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Gastrointestinal Disease in Children With Autism Spectrum Disorders

The general term for chronic inflammation in the intestines is Inflammatory Bowel Disease (IBD).

There are two traditionally recognized chronic diseases that cause inflammation of the gastrointestinal tract: ulcerative colitis and Crohn's disease. Patients with ASD's appear to suffer from another form of IBD, autistic enterocolitis, which manifests itself as inflammation of varying intensity anywhere in the gastrointestinal tract with associated prominent lymphoid nodular hyperplasia, in the setting of autism, and lacking the specific diagnostic features of ulcerative colitis or Crohn's disease. A growing number of published reports over the past number of years have detailed a variety of unique histochemical and molecular features of ASD-associated bowel inflammation that appears to distinguish it from both Crohn's disease and ulcerative colitis.

Evaluation of patients with ASD and co-morbid chronic gastrointestinal symptoms (go to new patients) consists of thorough review of the clinical history (with emphasis on the chronology of presenting gastrointestinal and developmental symptoms), clinical data obtained from the patients existing medical records, select laboratory testing, and a patient/parent interview. Patients in whom this these data suggest the presence of an inflammatory bowel disease, autistic enteritis/enterocolitis or an allergic/autoimmune esophago-gastro-enteropathy are often in need of a comprehensive diagnostic survey of the gastrointestinal tract, including gastrointestinal endoscopy and biopsy. Microscopic examination of biopsy obtained gastrointestinal tissue remains the gold standard in making an accurate diagnosis for purposes of appropriate therapeutic intervention.

During endoscopic procedures, a variety of lesions (link to photos) in the esophagus, stomach, small bowel, and colon are typically discovered. These lesions take the form of ulcerations, erosions, erythema, inflammatory polyps, and prominent lymphoid nodular hyperplasia. In addition to the lesions strongly associated with the co-occurring ASD diagnosis, additional diagnoses such as acid-reflux esophagits are frequently encountered. While the underlying cause of these lesions is still unknown, they often appear to result from an exaggerated, poorly regulated immune response involving the gastrointestinal mucosa, which is the lining of the GI tract. The most common clinical manifestations of these lesions are diarrhea, abdominal pain, constipation, abdominal distention, and growth problems. It is thought that behavioral symptoms traditionally attributed to autism may often in fact be symptoms of gastrointestinal disease or gastrointestinal pain.

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Autism and GI Disease: Chicken or Egg?

GI symptoms can precede, coincide with, or appear after the onset of neurological symptoms or regression. A current conceptual model linking the gastrointestinal pathology to cognitive deficits involves a biochemical sequence of events in which luminal contents, which consist primarily of ingested food and products of microbial degradation, are pathologically absorbed through the highly permeable inflamed intestinal mucosa before they are properly broken down intraluminally into smaller micromolecules. The absorbed macromolecules then undergo metabolic degradation and processing by pathways not normally employed, resulting in the production of byproducts that may be toxic to the developing brain. Though ultimately theoretical, this proposed mechanism is supported in its separate steps, both by published scientific data, the observations of clinicians caring for these children, and most importantly, the observations of countless parents.

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