Premium
Neurological Complications of Celiac Disease and Autoimmune Mechanisms: Preliminary Data of a Prospective Study in Adult Patients
Author(s) -
BRIANI C.,
ZARA G.,
TOFFANIN E.,
RUGGERO S.,
FERRARINI A.,
LAZZARI F.,
LUCA M.,
FAGGIAN D.,
GRASSIVARO F.,
ERMANI M.,
PEZZANI R.,
GIOMETTO B.,
D'ODORICO A.
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1361.056
Subject(s) - medicine , ataxia , subclinical infection , antibody , gastroenterology , prospective cohort study , peripheral neuropathy , antibody titer , immunology , titer , endocrinology , diabetes mellitus , psychiatry
A bstract : Antibodies to gangliosides and Purkinje cells have been reported in patients with celiac disease (CD) with neuropathy and ataxia, respectively. Whether these antibodies are pathogenic is not clear. The response of neurological symptoms and antibody titers to a gluten‐free diet is still controversial. The objective of our study was to assess whether neurological manifestations in CD patients correlate with antibody titers and a gluten‐free diet.Thirty‐five CD patients (9 males, 26 females, mean age 37.1 ± 12.6 yrs) were followed prospectively. At initial evaluation, 23 were on a gluten‐free diet, 12 were not. At recruitment and during follow‐up, patients underwent neurological and electrophysiological evaluation. IgG, IgM, and IgA anti‐ganglioside antibodies were assayed by ELISA; anti‐neuronal antibodies were assessed by immunohistochemistry and Western blot. Four patients, all males, had electrophysiological evidence of neuropathy; three had been on a gluten‐free diet for several months, and one was newly diagnosed. One had reduced tendon reflexes; another complained of distal paresthesias. With regard to anti‐ganglioside antibodies, three patients had a moderate increase in antibodies without symptoms or signs of neuropathy. No patients had ataxia or cerebellar dysfunction, although in four patients reactivity to neuronal antigens was found. In 17 patients, an electrophysiological follow‐up (mean duration of follow‐up, 9 months) showed no changes. In conclusion, the preliminary results of this prospective study indicate that neuropathy, usually subclinical, may accompany CD. Antibody titers do not seem to correlate with neurological symptoms/signs or diet. Ongoing follow‐up will help confirm these data and clarify the role, if any, of antibodies in neurological involvement in CD.