1. Bala KA, Dogan M, Kaba S, Mutluer T, Aslan O, Dogan SZ. {{Hormone disorder and vitamin deficiency in attention deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASDs)}}. {J Pediatr Endocrinol Metab}. 2016.
BACKGROUND: The aim of this study was to analyze thyroid hormones and antibodies, ferritin, vitamins B12 and D, adrenal and gonadal steroid levels, and celiac antibodies in children diagnosed with attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). METHODS: Between February 2014 and July 2014, a total of 77 children and adolescents (31 girls, 46 boys) who were admitted to the Van Training and Research Hospital were included in the study. The study population was divided into three groups including ADHD (n=34), ASD (n=16), and age- and sex-matched healthy controls (n=27). The diagnosis of ADHD was made on the basis of Diagnostic and Statistical Manual of Mental Disorders – Fifth Edition (DSM-5) and DSM-4 Turkish version with the diagnostic interview and Disruptive Behavior Disorder Rating Scale (DBDRS). The diagnosis of ASD was based on the DSM-4 and DSM-5 Turkish version with the diagnostic interview and the Childhood Autism Rating Scale (CARS). The blood samples were obtained between 8:00 and 9:00 A.M. RESULTS: There was a statistically significant difference in vitamin B12 and D levels and ferritin values among the three groups. The ASD group had the highest ferritin and the lowest vitamins B12 and D levels. Vitamin D levels of the ADHD group were significantly lower compared to the healthy controls. CONCLUSIONS: Our study results highlight the importance of supplementation of vitamins B12 and D in the ASD and ADHD patients.
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2. Coskun S, Simsek S, Camkurt MA, Cim A, Celik SB. {{Association of polymorphisms in the vitamin D receptor gene and serum 25-hydroxyvitamin D levels in children with autism spectrum disorder}}. {Gene}. 2016; 588(2): 109-14.
Vitamin D is implicated in several aspects of human physiology, and polymorphisms in the vitamin D receptor gene (VDR) are associated with a variety of neuropsychiatric disorders. The aims of this study are to determine whether VDR polymorphisms are associated with autism spectrum disorder (ASD), to examine serum 25-hydroxyvitamin D (25(OH)D) levels in ASD, and to explore whether VDR polymorphisms influence serum 25(OH)D levels. We investigated 480 subjects (237 children with ASD and 243 healthy controls) for the following VDR polymorphisms: TaqI, BsmI, FokI, ApaI, and Cdx2.Within the same samples, 25(OH)D levels were available only for 85 patients and 82 controls. The Cdx-2 variation was shown to deviate from Hardy-Weinberg equilibrium in the controls and was therefore excluded from the study. We found that the frequency of rare FokI TT, TaqI CC, and BsmI AA genotypes differed significantly between children with ASD and the controls (p=0.042, p=0.016, p=0.038, respectively). After correction for multiple testing, only the TaqI CC genotype remained significant. Further analysis using a recessive model showed that rare genotypes of these polymorphisms were significantly higher in patients compared to controls (p=0.045, p=0.005 and p=0.031, respectively). However, no significant association was found between ApaI and ASD. We found serum 25(OH)D levels to be significantly higher in children with ASD (p<0.001) and that the FokI polymorphism had an effect on serum 25(OH)D levels in children with ASD (p=0.041). Additionally, we found the haplotype GTTT (BsmI/TaqI/FokI/ApaI) conferred an increased risk for developing ASD (p=0.022; odds ratio [95% confidence interval]=2.322 [1.105-4.879]). This is the first clinical study evaluating the association between serum 25(OH)D levels and VDR polymorphisms in children with ASD. Our results demonstrated a significant association between TaqI, BsmI, and FokI polymorphisms and ASD and showed for the first time that FokI polymorphisms and haplotype GTTT (BsmI/TaqI/FokI/ApaI) are associated with an increased risk of ASD. Our findings support the hypothesis that 25(OH)D is involved in the pathophysiology of autism and that serum 25(OH)D levels may be affected by FokI polymorphisms in children with ASD. Our results should be considered as preliminary and needs confirmation by future studies. Lien vers le texte intégral (Open Access ou abonnement)
3. Happe FG, Mansour H, Barrett P, Brown T, Abbott P, Charlton RA. {{Demographic and Cognitive Profile of Individuals Seeking a Diagnosis of Autism Spectrum Disorder in Adulthood}}. {J Autism Dev Disord}. 2016.
Little is known about ageing with autism spectrum disorder (ASD). We examined the characteristics of adults referred to a specialist diagnostic centre for assessment of possible ASD, 100 of whom received an ASD diagnosis and 46 did not. Few demographic differences were noted between the groups. Comorbid psychiatric disorders were high in individuals with ASD (58 %) and non-ASD (59 %). Individuals who received an ASD diagnosis had higher self-rated severity of ASD traits than non-ASD individuals. Within the ASD group, older age was associated with higher ratings of ASD traits and better cognitive performance. One interpretation is that general cognitive ability and the development of coping strategies across the lifespan, do not necessarily reduce ASD traits but may mitigate their effects.
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4. Hens K, Peeters H, Dierickx K. {{Genetic testing and counseling in the case of an autism diagnosis: A caregivers perspective}}. {Eur J Med Genet}. 2016; 59(9): 452-8.
The search for genes that can explain the development of autism is ongoing. At the same time, genetic counselling and genetic testing can be offered to families with a child diagnosed with autism. However, given the complexity of autism, both with respect to its aetiology as well as with respect to its heterogeneity, such genetic counselling and testing raises specific ethical questions regarding the aim and scope. In order to map these questions and opinions we interviewed 15 Belgian autism professionals. We found that they believed that genetic counselling and genetic testing have certain benefits for families confronted with an autism diagnosis, but also that direct benefit to the child is limited to those cases where a genetic finding offers a certain prognosis and intervention plan. In cases where autism is the result of a syndrome or a known genetic variant that is associated with other health problems, detection can also enable prevention of these health issues. Benefits of genetic testing, such as relief of guilt and reproductive choice, are primarily benefits to the parents, although indirectly they may affect the wellbeing of the person diagnosed. These benefits are associated with ethical questions.
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5. Kilinc S, Herguner S. {{Oral Decongestant-Induced Mania in a Child with Autism Spectrum Disorder}}. {J Child Adolesc Psychopharmacol}. 2016.
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6. Mayes SD, Calhoun SL, Waxmonsky JG, Kokotovich C, Baweja R, Lockridge R, Bixler EO. {{Demographic Differences in Disruptive Mood Dysregulation Disorder Symptoms in ADHD, Autism, and General Population Samples}}. {J Atten Disord}. 2016.
OBJECTIVE: Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5) disruptive mood dysregulation disorder (DMDD) is a controversial new diagnosis. No studies have investigated DMDD symptoms (irritable-angry mood and temper outbursts) and demographics in general population and psychiatric samples. METHOD: Maternal ratings of DMDD symptoms and diagnoses, age, gender, IQ, race, and parent occupation were analyzed in general population (n = 665, 6-12 years) and psychiatric samples (n = 2,256, 2-16 years). RESULTS: Percentage of school-age children with DMDD symptoms were 9% general population, 12% ADHD-I, 39% ADHD-C, and 43% autism. Male, nonprofessional parent, and autism with IQ > 80 were associated with increasing DMDD symptoms, but demographics together explained only 2% to 3% of the DMDD score variance. CONCLUSION: Demographics contributed little to the presence of DMDD symptoms in all groups, whereas oppositional defiant disorder (ODD) explained most of the variance. Almost all children with DMDD symptoms had ODD suggesting that DMDD may not be distinct from ODD.
