Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children

Sabrá, Aderbal; Bellanti, Joseph A.; Colón, A. R.

doi:10.1016/s0140-6736(05)77837-5

Cited by 29 publications

(14 citation statements)

References 5 publications

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“…Findings of lymphoid nodular hyperplasia from biopsied specimens of autistic children have been controversial as several of the coauthors from the original study by Wakefield and associates (1998) [68] have retracted their conclusions and renounced the findings [69]. Lymphoid nodular hyperplasia has been found in conditions other than autism, including allergies [70]. At least two series of nonautistic children having colonoscopy for gastrointestinal symptoms have reported lymphoid nodular hyperplasia in 46 out of 140 and in 53 out of 74 cases [66,71].…”

Section: Clinical History Autismmentioning

confidence: 99%

The minicolumnopathy of autism: A link between migraine and gastrointestinal symptoms

Casanova

2008

Medical Hypotheses

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Gastrointestinal symptoms are common medical problems among autistic patients. A leaky gut and viruses have been proposed as possible culprits but evidence for these etiological agents remains elusive. In this article, we put forward an alternate etiology: abdominal migraines. Recent postmortem studies in autism indicate the presence of a minicolumnopathy and its relationship to both serotonergic abnormalities and a hyperexcitable cortex. These features of phenomenology are also observed in miganeurs. A putative relationship between autism and migraine is further suggested by similarities in clinical histories and laboratory evidence. Some commonalities include the presence of neuroinflammation, sensory overstimulation (e.g., flickering of fluorescent lights), "food allergies", benefits from similar diets, and the role of nitric oxide. Abdominal migraine therefore stands as a falsifiable hypothesis with added importance accrued to potential therapeutic interventions.

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Section: Clinical History Autismmentioning

confidence: 99%

The minicolumnopathy of autism: A link between migraine and gastrointestinal symptoms

Casanova

2008

Medical Hypotheses

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“…There is now evidence that some of these children have had their bowel/brain disease triggered by immunizing agents [19], though this has been refuted [20]. Also, ileal-lymphoid nodular hyperplasia has been reported in other conditions [21].…”

Section: Discussionmentioning

confidence: 99%

A Clinical Study of Secretin in Autism and Pervasive Developmental Delay

Lonsdale¹,

Shamberger²

2000

Journal of Nutritional & Environmental Medicine

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Purpose: The aim of this study was to examine the clinical effect of a single dose of secretin given to patients whose disease status lay within the autistic spectrum. Design: Open, uncontrolled trial. Materials and Methods: Sixty-four patients were registered for the study. They included 3 female adults and 2 male adolescents. There was a total of 16 dropouts. Thus there were 48 evaluable patients. Each patient received a complete vial of secretin, irrespective of current age and body weight. Any existing treatment that had already been started before the study began was allowed to continue. No new treatment was permitted for a minimum period of 8 weeks when study surveillance was completed. The parents or guardians performed clinical assessment on a weekly basis, using numerical scoring of symptoms in a questionnaire. The only laboratory study performed was a hair analysis at the outset and at the completion of the 8 weeks of surveillance. Results: Of 48 evaluable patients, there were 39 whose clinical response varied from minor to major behavioral and/or bowel function improvement and 9 in whom there was no sign at all of either a behavioral or gastrointestinal response. Only a few of these patients showed signi cant abnormalities in hair analysis and there was no signi cant difference in these changes as compared with a group of children who had been seen at our clinic for reasons other than autistic spectrum. The side effects observed were temporary irritability in a few patients and exacerbation of previously quiescent seizures in one child. Conclusions: We found a clearcut population of clinical "responders" as compared with a much smaller group of "non-responders." Little can be said about the dropout patients other than to conclude that total lack of response and expense were the most likely causes. We can certainly encourage and condone the use of secretin as a valuable weapon in attempting treatment of this devastating spectrum of disease. This study has not helped to de ne the indications to suggest a "responder" from a "non-responder."

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“…The intestinal changes are consistent with an autoimmune pathology and, in view of the increasing evidence for gut epithelial dysfunction in autism, are indicative of a speci®c and possibly important lesion. Bellanti and colleagues have presented preliminary evidence of similar ®ndings in some children with attention de®cit hyperactivity disorder, 34 suggesting that gastrointestinal pathology may be relevant to a broader spectrum of childhood developmental/behavioural disorders. Horvath et al have reported their ®ndings in the upper gastrointestinal tract in 36 autistic children, whose symptoms included chronic diarrhoea, gaseousness, abdominal discomfort and distension.…”

Section: The Gut In Autism: Clinical Presentation and Subclinical Dismentioning

confidence: 98%

The concept of entero‐colonic encephalopathy, autism and opioid receptor ligands

Wakefield

Puleston

Montgomery

et al. 2002

Aliment Pharmacol Ther

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There is growing awareness that primary gastrointestinal pathology may play an important role in the inception and clinical expression of some childhood developmental disorders, including autism. In addition to frequent gastrointestinal symptoms, children with autism often manifest complex biochemical and immunological abnormalities. The gut–brain axis is central to certain encephalopathies of extra‐cranial origin, hepatic encephalopathy being the best characterized. Commonalities in the clinical characteristics of hepatic encephalopathy and a form of autism associated with developmental regression in an apparently previously normal child, accompanied by immune‐mediated gastrointestinal pathology, have led to the proposal that there may be analogous mechanisms of toxic encephalopathy in patients with liver failure and some children with autism. Aberrations in opioid biochemistry are common to these two conditions, and there is evidence that opioid peptides may mediate certain aspects of the respective syndromes. The generation of plausible and testable hypotheses in this area may help to identify new treatment options in encephalopathies of extra‐cranial origin. Therapeutic targets for this autistic phenotype may include: modification of diet and entero‐colonic microbial milieu in order to reduce toxin substrates, improve nutritional status and modify mucosal immunity; anti‐inflammatory/immunomodulatory therapy; and specific treatment of dysmotility, focusing, for example, on the pharmacology of local opioid activity in the gut.

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Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children

Cited by 29 publications

References 5 publications

The minicolumnopathy of autism: A link between migraine and gastrointestinal symptoms

The minicolumnopathy of autism: A link between migraine and gastrointestinal symptoms

A Clinical Study of Secretin in Autism and Pervasive Developmental Delay

The concept of entero‐colonic encephalopathy, autism and opioid receptor ligands

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