Identification of abnormalities in the developmental trajectory during infancy of future schizophrenia cases offers the potential to reveal pathogenic mechanisms of this disorder. Previous studies of head circumference in pre-schizophrenia were limited to measures at birth. The use of growth acceleration of head circumference (defined as the rate of change in head circumference) provides a more informative representation of the maturational landscape of this measure compared to studies based on static head circumference measures. To date, however, no study has examined whether HC growth acceleration differs between pre-schizophrenia cases and controls. In the present study, we employed a nested case control design of a national birth cohort in Finland. Cases with schizophrenia or schizoaffective disorder (N=375) and controls (N=375) drawn from the birth cohort were matched 1:1 on date of birth (within 1month), sex, and residence in Finland at case diagnosis. Longitudinal data were obtained on head circumference from birth through age 1. Data were analyzed using a new nonparametric Bayesian inversion method which allows for a detailed understanding of growth dynamics. Adjusting for growth velocity of height and weight, and gestational age, there was significantly accelerated growth of head circumference in females with schizophrenia from birth to 2months; the findings remained significant following Bonferroni correction (p
The incidence of Neisseria gonorrhoeae with reduced susceptibility to quinolones increased from 0.18% (63 of 3285) in 1992 to 0.56% (15 of 2663) in 1993 and 0.62% (46 of 2846) in 1994. In all, 65 of the 67 isolates of Neisseria gonorrhoeae with decreased susceptibility to quinolones were characterised by pulsed-field gel electrophoresis (PFGE), auxotyping, serotyping and plasmid content. The strains were distributed among 14 auxotype/serovar (A/S) classes. Thirty isolates (46.2%) which were penicillin-susceptible with ciprofloxacin MIC90 of 0.12 mg/L and norfloxacin MIC90 of 1.0 mg/L belonged to a single A/S class, OUHL/IA-2. All but two of the 30 isolates had identical PFGE restriction profiles with NheI restriction endonuclease. Fifteen isolates (23.1%) with MICs in the intermediate (or resistant) categories for penicillin and with ciprofloxacin and norfloxacin MIC90 of 0.25 and 4.0 mg/L and (0.5 and 4.0 mg/L) respectively, belonged to A/S class P/IB-1. The 15 isolates showed nine different patterns with NheI and eight patterns with SpeI restriction endonucleases. Two of three beta-lactamase-producing (PPNG) isolates belonged to A/S class P/IB-5 and had a dissimilar PFGE restriction profile with NheI endonuclease; the other isolate belonged to A/S class P/IB-8. The remaining 17 isolates were distributed among 11 A/S classes. Three isolates within the common A/S class NR/IB-1 were subdivided into two types by PFGE as were three isolates belonging to A/S class NR/IB-2. Overall the 65 isolates of N. gonorrhoeae were distributed into 30 NheI and 26 SpeI macrorestriction profiles. All but one isolate harboured the 2.6-MDa cryptic plasmid and 18 isolates carried the 24.5-MDa transferable plasmid. The three PPNG isolates carried the 4.5-MDa Asian beta-lactamase-producing plasmid and a 25.2-MDa conjugative plasmid was found in the two TRNG isolates.
Thirteen infants and children with adenovirus type 7 infection proved by virus isolation are described. High fever, cough and dyspnea were the most frequent findings; in infants under 1 year of age wheezing was common. Four patients required artificial ventilation. Lobar collapse, consolidation and hyperinflation were frequent radiologic findings. None of the symptoms responded to antibiotic therapy or bronchodilator drugs. Three patients died (mortality rate of 23%). Pathologic findings were compatible with adenovirus type 7 pneumonia, and were characterized by a necrotizing bronchitis and bronchiolitis, patchy alveolar fibrinopurulent exudate and hyaline membrane formation. Some intra-alveolar epithelial cells showed strikingly abnormal nuclei and rare typical halo-outlined intranuclear inclusions were seen. Only one of eight survivors had evidence of significant chronic chest disease.
Cites: Am J Dis Child. 1967 Jul;114(1):36-414378107
Cites: Am J Hyg. 1958 May;67(3):367-7813533409
Cites: Am J Epidemiol. 1966 May;83(3):436-544286697
Cites: Prog Med Virol. 1965;7:253-3254283916
Cites: J Pediatr. 1966 Jan;68(1):142-44285229
Cites: Ann Intern Med. 1966 Mar;64(3):521-304286006
Cites: Am J Pathol. 1971 Dec;65(3):543-84330417
Cites: J Pediatr. 1971 Oct;79(4):605-114328651
Cites: S Afr Med J. 1971 Jan 30;45(5):107-114322988
Cites: J Can Assoc Radiol. 1969 Dec;20(4):218-244312230
Cites: Pediatrics. 1969 Oct;44(4):477-854310363
Cites: Mayo Clin Proc. 1968 Sep;43(9):635-444303957
Cites: AMA Arch Intern Med. 1958 Nov;102(5):816-913582270
The first aim of this study was to evaluate the association between different subgroups of autism spectrum disorders (ASDs) (childhood autism, Asperger syndrome, and pervasive developmental disorder/pervasive developmental disorder - not otherwise specified [PDD/PDD-NOS]) and congenital anomalies. Second, we assessed the association among intellectually disabled children with ASDs in the subgroups of childhood autism and PDD/PDD-NOS.
Nationwide population-based register data for children with a diagnosis of ASD (n=4449; 3548 males, 901 females) were collected during years 1987-2000 from the Finnish Hospital Discharge Register. Data on congenital anomalies were derived from the National Register of Congenital Malformations. Conditional logistic regression models were used as a statistical method. The association between ASD subgroups and congenital anomalies was stratified by the presence or absence of intellectual disability.
Congenital anomalies occurred more frequently in all subgroups of ASD than in comparison participants (adjusted odds ratio [OR] for major congenital anomalies 1.8, 95% confidence interval [CI] 1.5-2.2, p
Comment In: Dev Med Child Neurol. 2015 Jan;57(1):10-125312764
From the Department of Psychiatry, Columbia University Medical Center, and New York State Psychiatric Institute, New York; the Department of Epidemiology, Columbia University Mailman School of Public Health, New York; the Department of Health Security, National Institute for Health and Welfare, Kuopio, Finland; the Department of Child Psychiatry, University of Turku, Turku, Finland; the Department of Biostatistics, Columbia University Mailman School of Public Health, New York; the University of Oulu, Faculty of Medicine, Oulu, Finland; the Biobank Borealis of Northern Finland, Oulu University Hospital, Oulu, Finland; and the Department of Child Psychiatry, Turku University Hospital, Turku, Finland.
Autism is a complex neurodevelopmental disorder with a largely unknown etiology. To date, few studies have investigated prenatal exposure to toxins and risk of autism by using maternal biomarkers of exposure. Persistent organic pollutants are lipophilic halogenated organic compounds and include the insecticide dichlorodiphenyltrichloroethane (DDT), as well as its metabolite p,p'-dichlorodiphenyl dichloroethylene (p,p'-DDE), and polychlorinated biphenyls (PCBs). The objective of this study was to test whether elevated maternal levels of persistent organic pollutants are associated with autism among offspring.
The investigation was derived from the Finnish Prenatal Study of Autism, a national birth cohort study based on a nested case-control design. Cases of autism among children born between 1987 and 2005 were ascertained by national registry linkages. In cases of childhood autism and matched control subjects (778 matched case-control pairs), maternal serum specimens from early pregnancy were assayed for levels of p,p'-DDE and total levels of PCBs.
The odds of autism among offspring were significantly increased with maternal p,p'-DDE levels that were in the highest 75th percentile, with adjustment for maternal age, parity, and history of psychiatric disorders (odds ratio=1.32, 95% CI=1.02, 1.71). The odds of autism with intellectual disability were increased by greater than twofold with maternal p,p'-DDE levels above this threshold (odds ratio=2.21, 95% CI=1.32, 3.69). There was no association between total levels of maternal PCBs and autism.
These findings provide the first biomarker-based evidence that maternal exposure to insecticides is associated with autism among offspring. Although further research is necessary to replicate this finding, this study has implications for the prevention of autism and may provide a better understanding of its pathogenesis.
Speech/language, scholastic, and motor disorders are common in children. It is unknown whether exposure to selective serotonin reuptake inhibitors (SSRIs) during pregnancy influences susceptibility to these disorders.
To examine whether SSRI exposure during pregnancy is associated with speech/language, scholastic, and motor disorders in offspring up to early adolescence.
This prospective birth cohort study examined national population-based register data in Finland from 1996 to 2010. The sampling frame includes 845?345 pregnant women and their singleton offspring with data on maternal use of antidepressants and depression-related psychiatric disorders during pregnancy.
There were 3 groups of offspring: 15?596 were in the SSRI-exposed group, ie, had mothers diagnosed as having depression-related psychiatric disorders with a history of purchasing SSRIs during pregnancy; 9537 were in the unmedicated group, ie, had mothers diagnosed as having depression-related psychiatric disorders without a history of purchasing SSRIs during pregnancy; and 31?207 were in the unexposed group, ie, had mothers without a psychiatric diagnosis or a history of purchasing SSRIs.
Cumulative incidence of speech/language, scholastic, or motor disorders (829, 187, and 285 instances, respectively) from birth to 14 years. All hypotheses tested were formulated before data collection.
Of the 56?340 infants included in the final cohort, 28?684 (50.9%) were male and 48?782 (86.6%) were 9 years or younger. The mean (SD) ages of children at diagnosis were 4.43 (1.67), 3.55 (2.67), and 7.73 (2.38) for speech/language, scholastic, and motor disorders, respectively. Offspring of mothers who purchased SSRIs at least twice during pregnancy had a significant 37% increased risk of speech/language disorders compared with offspring in the unmedicated group. The cumulative hazard of speech/language disorders was 0.0087 in the SSRI-exposed group vs 0.0061 in the unmedicated group (hazard ratio, 1.37; 95% CI, 1.11-1.70; P?=?.004). There was a significantly increased risk of these disorders in offspring in the SSRI-exposed and unmedicated groups compared with offspring in the unexposed group. For scholastic and motor disorders, there were no differences between offspring in the SSRI-exposed group and in the unmedicated group.
Exposure to SSRIs during pregnancy was associated with an increased risk of speech/language disorders. This finding may have implications for understanding associations between SSRIs and child development.
Does IVF increase the risk of autism spectrum disorders (ASDs)?
No association between IVF and ASDs or any of its subtypes was found in this sample.
Certain prenatal factors may increase the risk of ASDs. Studies on the association between IVF and ASDs have shown inconsistent results. IVF is known to increase the risk of perinatal problems but many of them are related to multiple pregnancies.
This case-control study included 4164 autistic cases and 16 582 matched controls born in Finland in 1991-2005. The cases were diagnosed with ASDs by the year 2007. The maximum age at diagnosis was 16 years.
Four controls were matched to each case. For singletons the matching criteria were date of birth, place of birth, sex and residency in Finland. For twins the birth order within a twin pair was included as well. In the whole sample, there were 63 cases (1.51%) and 229 controls (1.38%) born after IVF.
No significant association was found between IVF and ASDs (adjusted odds ratio (OR): 0.9, 95% confidence interval (CI): 0.7-1.3) or its subtypes childhood autism (OR: 0.8, 95% CI: 0.4-1.5), Asperger's syndrome (OR: 0.9, 95% CI: 0.5-1.6) or other pervasive developmental disorder (OR: 1.0,?95% CI: 0.6-1.6). When only singletons were included, there was an association between IVF and Asperger's syndrome in an unadjusted analysis (OR: 2.0, 95% CI: 1.1-3.5) but this was not significant when adjusted for mother's socioeconomic status or parity. When the analyses were conducted separately for boys and girls, there was a significant association between IVF and Asperger's syndrome for boys in an unadjusted analysis (OR: 2.1, 95% CI: 1.2-3.7) but this was not significant in the final adjusted model.
Information both on IVF and on ASDs was based on registers and it is possible that there is some misclassification. No information on different subtypes of IVF or other assisted reproduction techniques was available. Statistical power may have been insufficient.
This study showed no increased risk of ASDs in children born after IVF but studies with larger sample sizes and information on different subtypes of IVF are needed to confirm the finding.
The study was supported by Autism Speaks, NIMH 1K02-MH65422 and NIEHS 1R01ES019004. There are no competing interests.
It is not yet definitively known whether dynamic features of head circumference growth are associated with autism. To address this issue, we carried out a nested matched case-control study using data from national well baby clinics in Finland; autism cases were identified from the Finnish Hospital and Outpatient Discharge Registry.
A nonparametric Bayesian method was used to construct growth velocity trajectories between birth and 2 years of age in autism cases and matched control subjects (n = 468 in main analyses, 1:1 matched control subjects). Estimates of odds ratios for autism risk in relation to the growth velocities were obtained using conditional logistic regression.
Growth velocity of head circumference at 3 months of age, adjusting for gestational age at birth and maternal age, is significantly associated with autism (p = .014); the finding was observed in subjects with comorbid intellectual disability (ID) (p = .025) but not in those without ID (p = .15). Height growth velocity among subjects with autism and without ID is significantly associated with autism at 6 months (p = .007), and weight growth velocity at 18 months without ID (p = .02) and 24 months without ID (p = .042) and with ID (p = .037).
Acceleration in head circumference growth is associated with autism with comorbid ID at 3 months but not subsequently. This association is unrelated to acceleration in height and weight, which are not strongly associated with autism until after 6 months.