The Best of Dr. Marios Hadjivassiliou and colleagues
Gluten Sensitivity as a Neurological Illness
”But antigliadin antibodies lack specificity”
IgG anti-gliadin antibodies have been the best diagnostic marker in the neurological population we have studied. IgG anti-gliadin antibodies have a very high sensitivity for CD but they are said to lack specificity. In the context of a range of mucosal abnormalities and the concept of potential CD, they may be the only available immunological marker for the whole range of gluten sensitivity of which CD is only a part. Further support for our contention comes from our HLA studies. Within the group of patients with neurological disease and gluten sensitivity (defined by the presence of anti-gliadin antibodies) we have found a similar HLA association to that seen in patients with CD: 70% of patients have the HLA DQ2 (30% in the general population), 9% have the HLA DQ8, and the remainder have HLA DQ1. The finding of an additional HLA marker (DQ1) seen in the remaining 20% of our patients may represent an important difference between the genetic susceptibility of patients with neurological presentation to those with gastrointestinal presentation within the range of gluten sensitivity.
”But antigliadin antibodies have been superseded by anti-endomysial and transglutaminase antibodies”
The introduction of more CD specific serological markers such as antiendomysium and more recently transglutaminase antibodies may have helped in diagnosing CD but their sensitivity as
markers of other manifestations of gluten sensitivity (where the bowel is not affected) is low. This certainly reflects our experience with patients with gluten sensitivity who present with neurological
dysfunction. Endomysium and transglutaminase antibodies are only positive in the majority but not in all patients who have an enteropathy. Patients with an enteropathy represent only a third of patients with neurological manifestations and gluten sensitivity. Antigliadin antibodies unlike endomysium and transglutaminase antibodies are not autoantibodies. They are antibodies against the protein responsible for gluten sensitivity.
From: The Neurology of Gluten Sensitivity: Science vs. Conviction
by Hadjivassiliou and Grunewald 2004
"There is also confusion about the role of antigliadin antibodies as a screening tool. Given that gluten sensitivity can exist without enteropathy, it is inappropriate to estimate sensitivity and specificity of these antibodies against the presence of enteropathy as the 'gold standard'. To assert that antigliadin antibodies lack specificity based on the fact that 10% of the healthy population may have them is a misconception. It is entirely plausible that 10% of the healthy population with circulating antigliadin antibodies have gluten sensitivity without recognized manifestations. The prevalence of coeliac disease itself is now recognized to be 20 times higher than what it was thought to be 20 years ago because most cases are clinically silent. It is important to realize that amongst the 10% antigliadin antibody positive people lurks those with 'silent' gluten sensitive enteropathy."
"It is ill-considered to suggest that antigliadin antibodies should not be used as a screening tool because they are found in “healthy” individuals. It is also irresponsible to suggest that neurological patients should not be screened for coeliac disease unless additional factors are present such as unexplained anaemia or evidence of malabsorption."
"Neurologic manifestations of gluten sensitivity are a scientific fact, not a theological issue. Whilst the debate continues, we owe it to our patients to screen them effectively for gluten sensitivity with the simple widely available antigliadin antibody test so that we do not in the meantime deprive them of a harmless but potentially effective treatment in the form of a gluten-free diet."
Sensory ganglionopathy due to gluten sensitivity. Sept 2010
Celiac disease presenting with motor neuropathy: effect of gluten free-diet May 2007
Myopathy associated with gluten sensitivity, Dec 2006
Dietary treatment of gluten neuropathy, Sept 2006
Neuropathy associated with gluten sensitivity, Nov 2006
Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia, Feb 2006
Cerebellar abnormalities on proton MR spectroscopy in gluten ataxia, July 2005 - free full text
Are lower gastrointestinal investigations necessary in patients with coeliac disease? Jun 2005
Multiple sclerosis and occult gluten sensitivity. Mar 2005
Making the diagnosis of coeliac disease: is there a role for push enteroscopy? Nov 2004
The immunology of gluten sensitivity: beyond the gut. Nov 2004
Gluten sensitivity masquerading as systemic lupus erythematosus. Nov 2004 - free full text
The Neurology of Gluten Sensitivity: Science vs. Conviction - 2004
Choreic syndrome and coeliac disease: a hitherto unrecognised association, Apr 2004
Dietary treatment of gluten ataxia. Sept 2003 - free full text
A primary care cross-sectional study of undiagnosed adult coeliac disease. Apr 2003
Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Mar 2003 - free full text
Gluten Sensitivity: Time to move from Gut to Brain. Jan/Feb 2003
The humoral response in the pathogenesis of gluten ataxia. Apr 2002
Gluten sensitivity as a neurological illness. May 2002 - free full text
Headache and CNS white matter abnormalities associated with gluten sensitivity. Feb 2001
Gluten sensitivity: a many headed hydra. Jun 1999 - free full text
Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Nov 1998
Neuromuscular disorder as a presenting feature of coeliac disease. Dec 1997 - free full text
Does cryptic gluten sensitivity play a part in neurological illness? Feb 1996