Celiac disease is an immune-mediated intolerance to gluten, which is found in grains such as wheat and barley. Its estimated prevalence is ∼1% and it remains underdiagnosed in many countries. It causes an enteropathy leading to macro- and/or micronutrient malabsorption, most commonly of iron, vitamin B12, vitamin D, and calcium. Deficiencies of only one or a few nutrients are the most common manifestation of non-diarrheal, “silent” celiac disease, which accounts for 50% of initial presentations.1 Immune- and nonimmune mechanisms provoke diverse neurologic complications in celiac disease including peripheral neuropathy and ataxia.2 ### Case report. We investigated a 58-year-old French-Canadian man with 1 year of progressive leg stiffness and gait unsteadiness. He had mild, longstanding, biopsy-proven celiac disease presenting with dermatitis herpetiformis in 1980. He had received replacement therapy for iron-deficiency anemia and vitamin B12 deficiency during the last decade. There were no other symptoms of celiac disease and he did not adhere to a gluten-free diet. Two of five siblings have celiac disease without neurologic symptoms. CSF and urine examinations were normal. Blood studies revealed a mild microcytic anemia (131 g/L) with acanthocytes; mildly elevated transaminases; serum α-tocopherol (vitamin E) 2.22 × 10−3); serum ceruloplasmin 200 mg/L); …
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Henri‐Bhargava et al. (2008) studied this question.
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