Evaluation, Diagnosis, and Treatment of Gastrointestinal Disorders in Individuals With ASDs: A Consensus Report

Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
PEDIATRICS (Impact Factor: 5.47). 01/2010; 125 Suppl 1(Supplement):S1-18. DOI: 10.1542/peds.2009-1878C
Source: PubMed


Autism spectrum disorders (ASDs) are common and clinically heterogeneous neurodevelopmental disorders. Gastrointestinal disorders and associated symptoms are commonly reported in individuals with ASDs, but key issues such as the prevalence and best treatment of these conditions are incompletely understood. A central difficulty in recognizing and characterizing gastrointestinal dysfunction with ASDs is the communication difficulties experienced by many affected individuals. A multidisciplinary panel reviewed the medical literature with the aim of generating evidence-based recommendations for diagnostic evaluation and management of gastrointestinal problems in this patient population. The panel concluded that evidence-based recommendations are not yet available. The consensus expert opinion of the panel was that individuals with ASDs deserve the same thoroughness and standard of care in the diagnostic workup and treatment of gastrointestinal concerns as should occur for patients without ASDs. Care providers should be aware that problem behavior in patients with ASDs may be the primary or sole symptom of the underlying medical condition, including some gastrointestinal disorders. For these patients, integration of behavioral and medical care may be most beneficial. Priorities for future research are identified to advance our understanding and management of gastrointestinal disorders in persons with ASDs.

Download full-text


Available from: Glenn T Furuta,
  • Source
    • "However, this is not necessarily the case for those with Disorders ASD. Gastrointestinal disorders can present as non-gastrointestinal problems (Buie et al., 2010a). For example, individuals may present with sleep problems or challenging behavior. "

    Comorbid Conditions Among Children with Autism Spectrum Disorders, Edited by Johnny L. Matson, 01/2015: chapter Gastrointestinal Disorders: pages 257-281; Springer., ISBN: 978-3-319-19183-6
  • Source
    • "© 2013 International Society for Autism Research, Wiley Periodicals, Inc. RESEARCH ARTICLE INSAR (loose frequent stools), constipation, and abdominal discomfort/pain. The American Academy of Pediatrics (AAP) consensus report [Buie et al., 2010a] "
    [Show abstract] [Hide abstract]
    ABSTRACT: To test whether gut permeability is increased in autism spectrum disorders (ASD) by evaluating gut permeability in a population-derived cohort of children with ASD compared with age- and intelligence quotient-matched controls without ASD but with special educational needs (SEN). One hundred thirty-three children aged 10-14 years, 103 with ASD and 30 with SEN, were given an oral test dose of mannitol and lactulose and urine collected for 6 hr. Gut permeability was assessed by measuring the urine lactulose/mannitol (L/M) recovery ratio by electrospray mass spectrometry-mass spectrometry. The ASD group was subcategorized for comparison into those without (n = 83) and with (n = 20) regression. There was no significant difference in L/M recovery ratio (mean (95% confidence interval)) between the groups with ASD: 0.015 (0.013-0.018), and SEN: 0.014 (0.009-0.019), nor in lactulose, mannitol, or creatinine recovery. No significant differences were observed in any parameter for the regressed versus non-regressed ASD groups. Results were consistent with previously published normal ranges. Eleven children (9/103 = 8.7% ASD and 2/30 = 6.7% SEN) had L/M recovery ratio > 0.03 (the accepted normal range cut-off), of whom two (one ASD and one SEN) had more definitely pathological L/M recovery ratios > 0.04. There is no statistically significant group difference in small intestine permeability in a population cohort-derived group of children with ASD compared with a control group with SEN. Of the two children (one ASD and one SEN) with an L/M recovery ratio of > 0.04, one had undiagnosed asymptomatic celiac disease (ASD) and the other (SEN) past extensive surgery for gastroschisis. Autism Res 2013, ●●: ●●-●●. © 2013 International Society for Autism Research, Wiley Periodicals, Inc.
    Autism Research 06/2014; 7(3). DOI:10.1002/aur.1350 · 4.33 Impact Factor
  • Source
    • "Oxidative stress and decreased methylation capacity are common in autism and abnormal epigenetic regulation may link the metabolic abnormalities to disruptions in brain development. Other comorbid features of autism, such as autoimmunity and gastrointestinal (GI) dysfunction [133, 134], may reflect similar manifestations of abnormal epigenetic regulation. A genome-wide comparison of DNA methylation in monozygotic twins discordant for autism found numerous differentially methylated regions associated with ASD, and the extent of these differences were correlated with severity of autistic trait scores [135]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Autism and autism spectrum disorders (ASDs) are behaviorally defined, but the biochemical pathogenesis of the underlying disease process remains uncharacterized. Studies indicate that antioxidant status is diminished in autistic subjects, suggesting its pathology is associated with augmented production of oxidative species and/or compromised antioxidant metabolism. This suggests ASD may result from defects in the metabolism of cellular antioxidants which maintain intracellular redox status by quenching reactive oxygen species (ROS). Selenium-dependent enzymes (selenoenzymes) are important in maintaining intercellular reducing conditions, particularly in the brain. Selenoenzymes are a family of ~25 genetically unique proteins, several of which have roles in preventing and reversing oxidative damage in brain and endocrine tissues. Since the brain's high rate of oxygen consumption is accompanied by high ROS production, selenoenzyme activities are particularly important in this tissue. Because selenoenzymes can be irreversibly inhibited by many electrophiles, exposure to these organic and inorganic agents can diminish selenoenzyme-dependent antioxidant functions. This can impair brain development, particularly via the adverse influence of oxidative stress on epigenetic regulation. Here we review the physiological roles of selenoproteins in relation to potential biochemical mechanisms of ASD etiology and pathology.
    03/2014; 2014(3):164938. DOI:10.1155/2014/164938
Show more