A symptom-based algorithm for calcium management after thyroid surgery: a prospective multicenter study

Objective: Evidence-based treatment guidelines for the management of postthyroidectomy hypocalcemia are absent. The aim of this study was to evaluate a newly developed symptom-based treatment algorithm including a protocolized attempt to phase out supplementation. Methods: In a prospective multicenter study, patients were treated according to the new algorithm and compared to a historical cohort of patients treated with a biochemically based approach. The primary outcome was the proportion of patients receiving calcium and/or alfacalcidol supplementation. Secondary outcomes were calcium-related complications and predictors for supplementation. Results: One hundred thirty-four patients were included prospectively, and compared to 392 historical patients. The new algorithm significantly reduced the proportion of patients treated with calcium and/or alfacalcidol during the first postoperative year (odds ratio (OR): 0.36 (95% CI: 0.23–0.54), P < 0.001), and persistently at 12 months follow-up (OR: 0.51 (95% CI: 0.28–0.90), P < 0.05). No severe calcium-related complications occurred, even though calcium-related visits to the emergency department and readmissions increased (OR: 11.5 (95% CI: 4.51–29.3), P <0.001) and (OR: 3.46 (95% CI: 1.58–7.57), P < 0.05), respectively. The proportional change in pre- to post operative parathyroid hormone (PTH) was an independent predictor for supplementation (OR: 1.04 (95% CI: 1.02–1.07), P < 0.05). Conclusions: Symptom-based management of postthyroidectomy hypocalcemia and a protocolized attempt to phase out supplementation safely reduce d the proportion of patients receiving supplementation, although the number of calcium-related hospital visits increased. For the future, we envision a more individualized treatment approach for patients at risk for delayed symptomatic hypocalcemia, including the proportional change in pre- to post- operative PTH

Gestational weight gain charts for different body mass index groups for women in Europe, North America, and Oceania

BackgroundGestational weight gain differs according to pre-pregnancy body mass index and is related to the risks of adverse maternal and child health outcomes. Gestational weight gain charts for women in different pre-pregnancy body mass index groups enable identification of women and offspring at risk for adverse health outcomes. We aimed to construct gestational weight gain reference charts for underweight, normal weight, overweight, and grades 1, 2 and 3 obese women and to compare these charts with those obtained in women with uncomplicated term pregnancies.MethodsWe used individual participant data from 218,216 pregnant women participating in 33 cohorts from Europe, North America, and Oceania. Of these women, 9065 (4.2%), 148,697 (68.1%), 42,678 (19.6%), 13,084 (6.0%), 3597 (1.6%), and 1095 (0.5%) were underweight, normal weight, overweight, and grades 1, 2, and 3 obese women, respectively. A total of 138, 517 women from 26 cohorts had pregnancies with no hypertensive or diabetic disorders and with term deliveries of appropriate for gestational age at birth infants. Gestational weight gain charts for underweight, normal weight, overweight, and grade 1, 2, and 3 obese women were derived by the Box-Cox t method using the generalized additive model for location, scale, and shape.ResultsWe observed that gestational weight gain strongly differed per maternal pre-pregnancy body mass index group. The median (interquartile range) gestational weight gain at 40weeks was 14.2kg (11.4-17.4) for underweight women, 14.5kg (11.5-17.7) for normal weight women, 13.9kg (10.1-17.9) for overweight women, and 11.2kg (7.0-15.7), 8.7kg (4.3-13.4) and 6.3kg (1.9-11.1) for grades 1, 2, and 3 obese women, respectively. The rate of weight gain was lower in the first half than in the second half of pregnancy. No differences in the patterns of weight gain were observed between cohorts or countries. Similar weight gain patterns were observed in mothers without pregnancy complications.ConclusionsGestational weight gain patterns are strongly related to pre-pregnancy body mass index. The derived charts can be used to assess gestational weight gain in etiological research and as a monitoring tool for weight gain during pregnancy in clinical practice.Peer reviewe

Maternal body mass index, gestational weight gain, and the risk of overweight and obesity across childhood : An individual participant data meta-analysis

Background Maternal obesity and excessive gestational weight gain may have persistent effects on offspring fat development. However, it remains unclear whether these effects differ by severity of obesity, and whether these effects are restricted to the extremes of maternal body mass index (BMI) and gestational weight gain. We aimed to assess the separate and combined associations of maternal BMI and gestational weight gain with the risk of overweight/obesity throughout childhood, and their population impact. Methods and findings We conducted an individual participant data meta-analysis of data from 162,129 mothers and their children from 37 pregnancy and birth cohort studies from Europe, North America, and Australia. We assessed the individual and combined associations of maternal pre-pregnancy BMI and gestational weight gain, both in clinical categories and across their full ranges, with the risks of overweight/obesity in early (2.0-5.0 years), mid (5.0-10.0 years) and late childhood (10.0-18.0 years), using multilevel binary logistic regression models with a random intercept at cohort level adjusted for maternal sociodemographic and lifestylerelated characteristics. We observed that higher maternal pre-pregnancy BMI and gestational weight gain both in clinical categories and across their full ranges were associated with higher risks of childhood overweight/obesity, with the strongest effects in late childhood (odds ratios [ORs] for overweight/obesity in early, mid, and late childhood, respectively: OR 1.66 [95% CI: 1.56, 1.78], OR 1.91 [95% CI: 1.85, 1.98], and OR 2.28 [95% CI: 2.08, 2.50] for maternal overweight; OR 2.43 [95% CI: 2.24, 2.64], OR 3.12 [95% CI: 2.98, 3.27], and OR 4.47 [95% CI: 3.99, 5.23] for maternal obesity; and OR 1.39 [95% CI: 1.30, 1.49], OR 1.55 [95% CI: 1.49, 1.60], and OR 1.72 [95% CI: 1.56, 1.91] for excessive gestational weight gain). The proportions of childhood overweight/obesity prevalence attributable to maternal overweight, maternal obesity, and excessive gestational weight gain ranged from 10.2% to 21.6%. Relative to the effect of maternal BMI, excessive gestational weight gain only slightly increased the risk of childhood overweight/obesity within each clinical BMI category (p-values for interactions of maternal BMI with gestational weight gain: p = 0.038, p <0.001, and p = 0.637 in early, mid, and late childhood, respectively). Limitations of this study include the self-report of maternal BMI and gestational weight gain for some of the cohorts, and the potential of residual confounding. Also, as this study only included participants from Europe, North America, and Australia, results need to be interpreted with caution with respect to other populations. Conclusions In this study, higher maternal pre-pregnancy BMI and gestational weight gain were associated with an increased risk of childhood overweight/obesity, with the strongest effects at later ages. The additional effect of gestational weight gain in women who are overweight or obese before pregnancy is small. Given the large population impact, future intervention trials aiming to reduce the prevalence of childhood overweight and obesity should focus on maternal weight status before pregnancy, in addition to weight gain during pregnancy.Peer reviewe

Group B Streptococcus Early-Onset Disease: New Preventive and Diagnostic Tools to Decrease the Burden of Antibiotic Use

The difficulty in recognizing early-onset neonatal sepsis (EONS) in a timely manner due to non-specific symptoms and the limitations of diagnostic tests, combined with the risk of serious consequences if EONS is not treated in a timely manner, has resulted in a low threshold for starting empirical antibiotic treatment. New guideline strategies, such as the neonatal sepsis calculator, have been proven to reduce the antibiotic burden related to EONS, but lack sensitivity for detecting EONS. In this review, the potential of novel, targeted preventive and diagnostic methods for EONS is discussed from three different perspectives: maternal, umbilical cord and newborn perspectives. Promising strategies from the maternal perspective include Group B Streptococcus (GBS) prevention, exploring the virulence factors of GBS, maternal immunization and antepartum biomarkers. The diagnostic methods obtained from the umbilical cord are preliminary but promising. Finally, promising fields from the newborn perspective include biomarkers, new microbiological techniques and clinical prediction and monitoring strategies. Consensus on the definition of EONS and the standardization of research on novel diagnostic biomarkers are crucial for future implementation and to reduce current antibiotic overexposure in newborns

Exonic deletions in AUTS2 cause a syndromic form of intellectual disability and suggest a critical role for the C terminus.

Genomic rearrangements involving AUTS2 (7q11.22) are associated with autism and intellectual disability (ID), although evidence for causality is limited. By combining the results of diagnostic testing of 49,684 individuals, we identified 24 microdeletions that affect at least one exon of AUTS2, as well as one translocation and one inversion each with a breakpoint within the AUTS2 locus. Comparison of 17 well-characterized individuals enabled identification of a variable syndromic phenotype including ID, autism, short stature, microcephaly, cerebral palsy, and facial dysmorphisms. The dysmorphic features were more pronounced in persons with 3'AUTS2 deletions. This part of the gene is shown to encode a C-terminal isoform (with an alternative transcription start site) expressed in the human brain. Consistent with our genetic data, suppression of auts2 in zebrafish embryos caused microcephaly that could be rescued by either the full-length or the C-terminal isoform of AUTS2. Our observations demonstrate a causal role of AUTS2 in neurocognitive disorders, establish a hitherto unappreciated syndromic phenotype at this locus, and show how transcriptional complexity can underpin human pathology. The zebrafish model provides a valuable tool for investigating the etiology of AUTS2 syndrome and facilitating gene-function analysis in the future

Association of gestational weight gain with adverse maternal and infant outcomes

Importance: Both low and high gestational weight gain have been associated with adverse maternal and infant outcomes, but optimal gestational weight gain remains uncertain and not well defined for all prepregnancy weight ranges. Objectives: To examine the association of ranges of gestational weight gain with risk of adverse maternal and infant outcomes and estimate optimal gestational weight gain ranges across prepregnancy body mass index categories. Design, setting, and participants: Individual participant-level meta-analysis using data from 196 670 participants within 25 cohort studies from Europe and North America (main study sample). Optimal gestational weight gain ranges were estimated for each prepregnancy body mass index (BMI) category by selecting the range of gestational weight gain that was associated with lower risk for any adverse outcome. Individual participant-level data from 3505 participants within 4 separate hospital-based cohorts were used as a validation sample. Data were collected between 1989 and 2015. The final date of follow-up was December 2015. Exposures: Gestational weight gain. Main outcomes and measures: The main outcome termed any adverse outcome was defined as the presence of 1 or more of the following outcomes: preeclampsia, gestational hypertension, gestational diabetes, cesarean delivery, preterm birth, and small or large size for gestational age at birth. Results: Of the 196 670 women (median age, 30.0 years [quartile 1 and 3, 27.0 and 33.0 years] and 40 937 were white) included in the main sample, 7809 (4.0%) were categorized at baseline as underweight (BMI <18.5); 133 788 (68.0%), normal weight (BMI, 18.5-24.9); 38 828 (19.7%), overweight (BMI, 25.0-29.9); 11 992 (6.1%), obesity grade 1 (BMI, 30.0-34.9); 3284 (1.7%), obesity grade 2 (BMI, 35.0-39.9); and 969 (0.5%), obesity grade 3 (BMI, ≥40.0). Overall, any adverse outcome occurred in 37.2% (n = 73 161) of women, ranging from 34.7% (2706 of 7809) among women categorized as underweight to 61.1% (592 of 969) among women categorized as obesity grade 3. Optimal gestational weight gain ranges were 14.0 kg to less than 16.0 kg for women categorized as underweight; 10.0 kg to less than 18.0 kg for normal weight; 2.0 kg to less than 16.0 kg for overweight; 2.0 kg to less than 6.0 kg for obesity grade 1; weight loss or gain of 0 kg to less than 4.0 kg for obesity grade 2; and weight gain of 0 kg to less than 6.0 kg for obesity grade 3. These gestational weight gain ranges were associated with low to moderate discrimination between those with and those without adverse outcomes (range for area under the receiver operating characteristic curve, 0.55-0.76). Results for discriminative performance in the validation sample were similar to the corresponding results in the main study sample (range for area under the receiver operating characteristic curve, 0.51-0.79). Conclusions and relevance: In this meta-analysis of pooled individual participant data from 25 cohort studies, the risk for adverse maternal and infant outcomes varied by gestational weight gain and across the range of prepregnancy weights. The estimates of optimal gestational weight gain may inform prenatal counseling; however, the optimal gestational weight gain ranges had limited predictive value for the outcomes assessed.Avon Longitudinal Study of Parents and Children (ALSPAC): Funded by grant 102215/2/13/2 from the UK Medical Research Council and Wellcome, core support from the University of Bristol, grant R01 DK10324 from the US National Institutes of Health, grant agreement 669545 from the European Research Council under the European Union’s Seventh Framework Programme (FP7/2007-2013), award MC_UU_12013/5 from the UK Medical Research Council, and Dr Lawlor is a National Institute for Health Research senior investigator (NF-SI-0611-10196). Cohort of Newborns in Emilia Romagna (CoNER): No funding reported. Danish National Birth Cohort (DNBC): The Danish Epidemiology Science Centre initiated and created the DNBC and this center was established by the Danish National Research Foundation via a major grant. Additional support was obtained from the Pharmacy Foundation, the Egmont Foundation, the March of Dimes Birth Defects Foundation, the Augustinus Foundation, and the Health Foundation. The 7-year follow-up study was supported by award 195/04 from the Lundbeck Foundation and award SSVF 0646 from the Danish Medical Research Council. Étude des Déterminants pré et postnatals du développement et de la santé de l’ENfant (EDEN): Supported by the French foundation for medical research, the French national agency for research, the French national institute for research in public health (IRESP: TGIR cohorte santé 2008 program), the French ministry of health, the French ministry of research, the INSERM bone and joint diseases national research and human nutrition national research programs, Paris-Sud University, Nestlé, the French national institute for population health surveillance, the French national institute for health education, the European Union FP7 programs (2007-2013; HELIX, ESCAPE, ENRIECO, and Medall projects), the French diabetes national research program through a collaboration with the French association of diabetic patients, the French agency for environmental health safety (now ANSES), the Mutuelle Générale de l’Education Nationale (a complementary health insurance), the French national agency for food security, and the French-speaking association for the study of diabetes and metabolism. Family and Children of Ukraine (FCOU): Supported by the Fogarty International Center at the US National Institutes of Health, the US National Institute of Environmental Health Sciences, the US Centers for Disease Control and Prevention, the US Environmental Protection Agency, and the National Academy of Medical Sciences of Ukraine. Genetica e Ambiente: Studio Prospettico dell’Infanzia in Italia (GASPII): Supported by the Italian ministry of health. Groningen Expert Center for Kids with Obesity (GECKO Drenthe): Supported by an unrestricted grant from Hutchison Whampoa Ltd and funding from the University of Groningen, Well Baby Clinic Foundation Icare, Noordlease, the Paediatric Association of the Netherlands, and Youth Health Care Drenthe. Genetics of Glucose regulation in Gestation and Growth (Gen3G): Supported by operating grant 20697 from the Fonds de recherche du Québec en santé, operating grant MOP 115071 from the Canadian Institute of Health Reseach, a grant from Diabète Québec, and operating grant OG-3-08-2622-JA from the Canadian Diabetes Association. Generation R: The general design of the study received financial support from Erasmus MC, University Medical Center Rotterdam, Erasmus University Rotterdam, the Netherlands Organization for Health Research and Development, the Netherlands Organisation for Scientific Research and the Ministry of Health, Welfare, and Sport, and the Ministry of Youth and Families. The research leading to these results received funding from the European Union Horizon 2020 Research and Innovation Programme under grant 733206 (LifeCycle Project). Dr Jaddoe received grant ERC-2014-CoG-648916 from the European Research Council. Dr Gaillard received grant 2017T013 from the Dutch Heart Foundation, grant 2017.81.002 from the Dutch Diabetes Foundation, and grant 543003109 from the Netherlands Organisation for Health Research and Development. Generation XXI: Funded by Programa Operacional de Saúde–Saúde XXI, Quadro Comunitário de Apoio III and Administração Regional de Saúde Norte (Regional Department of Ministry of Health), by POCI-01-0145-FEDER-016837 through the Operational Programme Competitiveness and Internationalization and national funding from the Foundation for Science and Technology (Portuguese Ministry of Science, Technology, and Higher Education) under the project PathMOB, by FCT PTDC/DTP-EPI/3306/2014 (Risco cardiometabólico na infância: desde o início da vida ao fim da infância), by POCI-01-0145-FEDER-006862 and UID/DTP/04750/2013 (Unidade de Investigação em Epidemiologia-Instituto de Saúde Pública da Universidade do Porto), and FCT investigator contract IF/01060/2015 awarded to Dr A. C. Santos. Growth, Exercise and Nutrition Epidemiological Study In preSchoolers (GENESIS): Supported by a research grant from Friesland Hellas. German Infant Nutritional Intervention plus environmental and genetic influences (GINIplus): Supported for the first 3 years by the Federal Ministry for Education, Science, Research, and Technology (intervention group) and Helmholtz Zentrum Munich (observation group). The 4-, 6-, 10-, and 15-year follow-up examinations were covered from the respective budgets of the 5 study centers (Helmholtz Zentrum Munich, Research Institute at Marien-Hospital Wesel, LMU Munich, TU Munich, IUF-Leibniz Research-Institute for Environmental Medicine at the University of Düsseldorf) and by funding from the European Commission 7th Framework Programme (MeDALL project), Mead Johnson, and Nestlé and grant FKZ 20462296 from the Federal Ministry for Environment (awarded to IUF Düsseldorf). Norwegian Human Milk Study (HUMIS): Funded by award FP7/2007-2013 from the European Commission 7th Framework Programme, grant 289346 from European Union EarlyNutrition project, and by funds for project 213148 from the Norwegian Research Council’s MILPAAHEL programme. INfancia y Medio Ambiente (INMA)-Sabadell: Funded by grant Red INMA G03/176 from the Instituto de Salud Carlos III in Spain and grant 1999SGR 00241 from the Generalitat de Catalunya-CIRIT. INMA-Valencia: Funded by grants FP7-ENV-2011 cod 282957 and HEALTH.2010.2.4.5-1 from the European Commission, grants G03/176, FIS-FEDER PI09/02647, PI11/01007, PI11/02591, PI11/02038, PI13/1944, PI13/2032, PI14/00891, PI14/01687, PI16/1288, Miguel Servet FEDER CP11/00178, CP15/00025, and CPII16/00051 from the Instituto de Salud Carlos III in Spain, and grants UGP 15-230, UGP-15-244, and UGP-15-249 from the Generalitat Valenciana, Foundation for the Promotion of Health and Biomedical Research of Valencia Region. INMA-Gipuzkoa: Funded by grants FISFIS PI06/0867, FIS-PS09/0009 0867, and Red INMA G03/176 from the Instituto de Salud Carlos III in Spain, grants 2005111093 and 2009111069 from the Departamento de Salud del Gobierno Vasco, and grants DFG06/004 and FG08/001 from the Provincial Government of Guipúzcoa. INMA-Menorca: This study was funded by grant Red INMA G03/176 from the Instituto de Salud Carlos III in Spain. Child, parents and health: lifestyle and genetic constitution (KOALA): Data collection from pregnancy up to the age of 1 year was supported by grants from Royal Friesland Foods, the Triodos Foundation, the Phoenix Foundation, the Raphaël Foundation, the Iona Foundation, the Foundation for the Advancement of Heilpedagogie, the Netherlands Organisation for Health Research and Development (2100.0090), the Netherlands Asthma Foundation (3.2.03.48 and 3.2.07.022), and the Netherlands Heart Foundation (2008B112). Krakow Cohort: Funded by grants R01ES010165 and R01ES015282 from the US National Institute of Environmental Health Sciences and by funding from the Lundin Foundation, the John and Wendy Neu Family Foundation, the Gladys and Roland Harriman Foundation, and the Anonymous Foundation. Influences of Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood plus the influence of traffic emissions and genetics (LISAplus): Mainly supported by grants for the first 2 years from the Federal Ministry for Education, Science, Research, and Technology, the Helmholtz Zentrum Munich, the Helmholtz Centre for Environmental Research-UFZ, the Research Institute at Marien-Hospital Wesel, and a pediatric practice in Bad Honnef. The 4-, 6-, 10-, and 15-year follow-up examinations were funded by the respective budgets of the involved partners (the Helmholtz Zentrum Munich, the Helmholtz Centre for Environmental Research-UFZ, the Research Institute at Marien-Hospital Wesel, a pediatric practice in Bad Honnef, and the IUF–Leibniz-Research Institute for Environmental Medicine at the University of Düsseldorf), by grant FKZ 20462296 from the Federal Ministry for Environment (awarded to IUF Düsseldorf), and by support from the European Commission 7th Framework Programme (MeDALL project). LUKAS Cohort: Funded by EVO/VTR grants, grants 139021 and 287675 from the Academy of Finland, grant QLK4-CT-2001-00250 from the European Union, and funding from the Juho Vainio Foundation, the Foundation for Pediatric Research, the Päivikki and Sakari Sohlberg Foundation, the Finnish Cultural Foundation, and the National Institute for Health and Welfare in Finland. Norwegian Mother and Child Cohort Study (MoBa): Supported by the Norwegian Ministry of Health and Care Services and the Ministry of Education and Research, contract N01-ES-75558 with the US National Institute of Environmental Health Sciences, and grants UO1 NS 047537-01 and UO1 NS 047537-06A1 from the US National Institute of Neurological Disorders and Stroke. Nascita e INFanzia: gli Effetti dell’Ambiente (NINFEA): Partially funded by the Compagnia San Paolo Foundation and by the Piedmont Region. Prevention and Incidence of Asthma and Mite Allergy (PIAMA): Supported by the Organization for Health Research and Development, the Organization for Scientific Research, the Asthma Fund, the Ministry of Spatial Planning, Housing, and the Environment, and the Ministry of Health, Welfare, and Sport (all organizations in the Netherlands). Piccolipiù Project: Financially supported by CCM grants during 2010 and 2014 from the Italian National Center for Disease Prevention and Control and funding (art 12 and 12 bis D.lgs 502/92) from the Italian Ministry of Health. PRegnancy and Infant DEvelopment (PRIDE Study): Supported by grants from the Netherlands Organization for Health Research and Development, the Radboud Institute for Health Sciences, and the Lung Foundation Netherlands. Project Viva: Funded by grants R01 HD034568 and UG3OD023286 from the US National Institutes of Health. Polish Mother and Child Cohort Study (REPRO_PL): Funded by grants DEC-2014/15/B/NZ7/00998 and FP7 HEALS 603946 from the National Science Centre in Poland and grant 3068/7.PR/2014/2 from the Polish Ministry of Science and Higher Education. Exposure of Preschool-Age Greek Children (RHEA): Financially supported by European Commission projects FP6-2003-Food-3-NewGeneris, FP6-STREP Hiwate, FP7-ENV.2007.1.2.2.2, FP7-2008-ENV-1.2.1.4 Envirogenomarkers, FP7-HEALTH-2009-single stage CHICOS, FP7-ENV.2008.1.2.1.6, FP7-HEALTH-2012, and 211250-Escape and proposals 226285 ENRIECO and 308333 HELIX and by the Greek Ministry of Health. Slovak PCB Study: Support was provided by grants R01 CA096525, R03 TW007152, P30 ES001247, P30 ES023513, and K12 ES019852 from the US National Institutes of Health. STEPS: This study was supported by the University of Turku, Abo Akademi University, the Turku University Hospital, the City of Turku, the Juho Vainio Foundation, and the Yrjö Jahnsson Foundation and by grants 121569 and 123571 from the Academy of Finland. Southampton Women’s Survey (SWS): Supported by funding from the Medical Research Council, the National Institute for Health Research Southampton Biomedical Research Centre, the University of Southampton, Dunhill Medical Trust, and the University Hospital Southampton National Health Service Foundation Trust, FP7/2007-2013 from the European Commission 7th Framework Programme, and grant 289346 from the European Union EarlyNutrition project

Impact of maternal body mass index and gestational weight gain on pregnancy complications: An individual participant data meta-analysis of European, North American and Australian cohorts.

OBJECTIVE To assess the separate and combined associations of maternal pre-pregnancy BMI and gestational weight gain with the risks of pregnancy complications and their population impact. DESIGN Individual participant data meta-analysis of 39 cohorts. SETTING Europe, North America and Oceania. POPULATION 265,270 births. METHODS Information on maternal pre-pregnancy BMI, gestational weight gain, and pregnancy complications was obtained. Multilevel binary logistic regression models were used. MAIN OUTCOME MEASURES Gestational hypertension, pre-eclampsia, gestational diabetes, preterm birth, small and large size for gestational age at birth. RESULTS Higher maternal pre-pregnancy BMI and gestational weight gain were, across their full ranges, associated with higher risks of gestational hypertensive disorders, gestational diabetes and large size for gestational age at birth. Preterm birth risk was higher at lower and higher BMI and weight gain. Compared to normal weight mothers with medium gestational weight gain, obese mothers with high gestational weight gain had the highest risk of any pregnancy complication (Odds Ratio 2.51 (95% Confidence Interval 2.31, 2.74)). We estimated that 23.9% of any pregnancy complication was attributable to maternal overweight/obesity and 31.6% of large size for gestational age infants was attributable to excessive gestational weight gain. CONCLUSIONS Maternal pre-pregnancy BMI and gestational weight gain are, across their full ranges, associated with the risks of pregnancy complications. Obese mothers with high gestational weight gain are at the highest risk of pregnancy complications. Promoting a healthy pre-pregnancy BMI and gestational weight gain may reduce the burden of pregnancy complications and ultimately the risk of maternal and neonatal morbidity. This article is protected by copyright. All rights reserved