Autoimmunity in autism( 95: 2285-2295). Use of immunohistochemi...)

95: 2285-2295). Use of immunohistochemical techniques had suggested a novel form of colitis, in which the epithelium of the colon was particularly affected (Journal of Pediatrics 2001; 138: 366-372), and, thus, possibly suggestive of autoimmunity. In the current study, the authors report a highly unusual form of small bowel abnormality, subtle on routine staining, but with distinct and apparent autoimmune features. Again the epithelium appears to be the focus of this immune response, with evidence of direct binding of self antibody to the surface of the epithelial cells (enterocytes), increased epithelial division and infiltration of T lymphocytes. The authors used an extensive panel of monoclonal antibodies, and made comparisons to children with celiac disease, cerebral palsy and mental retardation, and apparently normal controls, none of whom showed this pattern of abnormalities.

The findings thus support an autoimmune basis for the unexpected bowel abnormalities in children with autism. Many questions remain. In particular the relevance of these findings to the general autistic population, as these children had more obvious bowel symptoms than commonly seen. The authors avoid a direct suggestion that these bowel findings may be causal in autistic regression, but they cite reports that cognitive function is enhanced in some children with regressive autism when gut-based therapy is introduced. They also raise the possibility that the bowel changes may be a manifestation of a primarily genetic condition affecting several systems in which disturbance of brain function is simply more apparent. Further work thus clearly needs to be done to determine the role of the "gut-brain axis" in autism. However, confirmation that autoimmune responses really do contribute to cognitive regression in autistic children will raise the probability of a fundamental change in the treatment of autistic regression, based on modulating the immune response in children with early aut
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Contact: Frank Sissingh
molecularpsychiatry@mednet.ucla.edu
310-206-6739
Molecular Psychiatry
29-Apr-2002

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