N R Rosenberg1, M Vermeulen. 1. Department of Neurology, Academic Medical Centre, University of Amsterdam, Amsterdam, Netherlands. n.r.rosenberg@amc.uva.nl
Abstract
OBJECTIVE: To investigate whether there is an association between chronic peripheral neuropathy and coeliac disease. METHODS: The cause of chronic peripheral neuropathy was first investigated in a group of 478 patients. Published reports were then examined systematically for an association between chronic peripheral neuropathy and coeliac disease. Cases were divided into two groups: group A, polyneuropathy preceding duodenal biopsy and controls undergoing duodenal biopsies; group B, coeliac disease preceding polyneuropathy. Patients with cerebellar ataxia, small fibre neuropathy, or a cause for their neuropathy were excluded. RESULTS: In 425 of the 478 patients, a cause other than coeliac disease was established. In the patients with no determined cause for neuropathy, one had abnormally increased IgA antigliadin antibodies but duodenal biopsy was normal. Ten previous studies of patients with chronic peripheral neuropathies were reviewed. The incidence of biopsy proven coeliac disease in patients with polyneuropathy did not differ from the controls (group A). In patients with a proven coeliac disease (group B), polyneuropathy could not be diagnosed more often than in the general population. CONCLUSIONS: The results of both the clinical study and the literature review suggest that it is unlikely that chronic peripheral neuropathy without other neurological signs is associated with coeliac disease.
OBJECTIVE: To investigate whether there is an association between chronic peripheral neuropathy and coeliac disease. METHODS: The cause of chronic peripheral neuropathy was first investigated in a group of 478 patients. Published reports were then examined systematically for an association between chronic peripheral neuropathy and coeliac disease. Cases were divided into two groups: group A, polyneuropathy preceding duodenal biopsy and controls undergoing duodenal biopsies; group B, coeliac disease preceding polyneuropathy. Patients with cerebellar ataxia, small fibre neuropathy, or a cause for their neuropathy were excluded. RESULTS: In 425 of the 478 patients, a cause other than coeliac disease was established. In the patients with no determined cause for neuropathy, one had abnormally increased IgA antigliadin antibodies but duodenal biopsy was normal. Ten previous studies of patients with chronic peripheral neuropathies were reviewed. The incidence of biopsy proven coeliac disease in patients with polyneuropathy did not differ from the controls (group A). In patients with a proven coeliac disease (group B), polyneuropathy could not be diagnosed more often than in the general population. CONCLUSIONS: The results of both the clinical study and the literature review suggest that it is unlikely that chronic peripheral neuropathy without other neurological signs is associated with coeliac disease.
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