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Objectives: To describe the range of neuromuscular disorders which may be associated with cryptic coeliac disease., Methods: Nine patients were described with neuromuscular disorders associated with circulating antigliadin antibodies, whose duodenal biopsies later confirmed the diagnosis of coeliac disease. Neurological symptoms antedated the diagnosis of coeliac disease in all, and most had minimal or no gastrointestinal symptoms at the onset of the neuromuscular disorder., Results: Three patients had sensorimotor axonal peripheral neuropathy, one had axonal motor peripheral neuropathy, one had probable inclusion body myositis and axonal motor peripheral neuropathy, one had polymyositis and sensorimotor peripheral neuropathy, one had mononeuropathy multiplex, one had neuromyotonia, and one had polyneuropathy., Conclusion: A wide range of neuromuscular disease may be the presenting feature of coeliac disease. This represents the first report of inclusion body myositis and neuromyotonia associated with coeliac disease. Estimation of circulating antigliadin antibodies should be considered in all patients with neuromuscular disease of otherwise obscure aetiology.

Objectives: To prospectively study the clinical, neurophysiological and neuropathological characteristics of axonal neuropathies associated with positive antigliadin antibodies and the prevalence of such neuropathies in a cohort of patients with sporadic axonal neuropathy. Methods: Prospective screening (using antigliadin, antiendomysium and tissue transglutaminase antibodies) of patients with peripheral neuropathy attending a neurology clinic. Results: 215 patients with axonal neuropathy were screened. 141 patients had symmetrical sensorimotor neuropathy, 47 had mononeuropathy multiplex, 17 had motor neuropathy and 10 had small-fibre neuropathy. Despite extensive investigations of the 215 patients, 140 had idiopathic neuropathy. Positive immunoglobulin (Ig)G with or without IgA antigliadin antibodies was found in 34% (47/140) of the patients with idiopathic neuropathy. This compares with 12% prevalence of these antibodies in the healthy controls. The prevalence of coeliac disease as shown by biopsy in the idiopathic group was at least 9% as compared with 1% in the controls. The clinical features of 100 patients (47 from the prevalence study and 53 referred from elsewhere) with gluten neuropathy included a mean age at onset of 55 (range 24–77) years and a mean duration of neuropathy of 9 (range 1–33) years. Gluten-sensitive enteropathy was present in 29% of patients. The human leucocyte antigen types associated with coeliac disease were found in 80% of patients. Conclusions: Gluten sensitivity may be aetiologically linked to a substantial number of idiopathic axonal neuropathies. [ABSTRACT FROM AUTHOR]

Editorial. Focuses on coeliac disease or gluten sensitivity enteropathy. History of the treatment of coeliac disease; Association between neurological disorders and adult coeliac disease; Typical clinical manifestation of a patient with gluten sensitivity.