Coeliac disease is one of the most common chronic diseases encountered in the Western world with a serological prevalence of approximately 1%.
Yet the numbers of people estimated to have diagnosable coeliac disease in the UK but have yet to be identified against those that have been diagnosed is a remarkable 8:1.
Numerous related conditions have been attributed to this diagnosis and it is likely that there frequency and causal association will continue to be reviewed and altered accordingly. Some of the related conditions are indicated below.
Autoimmune diseases constitute clinically important associations, of which Type 1 diabetes mellitus and thyroid disorders are the most important. Addison’s disease and psoriasis are also increased in frequency when the patient has coeliac.
Several liver disorders, including primary biliary cirrhosis and primary sclerosing cholangitis, are also associated. Ischaemic heart disease and cerebrovascular disease risk increases with coeliac disease. The frequency of malignant complications of coeliac disease appears to be much lower than earlier studies have indicated, with lymphoma increased by approximately five-fold and the absolute number of tumours is small.
The increase in fracture risk in coeliac disease exists but is only modest. 
Although neurological and psychiatric conditions affect coeliac patients, no disorder specifically associated with coeliac disease has been identified.  The most commonly reported ones are epilepsy, depression and migraine.
Reproductive problems have been over exaggerated albeit that there remains a relationship between coeliac, infertility, miscarriage and lowered birth weight.
It is important that these co-morbidities are recognised because if not, symptoms will be falsely attributed to deliberate or inadvertent ingestion of gluten, rather than prompt a search for a second diagnosis. Furthermore, in a patient with an established diagnosis that is considered falsely to account for the whole clinical picture, coeliac disease is likely to remain undetected.
So, we can see that many systems of the body outside of the GI tract have been identified as ‘target organs’ for auto-immune response to wheat / gluten ingestion in sensitive individuals with varied and unrelated conditions.
To summarise and to highlight some of the clinical pearls that Dr O’Bryan will be covering in his 5th March 2011 lecture:
- Numerous auto-immune diseases are directly linked to Gluten Sensitivity & CD.
- Gluten Sensitivity can have a major role in determining whether the brain ages successfully or experiences a Neurodegenerative disease.
- Brain disorders such as ADHD, epilepsy, depression, anxiety and even eating disorders may be associated with Gluten Sensitivity and CD.
- Musculo-skeletal complaints such as arthritis, RA, myopathies, muscle wasting may be associated with Gluten Sensitivity & CD.
- 31% of patients with inflammatory myopathies are found to have Gluten Intolerance.
- Even osteoporosis may be the only sign of a wheat allergy that can be completely relieved or reversed on a gluten-free diet.
- 70% of unrelenting migraines were completely relieved on a gluten-free diet.
- Cognitive functional decline and underachievement in post-secondary education is 400% more likely with Gluten Sensitivity.
Gluten Sensitivity and CD may be a contributory cause to these conditions, in which it is the only presenting complaint:
Peripheral Neuropathies, Attention Deficit Disorders, Idiopathic Cardiomyopathy, Epilepsy, Multiple Sclerosis, Migraines, Chronic Fatigue Syndrome, Infertility, Miscarriages, Failure to Thrive in children, Myasthenia Gravis, Idiopathic Ataxia, Osteoporosis, Polyneuropathy, Rheumatoid Arthritis, Sjogren’s, Type 1 Diabetes, Addison’s Disease, Anxiety & Depression.
1. Recognise the history and incident frequency of Gluten Sensitivity & CD.
2. Recognise the likelihood of Gluten Sensitivity and CD being associated with various extra-intestinal manifestations.
3. Become familiar with the differential diagnosis of CD and Gluten Sensitivity through saliva, stool and serology results, with in-office examination clues.
4. Become familiar with the effectiveness of treatment for conditions associated with Gluten Sensitivity and CD in its different stages (Acute, Chronic & Rebuilding of damaged Tissue).
5. Learn about NEW testing and follow up monitoring of Gluten Sensitivity and CD.
Advances in our understanding of the pathogenic interactions between genetic, immunological and environmental factors involved in coeliac disease have provided us with promising explanations for the geographical variation, familial risk and sexual bias witnessed in coeliac disease. Universal awareness that nonstereotypical coeliac disease in all ages is on the rise and that the spectrum of associated risk is wider than first thought has refuelled the debate on the need for screening those individuals that are at ‘high risk’.
A. Vojdani, T. O’Bryan and G.H. Kellermann. The immunology of immediate and delayed hypersensitivity reaction to gluten. European Journal of Inflammation. Volume 6 No. 1, January – April 2008 Read Paper
 West J, Logan RF, Hill PG et al. Seroprevalence, correlates, and characteristics of undetected coeliac disease in England. Gut 52(7), 960–965 (2003). View Abstract
 Ludvigsson JF, Ludvigsson J, Ekbom A, Montgomery SM. Celiac disease and risk of subsequent Type 1 diabetes: a general population cohort study of children and adolescents. Diabetes Care 29(11), 2483–2488 (2006). View Abstract
 Sategna-Guidetti C, Volta U, Ciacci C et al. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. Am. J. Gastroenterol. 96(3), 751–757 (2001). View Abstract
 Elfstrom P, Montgomery SM, Kampe O, Ekbom A, Ludvigsson JF. Risk of primary adrenal insufficiency in patients with celiac disease. J. Clin. Endocrinol. Metab. 92(9), 3595–3598 (2007). View Abstract
 Ludvigsson JF, Elfstrom P, Broome U, Ekbom A, Montgomery SM. Celiac disease and risk of liver disease: a general population-based study. Clin. Gastroenterol. Hepatol. 5(1), 63–69, e1 (2007). View Abstract