Autistic enterocolitis: confirmation of a new inflammatory bowel disease in an Italian cohort of patients

Although the causes of autism are largely unknown, this life-long developmental disorder is now showing a strong increase of prevalence (1/500). An upper and lower intestinal disease has been recently described in these patients (pts) in spite of gastrointestinal symptoms have been reported by the parents back more many years. This disorder comprising ileocolonic lymphoid nodular hyperplasia (LNH) and chronic inflammatory colonic disease was called autistic enterocolitis: an association between autism and bowel disease was then proposed. Nine consecutive male pts (mean age 18 years, range 7-30 years) with a diagnosis of autism according to ICD-10 criteria that showed chronic intestinal symptoms (abdominal pain, bloating, constipation and/or diarrhoea) were enrolled. After routinely blood and stool tests, gastroscopy and colonoscopy with multiple biopsies were performed under sedation. A wireless enteroscopy capsule was also performed in 3 adult pts. Anemia and fecal blood positive test were found in 2 pts and 3 pts, respectively. Gastroscopy revealed mucosal gastritis in 4 pts, esophagitis in 1 pts and duodenitis in 1 pts. Histological findings showed a chronic inflammation of the stomach and duodenum in 6 pts (66%) but inconsistent with celiac disease. Macroscopic mucosal abnormalities (aphtoid ulcerations and loss of vascular pattern) were found in 1 pts (11%) at colonoscopy and a LNH in the terminal ileum in 4 pts (44%). Microscopic colitis with intraepithelial lymphocytes and eosinophyls infiltrations, mucosal atrophy and follicular hyperplasia was histologically present in all the pts (100%) whereas a chronic inflammation with iperemia and villous shortening of the terminal ileum was shown only in 6 (66%) pts. The wireless capsule revealed areas of bleeding or patchy erythema, mucosal erosions and ulcers in both jejunum and ileum in 1 patients whereas an atypical chronic jejunum and ileal erosive pattern was evident in the other two pts. These preliminary data are strongly consistent with previous descriptions of autistic enterocolitis and supported a not-coincidental occurrence. Moreover, they showed for the first time a small intestinal involvement, suggesting a panenteric localisation of this new IBD. The treatment to gain clinical remission has still to be tried and it will be extremely important to ameliorate the quality of life of such pts who are likely to be overlooked because of their life-long problems in the communication of symptoms.