SAN FRANCISCO—Gluten sensitivity in patients with neuropathy was more frequent than in a control group and much greater than in the general population, according to Lieutenant Colonel Eleanor E. Avery, MD. She advised that a gluten-free diet may be appropriate in patients with antigliadin antibodies, even in the absence of gastrointestinal symptoms.

“The results of our small pilot study are provocative and consistent with previous reports showing enhanced prevalence of gluten sensitivity in neuropathy patients as compared with the general population,” reported Lt. Col. Avery, of the Wilford Hall Medical Center at Lackland Air Force Base, Texas. She presented her findings at the 56th Annual Meeting of the American Academy of Neurology.

Peripheral neuropathy is a common diagnosis among patients with neuropathy, noted Lt. Col. Avery. “Most patients would like an ideology for their diagnosis as well as a specific treatment and prognosis,” she said. “Too often, the neuropathy is labeled as cryptogenic or idiopathic when no answer is found.” Neurologic complications generally occur in up to 10% of patients with established celiac disease; however, gluten sensitivity has been reported to cause neurologic complications even when enteric disease is not present. The prevalence of gluten-sensitive enteropathy is estimated to be between 0.4% and 1% in the United States. “So any prevalence in the neuropathy population that exceeds that might indicate an independent cause/effect relationship,” theorized Lt. Col. Avery.

SCREENING FOR NEUROPATHY

Patients who were examined by a neurologist and believed to have peripheral neuropathy symptoms were sent for standard laboratory screening. The patients’ blood was also sent for an antigliadin antibody panel and any other special tests that the neurologist deemed necessary. Serum was obtained from controls, who were patients hospitalized for other reasons and had no peripheral neuropathy signs or symptoms. The patients were not matched for age, sex, or race.

A total of 70 patients were screened for antigliadin antibodies. Of 45 patients with neuropathy who were tested, Lt. Col. Avery found that 15 patients (33%) had serum immunoglobulin G (IgG) or IgA antigliadin positivity or both IgA and IgG positivity. For controls, four of 25 subjects (16%) had antigliadin positivity. The odds ratio for patients versus controls was 2.58.

GLUTEN SENSITIVITY AND NEUROPATHY

Lt. Col. Avery believes that her findings are important because peripheral neuropathy can lead to significant morbidity. She emphasized that the disorder is typically a distal, symmetric axonal sensory neuropathy and was previously believed to be secondary to fat-soluble vitamin deficiency. “However,” she commented, “recent studies suggest that the neuropathy can occur in the absence of vitamin deficiency and in response to a gluten-free diet. This may indicate that isolated gluten sensitivity can precipitate an autoimmune disease directed at the peripheral nervous system even in the absence of celiac sprue.

“It is not known whether these patients have concomitant celiac disease,” Lt. Col. Avery added. “It has been postulated that gliadin itself is the inciting cause of disease and that neurologic manifestations occur secondary to direct toxicity of gluten without concomitant gastrointestinal disease. These observations may offer alternative treatment modalities, including dietary modification to the usual symptomatic therapies for idiopathic peripheral neuropathy.”

Lt. Col. Avery also said that testing antigliadin antibodies may be a reasonable addition to a standard neuropathy panel. Further studies are now under way to determine the prevalence of gluten sensitivity in a larger population of patients with peripheral neuropathy.

NR

—Colby Stong

Suggested Reading
Briani C, Ruggero S, Zara G, et al. Anti-ganglioside antibodies in children with coeliac disease: correlation with gluten-free diet and neurological complications. Aliment Pharmacol Ther. 2004;20:231-235.
Hadjivassiliou M, Grunewald R, Sharrack B, et al. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain. 2003;126(pt 3): 685-691.

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