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Neurological Deficits in Patients With Celiac Disease
Adi Vaknin-Dembinsky, MD;
Rami Eliakim, MD;
Israel Steiner, MD
Arch Neurol. 2002;59:647-648.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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INTRODUCTION
Celiac disease (CD) is an autoimmune enteropathy triggered by the ingestion
of gluten in genetically susceptible individuals.1
Developments in the understanding of the pathogenetic basis of the disease
and the introduction of serological diagnostic markers have enabled the delineation
of its epidemiological features and its clinical spectrum. This, in turn,
has led to increased interest in the possible neurological manifestations
and involvement in patients with this disorder.
CLINICAL DESCRIPTIONS
Celiac disease is clinically characterized by a malabsorption syndrome,
weight loss, abdominal distention, diarrhea, steatorrhea, malaise, iron deficiency
anemia, and bone disease. Most of these features were already noted in the
first description of the disorder, dated 200 AD:
The stomach being the digestive organ, labors in digestion when
diarrhea seizes the patient. If this diarrhea does not proceed from a slight
cause of only one or two days' duration, and if, in addition, . . . [Full Text of this Article]
DIETARY THERAPIES
OTHER LANDMARKS
THE NEUROLOGICAL FEATURES OF CD
From the Department of Neurology, Hadassah University Hospital, Jerusalem
(Drs Vaknin-Dembinsky and Steiner), and the Department of Gastroenterology,
Rambam Medical Center, Haifa (Dr Eliakim), Israel.
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