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 25 November 2017

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News

Researchers discover novel form of enteropathy in autistic children

A novel form of enteropathy has been demonstrated in autistic children, which is characterized by epithelial IgG and complement deposition.

News image

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Researchers from London, England, investigated small intestinal enteropathy in children with regressive autism.

They reported their findings in the latest issue of Molecular Psychiatry.

The investigators, from St Mark's Hospital and the Royal Free & University College Medical School, have previously reported lymphocytic colitis in children with regressive autism, with epithelial damage prominent.

Duodenal biopsies from 25 children with regressive autism were compared to 11 with celiac disease, 5 with cerebral palsy and mental retardation, and 18 histologically normal controls.

The density of intraepithelial and lamina propria lymphocyte populations were determined.

Mucosal immunoglobulin and complement C1q localization were also studied.

IgG deposition seen on basolateral epithelial surface in 92% of autistic children.
Molecular Psychiatry
Standard histopathology showed increased enterocyte and Paneth cell numbers in the autistic children.

Immunohistochemistry demonstrated increased lymphocyte infiltration in both epithelium and lamina propria with upregulated crypt cell proliferation, compared to normal and cerebral palsy controls.

The researchers found that intraepithelial lymphocytes and lamina propria plasma cells were lower than in celiac disease.

However, lamina propria T cell populations were higher, and crypt proliferation similar.

Most strikingly, IgG deposition was seen on the basolateral epithelial surface in 23/25 autistic children, co-localizing with complement C1q.

This was not seen in the other conditions.

Dr F. Torrente, of the Centre for Paediatric Gastroenterology at the Royal Free & University College Medical School, concluded on behalf of fellow colleagues, "These findings demonstrate a novel form of enteropathy in autistic children.

"This is characterized by increases in mucosal lymphocyte density and crypt cell proliferation, which occur with epithelial IgG deposition.

"The features are suggestive of an autoimmune lesion."

In an accompanying Editorial, Julio Licinio and colleagues from the UCLA Laboratory of Pharmacogenomics, in California, USA, comment, "As Torrente et al point out, the data could support different possibilities.

"One such possibility is the concept of local autoimmunity in the gut, leading to altered cognitive functioning by failure to detoxify neuroactive substances originating from the gut.

"The findings would also be consistent with multisystem autoimmunity."

They highlight that there are a number of studies that support Torrente et al's work on an autoimmune basis for autism.

The Editorial authors ask whether these independent findings conclusively support the concept of autoimmunity in autism.

They conclude that, only after various independent replication reports appear, will they be confident that the findings reported in the article are indeed relevant to autism.

Mol Psychiatr 2002; 7: 329, 375-82
25 April 2002

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