PEDIATRICS Vol. 108 No. 2 August 2001, p. e21
Kieslich M, Errazuriz G, Posselt HG, Moeller-Hartmann W, Zanella F, Boehles H.
Departments of Pediatrics, Johann Wolfgang Goethe University, Frankfurt/Main, Germany.

Celiac.com 08/24/2001 - It is well known that celiac disease causes destruction of the villi in the small intestine that results in malabsorption of nutrients in affected individuals. There is solid evidence that additional neurological complications can result, such as epilepsy, possibly associated with occipital calcifications or folate deficiency and cerebellar ataxia. An increase in brain white-matter lesions has been reported in patients with Crohn disease and ulcerative colitis, but until now, not in patients with celiac disease. A recent study published in the August 2, 2001 issue of Pediatrics has now demonstrated a similar increase of these lesions in patients with celiac disease.

The study was carried out by Dr. Kieslich and colleagues of the Departments of Pediatrics, Johann Wolfgang Goethe University, Frankfurt/Main, Germany, on 75 biopsy-proven celiac disease patients who were on a gluten-free diet. Most of the patients in the study were between 2.8 and 24.2 years old, and the mean age was 11.6 years. All of the patients underwent prospectively clinical neurological examinations, laboratory investigations, electroencephalography, computed tomography, and magnetic resonance imaging. According to the study the mean period of gluten exposure was 2.4 years, although it was likely longer as recent studies have shown that many celiacs are asymptomatic for many years before damage occurs that is severe enough to cause obvious symptoms.

The researchers found that ten of the patients had neurological manifestations such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development, although no folate deficiencies were found. Further, the hippocampal regions appeared normal, and no cerebral calcifications were found, however, the MRI results showed unilateral and bilateral T2-hyperintensive white-matter lesions in 15 patients (20%). According to the research, there does not appear to be a relationship between these lesions and dietary compliance or neurological or electroencephalographic abnormalities.

The researchers conclude that focal white-matter lesions in the brain may represent an extra-intestinal manifestation of celiac disease. They theorize that the lesions may be the result of a decreased blood supply caused by the constriction or obstruction of blood vessels due to inflammation, or caused by the destruction of the nerve fiber due to inflammation. Further, children with white-matter lesions, even if they do not have intestinal symptoms, should be tested for celiac disease. Last, more research needs to be done on people celiac disease of all ages to develop a proper predictive value, and to discover the exact cause of the lesions.

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