LUIGI GRECO NOVEMBER 14TH

2004

OMGE Practice Guideline

Celiac Disease

First Draft 1.0 summer 2004

Review Team: Professor J. Bai (chairman) Professor G.R. Corazza Professor D. Schuppan Professor M.J.G.Farthing Professor C. Catassi Professor L. Greco Professor H. Cohen Professor M. Fried Professor E Zeballos Drs J.H. Krabshuis

Sections: 1. Definitions 2. Key Points 3. Epidemiology 4. Pathology, natural history and associated conditions 5. Diagnosis of celiac disease 6. Management of celiac disease 7. Screening for Celiac Disease 8. Useful Websites 9. Guidelines, listserver, and further reading 10. Queries and Feedback from you

1 Definitions

Celiac sprue : An enteropathy affecting the (small) intestine in genetically predisposed children and adults, precipitated by the ingestion of gluten-containing foods.

Gluten: The storage proteins of wheat, rye and barley which give the dough its strong elastic character.

2 Key Points Key Points to remember:

The prevalence of celiac disease in a healthy adult population varies between one in 100 and one in 300

Many patients with celiac disease have minimal symptoms or present atypically

To make a diagnosis of celiac disease the patient should have:

o Characteristic histopathologic changes in an intestinal biopsy and

o Clinical improvement in response to a gluten free diet

o Produce specific autoantibodies (anti TGASE)

Serological tests have a role in:

Screen at risk and not at risk individuals

o Identifying patients for whom biopsy might be warranted

o Monitoring concordance with the diet : useless for this purpose, become positive months after the gluten induced damage ensued

o Investigating patients at increased risk of the disease

o Confirming a CD diagnosis

Patients with celiac disease should not eat wheat, rye, or barley

Patients need to follow a strict gluten free diet for the rest of their lives

Patients with celiac disease have an increased risk of death compared with the general population. But this excess death rate returns to normal after three to five years on a strict gluten free diet

On average CD is diagnosed >10 years late : ONCE !!! Not for children !

It is not true only Caucasians are affected

Oats are OK but must be pure; a small subgroup (5%) of coeliacs should not eat Oats

Corn and rice-based diets are OK

1st degree and (to a lesser extent) 2nd degree relatives are at an increased risk for CD

Think of the iceberg

3 Epidemiology Introduction Not so long ago it was thought that CD was a rare condition and that it occurred only in Caucasians, mostly in children with a typical presentation of weight loss and diarrhoea. We know now this is not true.

CD is common worldwide and affects around 1:100 to 1:300

The female to male ratio is 2:1

CD occurs frequently without GI symptoms

The risk of CD is raised in 1st and (less so in ) 2nd degree relatives

There is no substantial difference as regards symptomatic subjects and ‘not-at-risk’ subjects in all those countries or geographic areas where epidemiological studies were done.

CD epidemiology has iceberg characteristics – there are far more undiagnosed cases (below the waterline) than diagnosed cases (above the waterline)

The risks are much greater in first (up to 10%) and less so in 2nd degree relatives as well in people with diabetes and other autoimmune diseases, IBS (not enough data to be quoted !), Down’s syndrome and a number of other associated diseases (see 5.7)

There may be unfavourable associations between fertility and CD

Pregnancy may present a unfavourable course in undiagnosed CD patients, specially in those who had symptoms earlier.

A clinically severe picture can onset during pregnancy or puerperium in up to 17% of female cases.

3.1 Prevalence and Incidence The prevalence of CD , that is the number of cases that are present in a population at a given time, varies in different regions of the world. It is uncertain whether the number of new cases of CD found in a specific period in a given population (the incidence) is increasing locally or globally. Most commentators agree on the iceberg image – prevalence then refers to the total size of the iceberg – the area below the waterline represents the total number of un-diagnosed cases in a given population at a particular point in time. The area above the waterline – the tip of the iceberg – represents the number of clinically diagnosed cases.

The Iceberg

The Celiac Iceberg In 1991 Richard Logan published his idea of a Celiac Iceberg. In Europe for every case of celiac disease diagnosed there would be many that remained undiagnosed, either because they were latent, silent, misdiagnosed or asymptomatic. The ratio of diagnosed to undiagnosed in Europe is around 7-8:1 A key study in 2003 by Fasano et al (ref no 9) found a prevalence of CD as follows: At risk - first degree relatives : 1:22 At risk - second degree relatives : 1:39 At risk - symptomatic patients : 1:56 Not at-risk groups : 1:133

It is now accepted that the total size of the iceberg is more or less the same world-wide although the ‘waterline’ may differ from continent to continent. In Europe and the US for example – the prevalence is similar in a healthy population and in ‘at-risk’ groups but the iceberg appears to be more submerged in the US – fewer cases are diagnosed there than in Europe. Celiac disease goes hand in hand with the prevalence of DQ2 and to a minor degree DQ8. This is a necessary but not a sufficient condition for the development of CD. Gluten load is a key factor – there is no CD without gluten. There are further environmental triggers, for example Th1-weighted intestinal infections, most prominent e.g., in Saharawis. Populations that do not have DQ2, e.g., Chinese and Japanese are not expected to develop celiac disease except for those with DQ8.

4 Pathology, Natural History and Associated Conditions 4.1 Genetic predisposition

Celiac disease is a multigenic disorder associated with HLA-DQ2 (DQA1*05/DQB1*02) or HLA-DQ8 (DQA1*0301/DQB1*0302).

HLA-DQ2 is expressed in more than 90% of people with celiac disease. The expression of these HLA-DQ2 or HLA-DQ8 molecules is necessary, but not sufficient, to develop the disease. Results of studies in siblings (sib recurrence risk for celiac disease is 10%)

and identical twins (85% concordance, ref Greco GUT 2002) suggest that HLA genes are essential but not the only genes required to manifest the disease. HLA genes are estimated to contribute to about 1/3rd of the genetic variance of the disease. - Actually 4 genetic predisposition sites have been located and named in OMIM : Coeliac1 : HLA DQ Genes, Coeliac2 : CTLA4 site in Chromosome 2, Coeliac 3 : Chrom 5q31-33, and, recently Chromosome 19.

GENETIC PREDISPOSITION RISK

General population 1%

Individual DQ2 or DQ8 + 2%

First degree relatives, unknown HLA 10%

First degree relatives DQ2 or 8 + 20%

4.2 Pathogenesis

Recent evidence suggests that the gluten-induced up-regulation of zonulin, an intestinal peptide involved in the regulation of tight junctions is responsible at least in part for the aberrant increase in gut permeability that is characteristic of the early phase of celiac disease and the subsequent abnormal passage of gluten into the lamina propria. The protein is deamidated by tissue transglutaminase in the lamina propria and is then recognized by antigen-presenting cells bearing HLA-DQ2 or DQ-8, thereby triggering the autoimmune reaction of celiac disease 4.3 Natural history The natural history of CD remains unclear; further research is required to understand the natural history in asymptomatic CD patients. Most of our current knowledge is related to the natural history and clinical course of CD in diagnosed patients (most of them at the severe end of the clinical spectrum). If CD remains unrecognised it can increase the risk of life-threatening complications which are difficult to manage – for example intestinal lymphoma. Table 1 complications if CD remains undiagnosed:

- cancer (overall 1.3:1) (excluding colorectal cancer) - malignant lymphomas - small bowel neoplasia - oropharyngeal tumors - large intestine adenocarcinomas - unexplained infertility (12%) - osteoporosis (increased risk for classically symptomatic patients) - stunted growth - autoimmune diseases. A recent study found that undiagnosed celiac disease does not appear to be associated with unfavourable outcome of pregnancy.

4.4 Associated Conditions 4.4.1 Malignant disease

Malignant diseases are more frequent in patients with celiac disease. Small bowel adenocarcinoma, oesophageal and oropharyngeal squamous carcinoma and non-Hodgkin lymphoma occur more often in CD patients than in healthy controls. A gluten-free diet is thought to be protective against the development of malignant disease, although this might not be the case for the development of Enteropathy-associated-T-cell lymphomas in coeliacs diagnosed above the age of 50.

4.4.2 Osteoporosis Measurement of bone mineral density is recommended when celiac disease has been diagnosed because reduced bone density is common in both adults and children with CD. The reduction in bone density is more severe in symptomatic celiac disease than in the silent form and is associated with an increased risk of fracture. Bone mineral density improves after a gluten-free diet, but might not attain the normal range. 4.4.3 Fertility

Celiac disease may be associated with delayed menarche, premature menopause, amenorrhoea, recurrent abortions, and fewer children. Research results have found infertility in subsets of patients but also a normal number of pregnancies and children in other patients. Further research is needed.

Patients with celiac disease are also reported to have babies with low birthweight, increased perinatal mortality, and a shorter duration of breast feeding. Adherence to a gluten-free diet is associated with a return to normal outcomes.

Celiac disease may have clinical manifestations for the first time during pregnancy or puerperium. Undiagnosed celiac disease has been detected in infertile women who were screened for the disease, and but not in all studies.

Infertility in men is also associated with celiac disease. Furthermore, men with the disease also tend to have children with a shorter gestation and lower birthweight than those without the disease.

4.4.4 Autoimmune disorders Whether celiac disease is an inflammatory disorder with secondary autoimmune reactions or whether it is a primary autoimmune disease induced by a known exogenous factor remains unclear. Autoimmune disorders arise ten times more often in patients with celiac disease than they do in the general population. Such disorders include: Insulin dependent diabetes Thyroid disease

Sjögren's syndrome Addison's disease autoimmune liver disease cardiomyopathy neurological disorders.

When both autoimmune disease and celiac disease occur in a patient, celiac disease is frequently silent and as a result the autoimmune disorder is usually diagnosed first.

4.4.5 Dermatitis Herpetiformis

Dermatitis herpetiformis is considered as the skin manifestation of gluten sensitivity in patients with celiac disease .

Dermatitis herpetiformis (DH) is a severe itchy, blistering skin disease . The rash usually occurs on the elbows, knees, and buttocks. Although people with DH do not usually have digestive symptoms, they often have the same intestinal damage as people with CD.

DH is diagnosed by skin biopsy. DH is treated with a Gluten Free Diet (GFD) and medication to control the rash, for example with dapsone or sulfapyridine. The drug treatment may last several years.

Both the skin and the small bowel diseases are gluten dependent and are strongly associated with HLA DQ with no genetic differences to explain the two phenotypes.

5 Diagnosis of Celiac Disease

5.1 Introduction The clinical classification of CD has undergone change ; today most experts agree with a classification as follows Classical - mostly GI-symptoms Atypical - mostly non-GI symptoms – usually mono or oligo-symptomatic. Silent - no symptoms despite the presence of intestinal lesion 5.2 Differential Diagnosis CD presents a very complex and protean clinical picture and there are many diseases with mucosal changes similar to those of celiac disease. Table 2 Conditions with mucosal changes similar to celiac disease

Cow's milk intolerance

Chronic and persistent infantile diarrhoea

Tropical sprue

HIV enteropathy

Radiation damage

Recent chemotherapy

Graft-vs.-host disease

Chronic ischaemia

Giardiasis

Crohn's disease

Autoimmune enteropathy

Enteropathy-associated T-cell lymphoma

Combined immunodeficiency states

Gastroenteritis

Eosinophilic gastroenteritis

Severe malnutrition

Zollinger-Ellison syndrome

Refractory sprue

Collagenous sprue 5.3 Diagnostic Tests Only endoscopy with biopsy of the small intestine plus a positive celiac disease serology provide a definitive diagnosis .This is the gold standard.

Table 3 Diagnosis of Celiac Disease

Role of endoscopy for suspicion of celiac disease Although endoscopy may provide an indication for intestinal biopsy it may not be sufficiently sensitive to detect all manifestations of celiac disease in a population. The characteristic findings of an endoscopy include:

Flattened folds

Smaller size and or disappearing with maximum insufflation

Scalloped folds and mosaic pattern

increased intra-epithelial lymphocytes or plasma cells. Intestinal Biopsy Intestinal biopsies together with a positive serology represent the gold standard for diagnosing celiac disease. Multiple biopsies are taken from the second or third part of the duodenum. Endoscopy has become the most convenient method of obtaining biopsies of the small intestinal mucosa. Crosby capsule ingested non-invasively by the patients provides the best samples. Histological characteristics of celiac enteropathy Marsh's classification of small intestinal lesions : stage 0 pre-infiltrative mucosa stage I increase in the number of intra-epithelial lymphocytes t more than 30 per

100 enterocytes and infiltration of the lamina propria with lymphocytes. stage II crypt hyperplasia stage III villous atrophy; A partial, B subtotal, C total. stage IV total villous atrophy 5.4 The Global Aspect

The diagnosis of celiac disease can be made with different diagnostic technologies in different parts of the world depending on available resources but specificity and validity of the results may vary as ‘below-gold’ standard tools are used. Depending on available resources diagnostic options can be cascaded from a highly resourced setting where the above gold-standard can be used -- endoscopy followed by small bowel biopsy and specific serology for confirmation -- to a situation where very few resources are available and only the minimal can be done. The positive predictive value (and also the negative predictive value) of endoscopic markers of mucosal atrophy is very high in places where prevalence of celiac disease is very high.

The ‘serology’ option should be much re-evaluated : The anti –TGASE antibodies ARE THE ONLY PATHOGENETIC MARKER OF CD , dimensionally more specific than any histology. But they are not enough. So we should not talk any more of ‘serology’ which is related to the old fashioned AGA, which performed quite badly! Now we should speak of SPECIFIC AUTOANTIBODIES which are the hallmark of this autoimmune disease. In absence of the biopsy the criteria is : - presence of Auto-Antibodies - show the gluten-dependance of the auto-antibodies title and clinical sympthoms,

when present : so decrease of sympthoms and lowering of anti-TGASE title with gluten free diet. In children catch up growth, when applicable.

If endoscopy is not available 'serology only' remains a feasible method for diagnosing CD, also because serological tests are cheaper than endoscopy and biopsy and their statistical value is very similar. The easiest and cheapest serological test would be the dot ELISA . Once a bedside iGA anti tTG test is available and sufficiently sensitive and specific it would be ideal for low income regions. If a geographic area has very limited resources, clinical aspects become the most important diagnostic tool. A rice or corn-based GFD is the final and vital step in confirming a diagnosis of Celiac Disease. Table 4 Cascade for diagnosing CD

1. Autoantibodies and Endoscopy with intestinal biopsy (gold standard) 2. Endoscopy only 3. AUTOANTIBODIES

- EMA+tTG or IgA anti tTG and/or EmA (depending on availability and experience) - EmA alone - Dot ELISA ????? Still a dream, shall we quote it in a protocol ?

4. Combinations of the above ???? CONFUSING 5. Diagnosis based on ‘clinical aspects’ with clinical, histological or serological

improvement after corn or rice-based GFD CONFUSING

Although endoscopy is a very useful tool to detect CD it cannot be relied on as a single diagnostic procedure because the presence of markers of mucosal atrophy maybe highly suggestive of CD in places where the disease is common. By contrast, in other areas of the world a differential diagnosis needs to take account of other disorders prevalent in that part of the world – for example malnutrition, heavy chain disease etc) Nevertheless, the procedure is very helpful when markers are seen in the course of endoscopies ordered for other reasons. Then the endoscopist must be alert and proceed to intestinal biopsy.

5.5 Use of serum antibodies to diagnose Celiac Disease Table 5 Serological tests in celiac disease Serological test Sensitivity (%) Specificity (%) IgA EMA Indirect immunofluorescence 85-98 97-100 Guinea pig tTG 95-98 94-97 Human tTG 85-98 90-95 (Many false positives– especially in liver disease) 5.6 Key Symptoms Adults – GI symptoms

- Chronic diarrhoea (most common symptom) - weight loss - anemia - abdominal distension - lassitude & malaise

Children – GI symptoms

- failure to thrive, weight loss, downshift of weight or height centile, short stature

- vomiting - diarrhoea - recurrent abdominal pain - muscle wasting - ‘irritable’ bowel - hypoproteinemia - irritability and unhappiness

Adults and children – Non-GI symptoms - iron deficiency/anemia - dermatitis herpetiformis - peripheral neuropathy - folic acid deficiency - reduced bone density - unexplained infertility Consider CD in case of: - Unexplained folic acid - Iron or B12 deficiency - Reduced serum albumin - Unexplained hypertransaminasaemia - Osteoporosis and osteomalacia - Recurrent abdominal pain or bloating - Skin rashes

Why is Celiac Disease difficult to diagnose?

o Alternative diagnosis (often irritable bowel syndrome) o The condition may be asymptomatic o The condition may have latent periods o Clinicians are ‘unaware’ and there are several ‘myths’:

o CD is rare o CD occurs in Caucasians only o CD occurs mostly in Europe and the US o CD occurs only in childhood o CD can be cured after (a period of) treatment

5.7 Risks An elevated risk for CD exists in: - First and 2nd degree relatives (10% base, 20% if DQ2 or DQ8 +) - Down syndrome (12%) - Autoimmune thyroid disease (5%) - Chronic active hepatitis - Type 1 Diabetics (5-6%) - Lymphocytic colitis (15-27%) - Chronic fatigue syndrome (2%) Those with CD have an elevated risk for - cancer (overall 1.3:1) - malignant lymphomas - small bowel neoplasia - oropharyngeal tumors - Unexplained infertility (12%) - Osteoporosis (increased risk for classically symptomatic

patients).

6 Management of Celiac Disease

6.1 Management

The current treatment for celiac disease is a strict gluten-free diet for life. In the gluten-free diet wheat, barley, and rye are avoided. Oats are not toxic to patients with celiac disease or dermatitis herpetiformis. However, there is reluctance in some countries to advise liberal use of oats because of the difficulty in guaranteeing that commercially available oats are free of contamination with other grains. Rice and Corn can be part of a GFD.

Initial approach :

VERY FIRST : Do prescribe a ‘natural’ gluten-free regimen (this is a must by the physician who does the diagnosis, then , well after, the dietitian that many times is not so available promptly .

- Refer to dietician and or support group (see websites below) - Screen for iron and folate deficiency - USELESS, no medication, at therapeutic dosage, provides signifcant gluten. VERY VERY rare any report. - Advise bone density tests : NOT FOR ALL !!!! - Advise vitamin D and calcium supplementation if osteoporotic - Advise serological screening for 1st and 2nd degree relatives

Most patients have a rapid clinical response to a gluten-free diet, although the rate of response varies. Patients who are extremely ill might require admission, repletion of fluids and electrolytes, intravenous alimentation, and, occasionally, steroids. Patients should receive iron or folate supplementation if a deficiency in these minerals is documented. (THERE ARE NO CLEAR EBM evidences ! NO CONTROLLED TRIALS. Patients with flat mucosa are unlikely to absorbe well the iron, iron has to be provided by the gluten free diet, encouraging foods with high bioavailability of iron (meat etc) WE NEVER give (over last 30 years ) any iron or folate to about 16.000 cases treated .

Patients should also have a consultation with a dietitian who is knowledgable about gluten-free diets. However, not all dietitians are familiar with the intricacies of a gluten-free diet, and for this reason local or national support groups provide most of the required information.

For adults, quality of life is improved on a gluten-free diet even for those whose disease was detected by screening. Children on a gluten-free diet reported a quality of life comparable to that of a reference population. Adolescents have difficulty with dietary compliance.

6.2 The Gluten Free Diet

Table 6 Allowed foods in a Gluten Free Diet

POSITIVE MESSAGES REQUIRED FOR THE DOCTOR AND THE PATIENTS

rice beans,peas amaranth Meat

corn quinoa teff Fish

sorghum potato nuts Egg

millet soybean fruits Oats

Buckwheat (kasha) tapioca milk&cheeses 1)

The most effective treatment is a rigorous gluten-free-diet (GFD) for life. This means no wheat, rye or barley. Oats – provided it is pure and not contaminated with other grains (even minimal amounts of wheat, rye or barley) are safe to eat in 95% of cases.

Plain meat, fish, rice, corn, fruits, and vegetables do not contain gluten. Examples of foods that are safe to eat and those that are not can be found online by visiting the US website of the National Digestive Diseases Information Clearing House (NDDIC) as well as several online CD information sites listed in sections 8 and 9.

A gluten free diet is low on roughage . To avoid associated constipation advise to add regular dietary rice bran and isphagula husks for example. Fibers = entire rice, maize, potatoes, and a LOT of legumes

Correct any dietary deficiencies such as iron, folic acid, calcium and (very rarely) B12 deficiency.

6.3 Persistence of symptoms A common difficulty with the GFD is the presence of occult gluten in processed foods and/or medicines (although this is rare) , the persistence of symptoms is almost always caused by a continued ingestion of gluten. Reasons for persistence of symptoms - Gluten ingestion (most common reason) - Wrong diagnosis - Lactose or fructose intolerance - Other food intolerances - pancreatic insufficiency - Microscopic colitis - Bacterial overgrowth - Collagenous colitis or Sprue - IBS - Ulcerative jejunitis - Enteropathy-associated T-cell lymphoma - Autoimmune enteropathy - Refractory sprue

6.4 Refractory Celiac Sprue The diagnosis of refractory sprue is considered in patients with celiac disease who have persistent symptoms, villous atrophy, and failure to respond to a gluten-free diet. This might occur at presentation or after an initial response to a gluten-free diet Refractory celiac sprue is considered to be a low grade intraepithelial lymphoma, revealed by a severe malabsorption that is resistant to a gluten free diet. This diagnosis must be considered especially in coeliacs diagnosed above the age of 50 yrs.

7 Screening for celiac disease

7.1 Screening for Celiac Disease CANCER IS NOT THE MAIN REASON FOR SCREENING !!!! GOOD HEALTH AND GROWTH IS INDEED A GOOD REASON ! QUALITY OF LIFE ALSO ! Celiac disease reduces life expectancy because of a higher risk of malignancies: Small bowel lymphoma Small bowel adenocarcinoma Esophageal carcinoma EATL (Non Hodgkin lymphoma) Screening is therefore attractive and it meets the 5 WHO criteria for justifying general screening. There are however resource implications – is this the best use of available limited resources ? – and there are ethical implications! The current view is there is not enough evidence to support a decision to do mass screening of the general population nor is there enough evidence to assess the risks of undetected CD.

7.2 The Future . With the development of a possible powerful animal model for CD and the use of new proteomic approaches, there is the potential for isolating the critically important epitopes within gliadin and related proteins. Once these have been clearly identified, research can then focus on either modifying these proteins or improving tolerance of these proteins in CD patients or in those with a susceptibility to CD. In the interim, oats (in 95% of cases , corn and rice and possibly industrially purified wheat/starch protein can be used to expand the relatively limited range of a GFD (Robins; ref 14) The coeliac genetics research community has established a sound foundation for the identification of additional disease genes in the not-too-distant future - functional studies will play a critical role. (Sollid – Ref )

8 Useful Websites

Center for Celiac Research (University of Maryland) www.celiaccenter.org

The Celiac Disease Foundation www.celiac.org

The Celiac Sprue Association www.csaceliacs.org

The Celiac Disease and Gluten-free Diet Support Page www.celiac.com

The Gluten-free pantry www.glutenfree.com

World Gastroenterology Association www.omge.org

US National Institutes of Diabetes, Digestive, and Kidney Disorders:

Celiac Disease Foundation:

The Gluten Intolerance Group:

The Celiac Disease Foundation

http://digestive.niddk.nih.gov/ddiseases/pubs/celiac/

http://www.celiac.org/

http://www.gluten.net/

http://www.celiac.com/

American Gastroenterological Association http://www.gastro.org

American College of Gastroenterology www.acg.gi.org

British Society of gastroenterology www.bsg.org

Celiac Helpline www.celiac.co.uk

The Wheat free zone www.nowheat.com/grfx/nowheat/index.htm

US National Digestive Disease Clearinghouse (NDDIC) http://digestive.niddk.nih.gov/ddiseases/pubs/celiac/index.htm

OMGE ―Ask a Librarian‖ for Celiac Disease Research

support

www.omge.org

9 Guidelines, Listserver and Further Reading

9.1 Celiac Disease Guidelines

1. NIH – Consensus Development Conference Statement

Celiac Disease; June 28-30, 2004

http://consensus.nih.gov/cons/118/118cdc_intro.htm

2. Celiac Disease. Summary, Evidence Report/Technology Assessment Number 104,

AHRQ Publication Number 04-E029-1, June 2004-09-14 Agency for Healthcare Research

and Quality, Rockville, MD.

http://www.ahrq.gov/clinic/epcsums/celiacsum.htm

3. American Gastroenterological Association medical position statement: Celiac sprue Gastroenterology 2001 120: 1522-1525.

Pubmed-Medline

4. AGA technical review on celiac sprue Paul J. Ciclitira, Gastroenterology 2001 120: 1526-1540.

Pubmed-Medline

5. Interim Guidelines for the Management of Patients with Celiac Disease British Society of Gastroenterology

Revised by Professor P Ciclitira April 2002

http://www.bsg.org.uk/clinical_prac/guidelines/celiac.htm

6. Celiac Disease

North American Society for Pediatric Gastroenterology and Nutrition

http://www.naspgn.org/assets/diseaseInfo/pdf/Celiac.pdf

7. Celiac Disease List server

St. Johns Celiac Listserv Newsgroup

To subscribe

send an e-mail to the following address:

listserv@maelstrom.stjohns.edu

In the body of the letter put the following:

SUB CELIAC followed by your first and last name:

For example SUB CELIAC Bob Jones.

9.2 Further Reading

1 Celiac Disease

Green PHR, Jabri B

The Lancet; August 2003; 362/9381;383-391

Pubmed-Medline

2

Review article: The diagnosis of celiac disease.

Abdulkarim-A-S, Murray-J-A.

Alimentary Pharmacology and Therapeutics 15

APR 2003, 17/8 (987-995

Pubmed-Medline

3

Current approaches to diagnosis and treatment of celiac disease: An

evolving spectrum.

Fasano-A, Catassi-C.

Gastroenterology 2001, 120/3 (636-651)

Pubmed-Medline

4

Antiendomysium versus antigliadin antibodies in screening the general

population for celiac disease.

Catassi-C, Fanciulli-G, D-Appello-A-R, El-Asmar-R, Rondina-C,

Fabiani-E, Bearzi-I, Coppa-G-V.

Scandinavian Journal of Gastroenterology 2000, 35/7 (732-736)

Pubmed-Medline

5

Prevalence of celiac disease among blood donors in Brazil.

Gandolfi-L, Pratesi-R, Cordoba-J-C, Tauil-P-L, Gasparin-M,Catassi-C.

American Journal of Gastroenterology 2000, 95/3 (689-692

Pubmed-Medline

6

Why is celiac disease endemic in the people of the Sahara?

Catassi-C, Ratsch-I-M, Gandolfi-L, Pratesi-R, Fabiani-E, El-Asmar-R,

Frijia-M, Bearzi-I, Vizzoni-L.

Lancet , 21 AUG 1999, 354/9179 (647-648

Pubmed-Medline

7

Protagonist: European and North American populations should be screened for celiac disease.

Fasano A.

Gut 2003;52:168–9

Pubmed-Medline

8

Anatagonist: European and North American populations should be screened for celiac disease.

Kumar PJ

Gut 2003;52:170-171

Pubmed-Medline

9

Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: A large

multicentre study.

Fasano A, Berti I, Gerarduzzi T

Arch Intern Med 2003;163:286

Pubmed-Medline

10

Celiac Disease — How to Handle a Clinical Chameleon

Fasano A

NEJM June 19, 2003 Volume 348:2568-2570

Pubmed_Medline

11

Antibodies to human recombinant tissue transglutaminase may detect celiac disease patients

undiagnosed by endomysial antibodies.

Tesei N, Sugai E, Vazquez H, et al

Aliment Pharmacol Ther 2003, 17:1415–1423.

Pubmed-Medline

12

Additional factor in some HLA DR3/DQ2 haplotypes confers a fourfold increased genetic risk

of celiac disease.

Bolognesi E, Karell K, Percopo S, et al.:

Tissue Antigens 2003, 61:308–316.

Pubmed-Medline

13

Oats and the gluten-free diet.

Thompson T:

]J Am Diet Assoc 2003, 103:376–379.

Pubmed-Medline

14

Advances in Celiac Disease

Robins G, Howdle PD

Current Opinion in Gastroenterology; Volume 20(2)March 2004;95-103

Pubmed-Medline

15

Celiac sprue.

Farrell-R-J, Kelly-C-P.

New England Journal of Medicine, 17 JAN 2002; 346/3 (180-188)

Pubmed-Medline

16

Dermatitis herpetiformis: close to unravelling a disease

Karpati Sarolta

Journal of Dermatological Science; April 2004 ; 34/2;: 83-90

Pubmed-Medline

17

Stratification of bone fracture risk in patients with celiac disease.

Moreno-M-L, Vazquez-H, Mazure-R, Smecuol-E, Niveloni-S, Pedreira-S,

Sugai-E, Maurino-E, Gomez-J-C,Bai-J-C.

Clinical Gastroenterology and Hepatology, 2004, 2/2 (127-134),

Pubmed-Medline

18

Defining a proper setting for endoscopy in coeliac disease.

Vjero-K, Martucci-S, Alvisi-C, Broglia-F, Viera-F-T, Perego-M,

Corazza-G-R.

European Journal of Gastroenterology and Hepatology , 01 JUN 2003, 15/6 (675-678),

Pubmed-Medline

19

Pathomechanisms in celiac disease.

Dieterich-W, Esslinger-B,Schuppan-D.

International Archives of Allergy and Immunology 2003, 132/2 (98-108)

Pubmed-Medline

20

HLA-DQ relative risks for coeliac disease in European populations: A

study of the European Genetics Cluster on Coeliac Disease.

Margaritte-Jeannin-P, Babron-M-C, Bourgey-M, Louka-A-S, Clot-F,

Percopo-S, Coto-I, Hugot-J-P, Ascher-H, Sollid-L-M,Greco-L,Clerget-

Darpoux-F.

Tissue Antigens,2004, 63/6 (562-567),

Pubmed-Medline

21

When is a coeliac a coeliac?

Working Party Report UEGW Amsterdam 2001.

European Journal of Gastroenterology and Hepatology

2001; 13(9); 1123-1128

Pubmed-Medline

22

Case finding in Coeliac Disease seems beneficial, mass screening is still controversial.

Mulder-C-J-J, Bartelsman-J-F-W-M

Scandinavian Journal of gastroenterology

In Press

23

HLA in coeliac disease: Unravelling the complex genetics of a complex

disorder.

Louka-A-S,Sollid-L-M.

Tissue Antigens 2003, 61/2 ; (105-117)

Pubmed-Medline

24

Coeliac Disease: more than villous atrophy

Wahab-P-J, Meijer-J-W, Dumitra-D, Goerres- M-S, Mulder-C-J

Rom J Gastroenterol. 2002 Jun;11(2):121-7.

Pubmed-Medline

25

The Molecular Basis for Oat Intolerance in Patients with Celiac Disease

Arentz-Hansen-H, Fleckenstein-B, Molberg-O, Scott-H, Koning-F, Jung-G, Roepstorff-P, Lundin- K-E, Sollid- L-M.

Plos Med. 2004 Oct;1(1):e1.

Pubmed-Medline

Pubmed-Central