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Objective: To determine the association between adolescent hospitalization for suicide attempts and the subsequent risk of eating disorder hospitalization. Method: This was a cohort study of 162,398 adolescent girls in Quebec, Canada, including 7741 with suicide attempts before 20 years of age, matched to 154,657 adolescents with no attempt between 1989 and 2019. The main exposure measure was suicide attempt hospitalization. The main outcome measure was hospitalization for an eating disorder up to 31 years later, including anorexia nervosa, bulimia nervosa, and other eating disorders. We used adjusted Cox regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between adolescent suicide attempts and eating disorder hospitalization. Results: Adolescent girls admitted for a suicide attempt had 5.55 times the risk of eating disorder hospitalization over time (95% CI 3.74–8.23), compared with matched controls. Suicide attempt was associated with anorexia nervosa (HR 3.57, 95% CI 1.78–7.17) and bulimia nervosa and other eating disorders (HR 8.55, 95% CI 5.48–13.32). Associations were pronounced in girls with repeated suicide attempts. Girls who attempted suicide through self‐poisoning had an elevated risk of anorexia nervosa, whereas girls who used violent methods such as cutting or piercing had a greater risk of bulimia nervosa and other eating disorders. Suicide attempt was strongly associated with eating disorder hospitalization in the year following the attempt, but associations persisted throughout follow‐up. Discussion: Suicide attempt admission is associated with the long‐term risk of eating disorder hospitalization in adolescent girls. Public Significance: This study of adolescent girls suggests that suicide attempt admission is associated with the long‐term risk of hospitalization for eating disorders. The risk is greatest in the year after the attempt, but persists over time. Adolescents who present with a suicide attempt may benefit from screening for eating disorders and long‐term follow‐up to help prevent the exacerbation or development of eating disorders. [ABSTRACT FROM AUTHOR]

Aim: We assessed the association between caesarean birth and age‐specific risks of childhood cancer. Methods: We followed a cohort of 1 034 049 children between 2006 and 2020 in Quebec, Canada, from birth until age 14 years. The exposure was caesarean, operative vaginal, or spontaneous vaginal birth. The outcome included haematopoietic or solid tumours. We calculated hazard ratios (HR) and 95% confidence intervals (CI) for the association between mode of delivery and childhood cancer in age‐lagged analyses, adjusted for potential confounders. Results: A total of 249 415 (24.1%) children were born by caesarean and 97 411 (9.4%) by operative vaginal delivery. Compared with spontaneous vaginal birth, caesarean was associated with 1.16 times the risk of any cancer (95% CI 1.04–1.30), 1.12 times the risk of haematopoietic cancer (95% CI 0.92–1.36) and 1.21 times the risk of solid tumours (95% 1.06–1.39). Associations strengthened at 2 years of age and were greatest for lymphoma and sarcoma. Operative vaginal birth was not significantly associated with the risk of cancer. Conclusion: Caesarean birth may be associated with selected childhood cancers, including lymphoma and sarcoma early in childhood. The underlying reasons for the associations require further investigation, including whether mucosal dysbiosis or labour hormone exposure explain the excess risk. [ABSTRACT FROM AUTHOR]

Pneumonia is a leading cause of morbidity. Pneumonia is defined as a lung inflammation of infectious etiology. It can be subcategorized into Community Acquired Pneumonia, Hospital Acquired Pneumonia and Ventilator Acquired Pneumonia. Validated scores including the CRB-65, CURB-65 and PSI can guide decision-making between inpatient and outpatient management of pneumonia. While mild presentations can be managed through empiric treatment alone, more acute cases require identification of the infectious agent, initiation of empiric therapy, and subsequent de-escalation of treatment to the identified pathogen. This article aims to provide a framework for junior trainees to diagnose and manage pneumonia. [ABSTRACT FROM AUTHOR]

This study evaluated the association between placental pathology and gross morphology and the risk of autism spectrum disorders (ASD). We conducted a matched case–control study of children with confirmed ASD who were born between 2000 and 2017 at one of three university‐affiliated hospitals in Montreal, Quebec. Cases, who were identified through the Montreal Children's Hospital Autism Spectrum Disorders Program, were matched to babies (1:5) born at the same hospital and on the same day. Multi‐fetal births were excluded. Maternal demographics, pregnancy characteristics and placental pathologies were collected from hospital charts by abstractors blind to autism diagnoses. This current study consisted of data from a single‐site that had pathology reports available. Pearson chi‐square and Wilcoxon rank‐sum tests were used to estimate p‐values. Our study consisted of 107 ASD cases and 526 matched controls. Mothers of cases and controls were similar in terms of parity, gravidity, smoking status, BMI, rates of clinical chorioamnionitis, chronic hypertension, and gestational diabetes. Age at delivery of <25 years was more common among mothers of controls. Compared with controls, cases were more likely born male, <32 weeks of gestation, and weighing <1500 g. Cases and controls had similar rates of placental inflammation, vasculitis, and other placental pathologies. There were no differences in placental weight, placental thickness, umbilical cord length, and umbilical cord insertion between the two groups. In conclusion, placental pathology and gross morphology do not appear to be associated with ASD, suggesting that any perinatal determinants of autism are not likely to be mediated through placental pathology. Lay Summary: Data from a matched case–control study consisting of neonates born between 2000 and 2017 at one of three McGill‐affiliated hospitals were used to examine the relationship between placental pathology and morphology and the development of autism. No differences in placental pathology and gross morphology were found between those with and without autism, which suggests that placental abnormalities are unlikely to either cause or mediate the development of autism. [ABSTRACT FROM AUTHOR]

Background: Research is beginning to implicate early life characteristics in the development of pediatric nonalcoholic fatty liver disease, however the relationship with perinatal characteristics is poorly understood.Aims: We evaluated the association between perinatal characteristics and nonalcoholic fatty liver disease in childhood.Study Design: Nested case-control study.Subjects: 5104 children born in Quebec, Canada between 2006 and 2019. Exposures included maternal diabetes, obesity, prematurity, and other birth complications.Outcome Measures: The outcome was nonalcoholic fatty liver disease diagnosed in hospital before 14 years of age. We calculated adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between birth characteristics and nonalcoholic fatty liver disease.Results: A total of 104 children with nonalcoholic fatty liver disease were included. Gestational diabetes (OR 2.17, 95% CI 1.15-4.10), preexisting diabetes (OR 5.75, 95% CI 2.67-12.4), and maternal obesity (OR 3.06, 95% CI 1.71-5.45) were associated with childhood nonalcoholic fatty liver disease. Prematurity (OR 1.93, 95% CI 1.06-3.54) and neonatal intensive care unit admission (OR 2.18, 95% CI 1.10-4.33) were also associated with nonalcoholic fatty liver disease. However, there was no association with low birthweight, small-for-gestational age birth, and macrosomia.Conclusions: Maternal metabolic disorders and prematurity may initiate processes early in life that lead to the development of nonalcoholic fatty liver disease in childhood. [ABSTRACT FROM AUTHOR]

This study evaluated the association between placental pathology and gross morphology and the risk of autism spectrum disorders (ASD). We conducted a matched case-control study of children with confirmed ASD who were born between 2000 and 2017 at one of three university-affiliated hospitals in Montreal, Quebec. Cases, who were identified through the Montreal Children's Hospital Autism Spectrum Disorders Program, were matched to babies (1:5) born at the same hospital and on the same day. Multi-fetal births were excluded. Maternal demographics, pregnancy characteristics and placental pathologies were collected from hospital charts by abstractors blind to autism diagnoses. This current study consisted of data from a single-site that had pathology reports available. Pearson chi-square and Wilcoxon rank-sum tests were used to estimate p-values. Our study consisted of 107 ASD cases and 526 matched controls. Mothers of cases and controls were similar in terms of parity, gravidity, smoking status, BMI, rates of clinical chorioamnionitis, chronic hypertension, and gestational diabetes. Age at delivery of <25 years was more common among mothers of controls. Compared with controls, cases were more likely born male, <32 weeks of gestation, and weighing <1500 g. Cases and controls had similar rates of placental inflammation, vasculitis, and other placental pathologies. There were no differences in placental weight, placental thickness, umbilical cord length, and umbilical cord insertion between the two groups. In conclusion, placental pathology and gross morphology do not appear to be associated with ASD, suggesting that any perinatal determinants of autism are not likely to be mediated through placental pathology. LAY SUMMARY: Data from a matched case-control study consisting of neonates born between 2000 and 2017 at one of three McGill-affiliated hospitals were used to examine the relationship between placental pathology and morphology and the development of autism. No differences in placental pathology and gross morphology were found between those with and without autism, which suggests that placental abnormalities are unlikely to either cause or mediate the development of autism., (© 2021 International Society for Autism Research and Wiley Periodicals LLC.)