{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T15:56:41Z","timestamp":1785254201780,"version":"3.55.0"},"reference-count":19,"publisher":"American Academy of Pediatrics (AAP)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,8,1]]},"abstract":"<jats:sec>\n                  <jats:title>Objective.<\/jats:title>\n                  <jats:p>Celiac disease (CD), or gluten sensitivity, is considered to be a state of heightened immunologic responsiveness to ingested gluten proteins in genetically predisposed individuals. The gastrointestinal manifestation suggests a severe enteropathy of the small intestine with malabsorption, steatorrhea, and weight loss because of a deranged mucosal immune response. Neurologic complications occur, especially epilepsy, possibly associated with occipital calcifications or folate deficiency and cerebellar ataxia. There have been reports of brain white-matter lesions as an extraintestinal manifestation in Crohn disease and ulcerative colitis but not in CD.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods.<\/jats:title>\n                  <jats:p>In this study, 75 diet-treated mainly pediatric patients with biopsy-proven CD underwent prospectively clinical neurologic examinations, laboratory investigations, electroencephalography, computed tomography, and magnetic resonance imaging. The age range was 2.8 to 24.2 years with a mean of 11.6 years. The mean period of gluten exposure was 2.4 years.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results.<\/jats:title>\n                  <jats:p>Ten patients had neurologic findings such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development. No folate deficiency was found. The hippocampal regions showed no abnormalities. Computed tomography did not reveal any cerebral calcifications, but magnetic resonance imaging detected unilateral and bilateral T2-hyperintensive white-matter lesions in 15 patients (20%). There was no correlation between these lesions and dietary compliance or neurologic or electroencephalographic abnormalities. The mean gluten exposure time of these patients was slightly increased (not significant).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions.<\/jats:title>\n                  <jats:p>Focal white-matter lesions in the brain may represent an extraintestinal manifestation of CD. They may be ischemic in origin as a result of a vasculitis or caused by inflammatory demyelination. They seem to be more typical of pediatric CD than cerebral calcifications. Their prognostic value is unclear and needs to be elucidated in additional studies. CD should be suggested as a differential diagnosis in children with unclear white-matter lesions even without intestinal symptoms.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1542\/peds.108.2.e21","type":"journal-article","created":{"date-parts":[[2004,8,13]],"date-time":"2004-08-13T23:55:51Z","timestamp":1092441351000},"page":"e21-e21","source":"Crossref","is-referenced-by-count":103,"title":["Brain White-Matter Lesions in Celiac Disease: A Prospective Study of 75 Diet-Treated Patients"],"prefix":"10.1542","volume":"108","author":[{"given":"Matthias","family":"Kieslich","sequence":"first","affiliation":[{"name":"From the Departments of Pediatrics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Germa\u0301n","family":"Erra\u0301zuriz","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans Georg","family":"Posselt","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Walter","family":"Moeller-Hartmann","sequence":"additional","affiliation":[{"name":"Neuroradiology, Johann Wolfgang Goethe University, Frankfurt\/Main, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Friedhelm","family":"Zanella","sequence":"additional","affiliation":[{"name":"Neuroradiology, Johann Wolfgang Goethe University, Frankfurt\/Main, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hansjosef","family":"Boehles","sequence":"additional","affiliation":[{"name":"From the Departments of Pediatrics and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2001,8,1]]},"reference":[{"key":"2021121003514956900_B1","doi-asserted-by":"crossref","first-page":"172","DOI":"10.1111\/j.1651-2227.1987.tb10442.x","article-title":"Late onset coeliac disease in the monozygotic twin of a coeliac child.","volume":"76","author":"Salazar de Sousa","year":"1987","journal-title":"Acta Paediatr Scand"},{"key":"2021121003514956900_B2","doi-asserted-by":"crossref","first-page":"1503","DOI":"10.1111\/j.1572-0241.2000.02087.x","article-title":"Gluten sensitivity in monozygous twins: a long-term follow up of five pairs.","volume":"95","author":"Bardella","year":"2000","journal-title":"Am J Gastroenterol"},{"key":"2021121003514956900_B3","first-page":"267","article-title":"The genetic epidemiology of coeliac disease.","volume":"1","author":"Ellis","year":"1986","journal-title":"Genet Epidemiol Suppl"},{"key":"2021121003514956900_B4","doi-asserted-by":"crossref","first-page":"76","DOI":"10.1006\/mgme.2000.3045","article-title":"Genetics of celiac disease","volume":"71","author":"Clot","year":"2000","journal-title":". 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