Heightened responsiveness to gluten is not confined to the gut
- M Hadjivassiliou, Senior registrar in neurology. (firstname.lastname@example.org),
- R A Grünewald, Acting head, academic section of clinical neurology.,
- G A B Davies-Jones, Consultant neurologist.
- Department of Neurology, Royal Hallamshire Hospital, Sheffield S10 2JF
In a lecture entitled “On the coeliac affection”1 given in London in 1887 Dr Samuel Gee first described the condition we now refer to as coeliac disease or gluten sensitive enteropathy. With clinical manifestations confined to the gastrointestinal tract or attributable to malabsorption, it was logical to assume that the key to the pathogenesis of this disease resided in the gut. However, focusing diagnostic criteria on the gut (as most physicians still do) has delayed the appreciation of the wider spectrum of gluten sensitivity.
The treatment of coeliac disease remained empirical until 1940-50, when the Dutch paediatrician Willem Dicke noted the deleterious effect of wheat flour on individuals with coeliac disease.2 Removal of all dietary products containing wheat resulted in complete resolution of the gastrointestinal symptoms and a resumption of normal health. The introduction of the small bowel biopsy in 1950-60 confirmed the gut as the target organ in coeliac disease. The characteristic features of villous flattening, crypt hyperplasia, and increase in intraepithelial lymphocytes …