestational weeks 9 and 16, and then tapers until term 7, but IPTp-SP studies almost exclusively measure parasitaemia only once, at or near delivery, producing a point estimate that has been influenced by the total amount of antimalarial drug administered during the antenatal period and by near-to-term therapy. Thus, antenatal exposure to malaria infection is often understated in IPTp-SP studies. A proxy measure for malaria transmission intensity is needed. This proxy should lend itself to stratification by gravidae because malaria infection in endemic areas is known to be more prevalent and intense in primi- and secundigravidae than among multigravidae 7. The proxy we chose is the prevalence of malaria infection among children. A systematic review of the literature on malaria in pregnancy was completed in August 2014. The protocol can be found in the International Prospective Register of Systematic Reviews (PROSPERO; CRD42014007618). In brief, we searched PubMed, MEDLINE, EMBASE, the WHO International Clinical Trials Registry and reference lists to identify pregnancy studies that reported: (i) the proportion of pregnant women who were exposed to ≥2 doses of IPTp-SP compared to placebo, or to no doses of IPTp-SP, and (ii) the incidence of LBW by treatment group. We imported records into EndNote X7 software (Thomson Reuters), removed duplicates and screened each record against pre-determined eligibility criteria. Discrepancies in eligibility assessment were settled by a third-party expert. We reviewed full-text articles against the same criteria. Studies were excluded if they were conducted: (i) before 1990, (ii) outside sub-Saharan Africa, (iii) without reporting the effect of IPTp-SP on LBW, (iv) with selective enrolment of pregnant women from high-risk groups such as those with HIV or (v) utilised active antimalarial drug comparators against IPTp-SP. Figure 1 illustrates our selection process, the number of studies excluded and the reasons for their exclusion in accordance with guidelines from the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Table S1 is the PRISMA checklist. We extracted data without blinding to author or publication, but we did so in duplicate and independently, and then applied methods of Grading of Evidence, Assessment, Development and Evaluation (GRADE) to appraise data quality. RevMan 5.2 software was used to determine the risk of bias among individual pregnancy studies and across studies (Oxford, UK). We conducted a standard meta-analysis employing Stata/IC version 13 software (Stata Corporation) using the results of our systematic review without regard for malaria transmission intensity on LBW outcomes. We pooled the incidence of LBW by gravidae and by exposure to ≥2 doses of IPTp-SP vs. placebo or no doses, and assessed our results with the Q statistic. We employed two methods to estimate the malaria transmission intensity that was likely to have been present in each IPTp-SP study site. Our first approach was to use the 2007 prevalence estimates of Plasmodium falciparum infection among children 2–10 years of age (2007 PfPR2–10) as calculated by the Malaria Atlas Project (MAP) for the same locations where IPTp-SP studies had been conducted. However, because all our IPTp-SP studies had been conducted prior to 2007, with the exception of one multi-year trial that ended in 2007, we sought prevalence estimates that better aligned with the years of the pregnancy studies. For this, we obtained national cross-sectional survey data sets from MAP of P. falciparum prevalence for each of the 12 countries where the IPTp-SP studies had been conducted. We then developed four matching rules shown in Table 1 to identify point estimates from the cross-sectional data that were most likely to reflect the malaria transmission intensity to which pregnant women were exposed. Before applying these matching rules, we extracted geospatial coordinates for each IPTp-SP study and cross-sectional survey using the GEOnet Names Server 8 and then used ArcGIS 10 software (Environmental Systems Research Institute) to calculate straight-line distances between the locations of IPTp-SP studies and cross-sectional surveys. This allowed us to restrict matching of IPTp-SP studies to survey data that had been collected within <100 miles of each other as described in rule 1, a distance used in previous malaria modelling of pregnancy and paediatric data 9. Similarly, we obtained elevation estimates from the Consortium for Spatial Information 10 for locations of the IPTp-SP studies and survey data. We used these estimates as part of an elevation criterion in rule 3 that took into account the fact that malaria infection declines sharply at altitudes ≥1200 m compared to lower elevations 11. We also included a temporal criterion in the matching rules, stipulating that survey data needed to have been collected within ±2 years of the IPTp-SP studies to be paired. All four matching rules required that cross-sectional surveys and pregnancy studies had to have been conducted in areas from the same malaria transmission category as designated by MAP: high (>40% P. falciparum prevalence among 2–10 year olds), intermediate (5–40%) and low (<5%). This accounted for the possibility that IPTp-SP studies and cross-sectional surveys may have been conducted in proximate locations that had very different intensities of malaria transmission. To reflect the gravidae-specific nature of parasitaemia among pregnant women in endemic areas when pairing prevalence estimates of malaria in children, we made some assumptions based on reports from Sierra Leone 12 and Kenya 13 that suggest the prevalence of parasitaemia among children is comparable to maternal parasitaemia as presented in Table 2. We then applied our matching rules sequentially. If survey data could not be matched to an IPTp-SP study using rule 1, then rule 2 was applied, and so on until we identified all point prevalence estimates from survey data that could be considered the best possible matches for each IPTp-SP study as illustrated in Figure 2. Using random-effects models, we pooled survey data that were paired with IPTp-SP studies under rules 1, 2 or 3. If survey data could not be matched under these rules, we imposed the 2007 PfPR2–10 estimate for the same location where the IPTp-SP study had been conducted. With data from IPTp-SP studies paired to malaria prevalence estimates, whether using 2007 PfPR2–10 or our pooled estimates, we applied standard meta-regression models 14, 15 to LBW outcomes reported in the IPTp-SP studies. This allowed us to correct for the variances of treatment effect within pregnancy studies, and the residual heterogeneity across pregnancy studies, and to estimate the effect of malaria transmission intensity on the protection conferred by IPTp-SP against LBW. Because the Pfdhps 581G mutation may have acted as an important effect modifier, we used the geographical database of molecular biomarkers as described elsewhere 16 to obtain point prevalence estimates of the 581G mutation associated with ‘super resistance’ to SP among parasites from the same locations where IPTp-SP studies had been conducted. We included mutation prevalence estimates if they had been collected from <100 miles of the IPTp-SP studies and within ±2 years of when the IPTp-SP studies had been conducted. This radius was expanded to 100–250 miles if no data were available from <100 miles. If multiple point estimates were found, we pooled them using standard meta-analysis. We then conducted a sensitivity analysis of the 581G mutation on our results. Studies of IPTp-SP stratified by gravidae that met inclusion criteria are summarised in Table 3 17-25. Nine studies involving 10 279 pregnant women were included in our analysis. Seven studies reported LBW outcomes from 12 unique sites for primi- and secundigravidae who were exposed to ≥2 doses of IPTp-SP (N = 2314) vs. placebo or no doses (N = 1954). In addition, seven studies from 10 unique sites reported LBW outcomes among multigravidae who received ≥2 doses of IPTp-SP (N = 2941) compared to placebo or no doses (N = 3070). Funnel-plot analysis in Figure S1 suggests that relatively small IPTp-SP studies failing to protect against LBW may have been under-represented in our sample. Our appraisal of evidence using GRADE methods is summarised in Table S2. Figure S2 illustrates the risk of bias within individual IPTp-SP studies, and Figure S3 shows the combined risk of bias across IPTp-SP studies. Five of the nine studies were randomised clinical trials, whereas four were observational studies. There is an unclear risk of selection bias and detection bias in one-half of the studies. Random-effects models produced statistically strong evidence among pregnancy studies; among primi- and secundigravidae, ≥2 doses of IPTp-SP vs. placebo or no IPTp-SP reduced the odds of delivering a LBW newborn by one-half [odds ratio (OR) = 0.54; 95% CI: 0.35, 0.84; I2 = 69.0%; P < 0.00]. The reduction was 30% among multigravidae (OR = 0.70; 95% CI: 0.51, 0.95; I2 = 48.9%; P = 0.04). To explore whether heterogeneity could be reduced, we stratified LBW outcomes as reported in observational studies vs. RCTs. We found less heterogeneity among the observational studies (I2 = 34.7%; P = 0.190) than among RCTs (I2 = 76.5%; P < 0.000) for primi- and secundigravidae. In contrast, there was less heterogeneity in RCTs among studies in multigravidae (I2 = 38.8%; P = 0.133) compared to observational studies (I2 = 63.7%; P = 0.064). We used 12 national cross-sectional data sets from MAP containing 11 548 surveys to estimate the malaria transmission intensity at each IPTp-SP study site. Table 4 shows the matching rules that we used and our pooled prevalence estimates of malaria parasitaemia. Among primi- and secundigravidae, the pooled prevalence ranged between 25.1% and 59.1%, whereas MAP estimates were between 20.5% and 66.4%. Among multigravidae, pooled prevalence estimates ranged from 6.7% to 39.3%, in contrast to MAP estimates which were between 20.5% and 66.4%. To explore the potential effect of malaria transmission intensity on the association between IPTp-SP and LBW, we produced four separate meta-regression models. In Model 1, we used our pooled prevalence estimates among primi- and secundigravidae for the measure of malaria transmission intensity. In our second model, also for primi- and secundigravidae, we applied MAP estimates for malaria transmission intensity. In Models 3 and 4 for multigravidae, we used our pooled prevalence estimates and MAP estimates, respectively. None of the models suggested that variation in the ORs of LBW could be explained by malaria transmission intensity: Model 1 (P = 0.83), Model 2 (P = 0.78), Model 3 (P = 0.30) and Model 4 (P = 0.93). Sensitivity testing among matching rules did not produce any statistically significant difference. Using a geographical database of molecular biomarkers as described elsewhere 16, we obtained prevalence estimates of Pfdhps 581G from 44 locations that had been measured within ±2 years of the IPTp-SP studies. There were 20 locations within <100 miles of the pregnancy study sites and 24 locations within 100–250 miles as shown in Table 5 26-40. The highest prevalence estimates of 581G were calculated using data from four biomarker studies – Karema 32, Alker 30, Lynch 31 and Taylor 29 – that could be paired with two pregnancy studies – Likwela et al. 17 and Ndyomugyenyi 18. Specifically, these four biomarker studies had 581G prevalence data from six locations that were related to the Likwela 17 pregnancy study (Rutshuru). We combined these point estimates using random-effects models to produce a pooled estimate of 52.4% [95% confidence intervals (CI): 47.5–57.4%). We were able to relate five biomarker studies that reported measurements of the 581G mutation to the Ndyomugyenyi 18 pregnancy study. We pooled these using random-effects models to generate an estimate of 52.6% (95% CI: 47.6–57.5%). The biomarker study by Karema 32 that reported the population prevalence of 581G to be 61.1% also observed dhfr-164L at a frequency of 11.4%. Similarly, population prevalence estimates of 581G detected by Lynch 31 were 45.8% (Rukungiri) and 45.0% (Kabale), whereas lower frequencies, 4.2% and 13.7%, were identified for 164L in the same locations, respectively. The dhfr-164L mutation is also associated with the failure of SP to clear malaria parasites and is more commonly found in South American and South-East Asia. Twelve biomarker studies reported the 581G mutation that could be related spatially and temporally to the remaining pregnancy studies. These prevalence estimates ranged between 0.0% and 10.1% (95% CI: 3.5, 16.8). Overall, 581G prevalence points presented a binomial structure – frequencies of 581G ≤10.1% and those >10.1% – which we used to stratify IPTp-SP studies. Random-effects models shown in Figure 3 indicate that ≥2 doses of IPTp-SP reduced the odds of LBW among primi- and secundigravidae (OR = 0.49; 95% CI: 0.29, 0.81; I2 = 67.7%; P < 0.00) and multigravidae (OR = 0.56; 95% CI: 0.37, 0.86; I2 = 48.7%; P < 0.03) in areas where the prevalence of 581G was ≤10.1%. Where the prevalence of 581G was >10.1%, the protective effect of IPTp-SP persisted among primi- and secundigravidae, although at lower levels, as illustrated in Figure 4. Among multigravidae, random-effects models showed that IPTp-SP confers protection against LBW in areas where the prevalence of 581G was ≤10.1% (OR = 0.56; 95% CI: 0.37, 0.86; P = 0.07), a finding of borderline statistical significance. In contrast, there was no evidence from fixed-effects or random-effects models that multigravidae were protected against LBW at sites where the prevalence of 581G was >10.1% (OR = 0.96; 95% CI: 0.70, 1.34; I2 = 72.0%; P < 0.47). The interaction between malaria transmission intensity and the prevalence of 581G was borderline significant: P = 0.06 among primi- and secundigravidae, and P = 0.04 among multigravidae. Thus, meta-regression of malaria transmission intensity, stratified by the prevalence of 581G, was only able to explain some of the variation in protective effect of IPTp-SP against LBW. To our knowledge, this is the first use of age-stratified rates of paediatric parasitaemia to model the gravidity-specific relationship of malaria in pregnancy in endemic settings, and our results conform to established epidemiological patterns among pregnant women. In addition, IPTp-SP studies identified through our systematic review were protective against LBW to levels that are comparable to other studies. We do not consider the age of the data to be a limitation because we paired LBW outcomes to parasite prevalence estimates from the same time periods. Lacking prevalence estimates for the 581G mutation between 10.1% and 52.4%, we can only conclude that the prevalence threshold of this mutation is >10.1% above which IPTp-SP no longer protects against the incidence of LBW. It is tempting to state the cut-off should be >52.4%, but the threshold may be much lower, especially considering the alarming results from Tanzania where placental infection was significantly higher in 84% of women (n = 104) given any dose of IPTp-SP compared to 16% of women (n = 104) who received none (P = 0.03) 41, 42. The prevalence of the 581G mutation in this study area was 55% (95% CI: 44.7, 65.2; N = 87) 43. Our results should be interpreted with caution. We were limited by the relative paucity of data that relate the efficacy of IPTp-SP to the intensity of malaria exposure during pregnancy that has been stratified by gravidae. Moreover, there may have been selection bias in six of the nine studies we identified because of the absence of random sequence generation or allocation concealment. In addition, there was considerable heterogeneity among pregnancy studies. We are, however, hesitant to draw any conclusions from stratifying studies by design, and doing so did not consistently reduce heterogeneity. We were unable to detect a malaria transmission threshold below which IPTp-SP is no longer protective against LBW, a possible consequence of there being too few data points. However, an unpublished analysis of Multiple Indicator Cluster Surveys also found that IPTp-SP continued to protect against LBW until very low levels of transmission and, similar to our analysis, could not define a cut-off point of transmission below which IPTp-SP is no longer protective against LBW (Eisele TP, personal communication). Our inability to detect a transmission threshold may be due to other factors. We do not know the prevalence of placental infection in very low-transmission settings and it is entirely possible that declines in peripheral parasitaemia are not reflected in equivalent reductions of placental infection. If that is the case, then IPTp-SP may provide important and continued protection against placental carriage and the incidence of LBW in areas of very low endemicity. Another possible explanation is that the causal pathway to LBW is multifactorial and that IPTp-SP offers some protection against other causes of LBW. SP has been used as chemoprophylaxis against Toxoplasma gondii infection and Pneumocystis carinii pneumonia 44. Sulphadoxine is related to sulphamethoxazole, the partner compound used with trimethoprim to form co-trimoxazole which is commonly prescribed for urinary tract infections 45. Sulphonamide has also been used to treat Gardnerella vaginalis 46, a bacterium found in women with bacterial vaginosis which can double the odds of having a LBW baby (OR = 2.0; 95% CI: 1.3, 2.9) compared to pregnant women without bacterial vaginosis 47. A meta-analysis reported the prevalence of bacterial vaginosis to be 50.8% (95% CI: 43.3, 58.4) among pregnant women attending antenatal care in East and Southern Africa and 37.6% (95% CI: 18.0, 57.2) in West and Central Africa 48. Additional insight could be gained from prospective case–control studies that measure the incidence of LBW among women who had received ≥2 doses of IPTp-SP vs. women who had not to have received IPTp-SP during their pregnancies. Such studies, however, can readily be confounded. Although the 581G mutation is not widely found throughout sub-Saharan Africa, the codon has been detected in 10 countries 49 and selection can be alarmingly rapid. A study in Kenya reported the prevalence of 581G to be 85.1% (95% CI: 80.0%, 89.4%) where no parasites had expressed the mutation 3 years prior 50. Before declaring a specific level of malaria transmission or 581G prevalence at which IPTp-SP no longer provides a cost-effective benefit, placebo-control trials may be needed in a range of low-transmission settings that have sufficient power for subanalysis by gravidae and include robust micro-biological testing that would enable exploration of potential protection conferred by IPTp-SP against infections apart from malaria. To our knowledge, there are no such studies underway. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article." @default.
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• W1947887788 date "2015-09-30" @default.
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• W1947887788 title "Influence of malaria transmission intensity and the 581G mutation on the efficacy of intermittent preventive treatment in pregnancy: systematic review and meta‐analysis" @default.
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• W1947887788 doi "https://doi.org/10.1111/tmi.12595" @default.
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