+90 (312) 472 17 69

CELIAC DISEASE

CELIAC DISEASE OR GLUTEN ENTEROPHYSIS

“In case of complaints and illnesses that you cannot explain the reason, please have CELIAC in mind”

Dr. Ceyhun NURİ

DEFINITION

It is an intestinal disease characterized by destruction of structures called villus, which plays a role in food absorption especially in the upper small intestines in people who are susceptible to genetic infrastructure against proteins found in cereals such as wheat, rye, barley, oats, and gluten.

EPIDEMIOLOGY

Approximately 10,000 years ago, consumption of meat, vegetables, and fruits decreased gradually as people increased consumption of cereals, milk and processed products, along with the built-in pasture of hunting, gathering and nomadic life. This disease, which seems to be a rare event, has begun to grow dramatically with the globalization and the reach of the food, seeds from different race and geographical regions to every part of the world, and serious food mismatch (Food Intolerance) against nutrients all over the world. People start to feed on their temperaments. People start to feed against their temperaments. In some culturally or tribally living communities that are still isolated,  (some tribes of Africa, East China, Pacific Islands, South East Asia, Japan)celiac is a very rare disease.

Celiac Disease is the leading cause of malabsorption seen in children. It is more common in women than in men. The frequency of first degree relatives and single eggs (Monozygotic) twins is ten times higher. Because of the underlying immune system irregularity, the rate of other autoimmune diseases (Addison, Sjögren, Thyroiditis, Type I DM, Osteoporosis, Primer Biliary Cirrhosis, Down syndrome, Selective IgA deficiency etc.) is high.

PATHOPHYSIOLOGY

Classic View of Formation Mechanism

This disease, which can manifest itself at any age, is known to be an autoimmune reaction. In other words, the immune system elements in the small intestine mucus are destroying the physiological structures (villus etc.) due to the excessive reaction against the intestinal cells. But it is not known why this autoimmune reaction occurs.

Dr. Ceyhun NURI’s View of Formation Mechanism:

In the results of the research published in CELL RESEARCH on September 20, 2011, it is explained as follows: Every food consumed, every plant that is eaten, has micro RNAs of that plant and they reach the tissues together with the circulation after they are absorbed from the intestines. These microRNAs begin to interfere with the genes of the individual. In a study by Zhang and his friends, they found that rice and wheat, carrying MIR156a microRNAs, boosted human LDL cholesterol. So, as we have mentioned above, if we take the globalization, the western type and the malicious reverse nutrition into account, it is possible to reach the following result. It is not right to look at food only in terms of proteins, fats, carbohydrates and calories. We should not lose sight of which genetic information they carry us. In this case, the proteins and enzymes that are encoded and synthesized by DNA that starts to change start to deteriorate. When the protein is degraded, the metabolism begins to change as the enzyme reacts to the other reactive side. And the wrong encoding (Mutation) in this DNA begins to be transmitted from the generation to the generation. Although it is thought that many genetic disorders play a role in the development of celiac disease, the main responsible structure is DQ2ve DQ8. It is also thought that they play a role in the onset and course of celiac disease with viruses (Adenovirus type 12, type 7, Rubella, Human Herpesvirus 1, Hepatitis C, and HIV) with very high degree of amino acid sequence similarity with gliadin.

Environmental factors play a very important role in the development of the disease. It leads to the deterioration of the intestinal protection shield (Probiotic bacteria, Intestinal sealing wall) rich in fermented products (yoghurt, kefir, etc.), refined flour and sugary foods. The immune system (IgE, Leukocyte, NK, Leukotriene, ANA, etc.) reacts excessively to increased allergens and toxins when the excessive foreign matter entering the body is not cleared by the liver.

For digestion, several enzymes (Lactase, Protease, Lipase, Maltase, Peptidase, etc.) should be secreted from many organs such as stomach, intestine, liver, gall bladder, and pancreas. But, as you can see, due to the wrong genetic information, these enzymes are either not secreted or are produced with different qualities (enzymes that take an active role in the metabolism of gluten and similar proteins). In this case, a portion of undigested food particles (amino acids) begin to accumulate in the intestines. They begin to form a dead layer and plugs on the intestinal surface. This results in the movement of some centers where the elements of the immune system, such as bone marrow, lymph nodes, are produced. As a result, a dense autoimmune, inflammatory response to the intestinal surface begins to develop. Humoral and cytotoxic cellular immune responses are developed against gliadin (especially its 33-mer peptide) in glutenin, predominantly IgA, more weakly IgG. (“Human leukocyte antigen” (HLA) class IL, HLA-DQ2, DQ8, Th1 / Th0 CD4 + Gluten-sensitive T cells). So, the body opens the war against the intestinal surface. In this battle, villus atrophy, crypt hyperplasia and small intestinal surface result in catastrophic damage. An increase in immature epithelial cells is observed on the intestinal surface due to this process. Although destruction mostly affects the proximal, that is, the beginning part of the small intestine, distal (lower) parts are also affected. As a result, body nutrients cannot be absorbed, body loss starts, frequent diarrhea occur. As the absorption decreases, weight, height losses will appear, as the absorption of calcium deteriorates, bone disorders will start.

CLINIC

Symptoms and signs of celiac disease may be quite variable. Most complaints and findings are related to impaired proximal intestinal absorption. The most common symptom is frequent, abundant, oily, light colored, foul-smelling, dull-looking stool.

Symptoms often start to appear in infants after the first six months with additional food, especially cereals. They typically come with complaints of gastrointestinal system such as height-weight deficiency, frequent nausea, juvenile stools, chronic diarrhea, anorexia, unexplained weight loss, abdominal distension, reflux, and malabsorption.

Although it seems like an illness in which the intestinal problems are frontal, the intestinal symptoms and signs are very common in these patients because all the absorption and breakthrough processes are affected.

In these patients, musculoskeletal symptoms such as rickets, osteoporosis, dental enamel spoilage, shortness of stature, arthralgia (pain in joints), and myopathy can be seen due to impairment of calcium and vitamin D metabolism.

Hematologic symptoms such as anemia (anemia), leukopenia, thrombocytopenia due to impaired absorption of iron, folate, B12, VE, and K vitamins in the stomach and intestine may occur.

Neuropsychiatric symptoms such as epilepsy, peripheral neuropathy, depression, dementia, schizophrenia, impairment of perception, headache, cerebellar ataxia, attention deficit are the complaints of the gastrointestinal system in celiac disease.

Complaints related to skin and mucous membranes such as mouth apthas, dermatitis herpetiformis can be seen.

Celiac Disease can come from under the complaints of delayed puberty, menstrual irregularities, recurrent abortion, infertility, elevated liver enzymes, chronic hepatitis, chronic fatigue, hair loss, intestinal lymphoma, thyroiditis and many more.

This list of indications may be extended further. But let’s briefly say that. We have given names to these signs / findings so that we can understand and negotiate. If the body functions like absorption, metabolism, production, detoxification, cleansing ability, circulation, respiration, neural communication, oscillation etc. are impaired, we will have more complaints than we can count.

DIAGNOSIS

Although it is a very common disease in our society, most people do not know that their complaints depend on this disease. If the patients suffer from loss of appetite, height, swelling, chronic diarrhea, chronic constipation, recurrent abdominal pain or vomiting, hypoplasia of teeth minerals, unexplained shortness, delayed puberty, refractory iron deficiency anemia, osteoporosis, and frequent illness etc., the first disease that should come to mind is celiac. And serologic screening tests must be performed in these patients.

Serologic screening tests should also be performed in first-degree relatives of patients diagnosed with celiac disease, autoimmune thyroiditis, Type I DM, Down / Williams / Turner syndrome, selective IgA deficiency and other autoimmune diseases.

The diagnosis is made by findings such as lymphocyte (IEL) increase, crypt hyperplasia, villus atrophy, intestinal mucosal flattening in the epithelial mucosal epithelium of the intestine, which is actually detected in the biopsy of IB. However, making the easier serological tests before this invasive procedure is considered the first step in diagnosis today.

Serological tests are the most valuable methods for screening purposes. In these serological tests 1) the proteins in the food (gluten). 2) Trying to detect antibodies against the structural proteins (endomyosin, reticulin, transglutaminase) in the intestinal mucosa.

Serological tests used for screening (in IgA, IgG construct):

Antigliadin antibody (AGA)

Serological tests used in the diagnosis and follow-up of the disease (in Iga structure):

  • Anti-Tissue Transglutaminase Antibody (Anti-TG)
  • Anti-endomicin antibody (EMA)
  • Anti-reticulin antibody (ARA)

NOTE:

  1. It would not be right to look at the Ig structure of the antibody under 2 years of age and situations with IgA deficiency (may give false negative results). In these cases, it would be more accurate to look at the antibodies in the IgG construct.
  2. In today’s conditions, if we consider the techniques, cost, and reliability of these tests, our approach to testing will be more accurate:
  • Anti-tissue transglutaminase antibody (Anti-dTG) for screening
  • Anti- endomysium antibody (EMA) to support diagnosis of celiac disease in suspicious cases
  • Antigliadin antibody (AGA) under 2 years of age
  • Anti-dTG IgG, AGA IgG in selective IgA deficiency with

Biopsy

It is still seen as a golden approach in the diagnosis of celiac disease. In all cases where anti-dTG and / or EMA positive is detected, small intestine biopsy should be performed to confirm the diagnosis of celiac disease.

Diagnosis and follow-up of celiac disease is absolutely necessary in other hematological, biochemical, radiological examinations:

– Whole Blood Count

 

-Iron, Ferritin, Iron

Bonding Capacity

 

– Zinc, Zinc binding

its capacity

-Vitamin B12

 

-Insulin (Hunger), Hunger- blood sugar

 

-CRP, RF, ES Speed

 

– Calcium, Phosphorus

-Magnesium

-Alkaline Phosphatase

 

– Liver enzymes

 

-Total protein, albumin

 

-Electrolytes

 

– microscopic inspection of stool

 

-PTH, vitamin D

 

-Hand-wrist graphy

 

-Bone densitometry

 

-IgA, IgG, IgM

-PT, PTT

-Thyroid function tests

 

– Thyroid antibodies (TG, Anti Tg, Anti TPO)

 

— Autoantibodies (ANA, dsDNA, AMA, ASMA, LKM 1)

 

-EEG

 

– Cranial MR

 

– Tissue group

 

TREATMENT

Classical Treatment Approach

There is no treatment for celiac disease.

The general belief is that this reaction against gluten is persistent in the body, so it insists on the application of lifelong gluten-free diet.

Dr. Ceyhun NURİ’s Treatment Approach:

There is ABSOLUTELY a Treatment for Celiac Disease!!!

No one has to be convicted of lifelong gluten-free speech if you solve the causes and connections of the autoimmune response.

As we mentioned earlier, the most important point is to correct the genetic background. And there are plants and seeds that will regulate it and turn the body back to its main balanced order (HOMEOSTAZIS).

It is imperative that the elements that are determined to be deficient in treatment are conducted. Many other substances that are absolutely important contributors to cell repair such as vitamin B12, folic acid, zinc, calcium, vitamin D, which are very important in the neurological structure, help to transport oxygen to the cell, must be quickly compensated.

It is useful to point out that we need to meet the deficit by taking minerals, elements, proteins, vitamins, which we really need from our natural sources like meat, vegetables, fruit, and sun. But it is not possible for us to take advantage of these natural sources until treatment and order are established in humans, such as celiac disease, that lacks absorption, ingestion, digestion, and production of intestinal enzymes.

COMPLICATIONS THAT CAN BE DEVELOPED IF NOT TREATED

In patients who have not been diagnosed and treated for a long time, many autoimmune diseases that may develop due to the same immune background can be added to the clinic. Aging, Osteoporosis, Ulcerative jejunoileitis, T-cell intestinal lymphoma, Anemia, Rickets, Hepatitis, Cerebral cirrhosis, Epilepsy, Osteoporosis in the elderly, Ulcerative jejunoileitis, T-cell intestinal lymphoma, Anemia, Rickets, Hepatitis, Brain cirrhosis, Epilepsy, Cerebellar ataxia, Neuropathy It is possible to encounter many conditions such as Myocarditis, Cardiomyopathy, Kidney problems, Adrenal insufficiency, Infertility, Depression, Resistant obesity and many more. Neuropathy, Myocarditis, Cardiomyopathy, Kidney problems, Adrenal insufficiency, Infertility, Depression, Resistant obesity and many more.

If treatment is delayed, other nutrients that digest here will begin to be affected, secondary to damage to the epithelium on the surface of the intestine. The production of lactase enzyme, which plays a role in the digestion of milk and dairy products, will deteriorate and nutrition will eventually deteriorate. A similar situation is seen in the digestion of carbohydrates, sugars and other nutritional ingredients (sucrose, maltase, etc.)

RECOMMENDATIONS TO DR.CEYHUN NURI:

– Gluten-free diet must be strictly applied until the patient’s background is resolved. Rice and corn for these patients are considered safe grain foods because they do not contain toxic prolamin.

-It has been shown in many studies that long-term delivery of the baby’s milk to the baby and initiation of simultaneous appetizers after 6 months protects against celiac disease and many other diseases. We find it useful to breastfeed until the age of two.

– It is better to avoid milk, fruit and fruit juices in the first weeks until the surface of the gut is regenerated (repaired). (Disaccharides secondary to the destruction of the intestinal epithelium, due to lack of lactase enzyme)

– To help repair the intestinal mucosa, three times a day on an empty stomach a sweet spoon of pure corn oil consumption will make a positive contribution to the process.

– It will be very useful to increase the consumption of products supporting the biological life of the bowel and the intestines (home-made yoghurt, kefir, fig, date, garlic, etc.)

– You should consume 2-3 cups of plantago tea a day, which is useful for repairing the rough surface structure.

Dr. Ceyhun NURİ

For more information, please contact us at our contact details.

RESOURCES:

  1. Maki M, Lohi O. Celiac Disease. In: Walker WA, Goulet O, Kleinman RE, Sherman PM, Shneider BL, Sanderson IR (eds). Pediatric Gastrointestinal Disease. 4th ed. Ontario: B.C. Decker, 2004: 932-43.
  2. Hill ID, Dirks MH, Liptak GS, et al. North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. Guideline for the Diagnosis and Treatment of Celiac Disease in Children: Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr 2005; 40: 1-19.
  3. Farrell RJ, Kelly CP. Celiac Sprue. N Engl J Med 2002; 346: 180-8.
  4. Fasano A, Catassi C. Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum. Gastroenterology 2001; 120: 636- 51.
  5. Fasano A, Catassi C. Coeliac disease in children. Best Pract Res Clin Gastroenterol 2005; 19: 467-78. 6. Marsh M. Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity (‘celiac sprue’). Gastroenterology 1992; 102: 330-54.
  6. Catassi C, Rätsch IM, Gandolfi L, et al. Why is coeliac disease endemic in the people of the Sahara? Lancet 1999; 354: 647-8.
  7. Rostami K, Malekzadeh R, Shahbazkhani B, et al. Coeliac disease in Middle Eastern countries: a challenge for the evolutionary history of this complex disorder? Dig Liver Dis 2004; 36: 694-7.
  8. Dowd BD, Walker-Smith JA. Samuel Gee, Aretaeus, and the coeliac affection. BMJ 1974; 2: 45-7. 10. Toscano E. Historical views on celiac disease: the contribution of Adolf Baginsky (1843-1918). Acta Paediatr 2004; 93: 417-8.
  9. Dalgıç B, Sarı S, Baştürk B, Ensari A, et al, Turkish Celiac Disease Study Group. Prevalence of celiac disease in Turkish school children. 43rd Annual Meeting of the ESPGHAN 2010, Abstract CD; PO-G-171: 221.
  10. Demirçeken FG, Kansu A, Kuloğlu Z, et al. Human tissue transglutaminase antibody screening by immunochromatographic line immunoassay for early diagnosis of celiac disease in Turkish children. Turk J Gastroenterol 2008; 19: 14-21.
  11. Ertekin V, Selimoğlu MA, Kardaş F, et al. Prevalence of celiac disease in Turkish children. J Clin Gastroenterol 2005; 39: 689-91.
  12. Gursoy S, Guven K, Simsek T, et al. The prevalence of unrecognized adult celiac disease in Central Anatolia. J Clin Gastroenterol 2005; 39: 508-11.
  13. Tatar G, Elsurer R, Simsek H, et al. Screening of tissue transglutaminase antibody in healthy blood donors for celiac disease screening in the Turkish population. Dig Dis Sci 2004; 49: 1479-84.
  14. Karaaslan H, Bektaş M, Bozkaya H, et al. Gönüllü kan donörlerinde gluten enteropatisi seroprevalansı. 20. Ulusal Gastroenteroloji Haftası, Ku- şadası. Turk J Gastroenterol 2003; 14 (Supp1): 18.
  15. Mustalahti K, Catassi C, Reunanen A, et al, Coeliac EU Cluster, Project Epidemiology. The prevalence of celiac disease in Europe: Results of a centralized, international mass screening project. Ann Med 2010; 42: 587-95.
  16. Roka V, Potamianos SP, Kapsoritakis AN, et al. Prevalence of coeliac disease in the adult population of central Greece. Eur J Gastroenterol Hepatol 2007; 19: 982-7.
  17. Mongi BH, Kallel-Sellami M, Kallel L, et al. Prevalence of celiac disease in Tunisia: mass-screening study in schoolchildren. Eur J Gastroenterol Hepatol 2007; 19: 687-94.
  18. Akbari MR, Mohammadkhani A, Fakheri H, et al. Screening of the adult population in Iran for coeliac disease: comparison of the tissue-transglutaminase antibody and anti-endomysial antibody tests. Eur J Gastroenterol Hepatol 2006; 18: 1181-6.
  19. Remes-Troche JM, Ramírez-Iglesias MT, Rubio-Tapia A, et al. Celiac disease could be a frequent disease in Mexico: prevalence of tissue transglutaminase antibody in healthy blood donors. J Clin Gastroenterol 2006; 40: 697-700.
  20. Mankaï A, Landolsi H, Chahed A, et al. Celiac disease in Tunisia: serological screening in healthy blood donors. Pathol Biol (Paris) 2006; 54: 10-3.
  21. Brar P, Lee AR, Lewis SK, et al. Celiac disease in African-Americans. Dig Dis Sci 2006; 51: 1012-5. Epub 2006.
  22. Antunes H, Abreu I, Nogueiras A, et al. First determination of the prevalence of celiac disease in a Portuguese population. Acta Med Port 2006; 19: 115-20. Epub 2006.
  23. Melo SB, Fernandes MI, Peres LC, et al. Prevalence and demographic characteristics of celiac disease among blood donors in Ribeirão Preto, State of São Paulo, Brazil. Dig Dis Sci 2006; 51: 1020-5. Epub 2006.
  24. Stroikova M, Augul N, Gureev J, et al. Screening of blood donors for tissue transglutaminase antibodies in the Ryazan area (Russia). Dig Liver Dis 2006; 38: 617-9. Epub 2006.
  25. Mäki M, Mustalahti K, Kokkonen J, et al. Prevalence of celiac disease among children in Finland. N Engl J Med 2003; 348: 2517-24.
  26. Rutz R, Ritzler E, Fierz W, Herzog D. Prevalence of asymptomatic celiac disease in adolescents of eastern Switzerland. Swiss Med Wkly 2002; 132: 43-7.
  27. West J, Logan RF, Hill PG, et al. Seroprevalence, correlates, and characteristics of undetected coeliac disease in England. Gut 2003; 52: 960-5.
  28. Cilleruelo Pascual ML, Román Riechmann E, Jiménez Jiménez J, et al. Silent celiac disease: exploring the iceberg in the school-aged population. An Esp Pediatr 2002; 57: 321-6.
  29. Hovell CJ, Collett JA, Vautier G, et al. High prevalence of coeliac disease in a population-based study from Western Australia: a case for screening? Med J Aust 2001; 175: 247-50.
  30. Korponay-Szabó IR, Kovács JB, Czinner A, et al. High prevalence of silent celiac disease in preschool children screened with IgA/IgG antiendomysium antibodies. J Pediatr Gastroenterol Nutr 1999; 28: 26-30.
  31. Johnston SD, Watson RG, McMillan SA, et al. Prevalence of coeliac disease in Northern Ireland. Lancet 1997; 350: 1370.
  32. Catassi C, Fabiani E, Rätsch IM, et al. The coeliac iceberg in Italy. A multicentre antigliadin antibodies screening for coeliac disease in schoolage subjects. Acta Paediatr Suppl. 1996; 412: 29-35.
  33. Cummins AG, Roberts-Thomson IC. Prevalence of celiac disease in the Asia-Pacific region. J Gastroenterol Hepatol 2009; 24: 1347-51.
  34. Maki M, Kakkonen K, Lahdeaho ML, et al. Changing pattern of childhood celiac disease in Finland. Acta Paediatr Scand 1988; 77: 408-12.
  35. Metha G, Taslaq S, Littreford S, et al. The changing face of the celiac disease. Br J Hosp Med (Lond) 2008; 69: 84-7.
  36. Patel D, Kalkat P, Basisch D, Zipser R. Celiac disease in elderly. Gerontology 2005; 51: 213-4.
  37. Vilppula A, Collin P, Maki M, et al. Undetected coeliac disease in the elderly: a biopsy-proven population-based study. Dig Liver Dis 2008; 40: 809-13.
  38. Elsürer R, Tatar G,Şimşek H, et al.Celiac disease in Turkish population.Dig Dis Sci 2005; 50: 136-42.
  39. Ivarsson A, Persson LA, Nyström L, et al. The Swedish coeliac disease epidemic with a prevailing twofold higher risk in girls compared to boys may reflect gender specific risk factors. Eur J Epidemiol 2003; 18: 677-84.
  40. Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at risk and not at risk groups in the United States: a large multicenter study. Arch Intern Med 2003; 163: 286-92.
  41. Hill I, Fasano A, Schwartz R, et al. The prevalence of celiac disease in at risk groups of children in the United States. J Pediatr 2000; 136: 86-90.
  42. Mustalahti K. Unusual manifestations of celiac disease. Indian J Pediatr 2006; 73: 711-6.
  43. Cataldo F, Marino V. Increased prevalence of autoimmune diseases in first-degree relatives of patients with celiac disease. J Pediatr Gastroenterol Nutr 2003; 36: 470-3.
  44. Ventura A, Magazzù G, Greco L. Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disaese. Gastroenterology 1999; 117: 297-303.
  45. Ivarsson A, Hernell O, Stenlund H, Persson LA. Am breast-feeding protects against celiac disease. J Clin Nutr 2002; 75: 914-21.
  46. Guandalini S. The influence of gluten: weaning recommendations for healthy children and children at risk for celiac disease. Nestle Nutr Workshop Ser Pediatr Program. 2007; 60: 139-51; discussion 151-5.
  47. Fälth-Magnusson K, Franzén L, Jansson G, et al. Infant feeding history shows distinct differences between Swedish celiac and reference children. Pediatr Allergy Immunol 1996; 7: 1-5.
  48. Peters U, Schneeweiss S, Trautwein EA, Erbersdobler HF. A case-control study of the effect of infant feeding on celiac disease. Ann Nutr Metab 2001; 45: 135-42.
  49. Akobeng AK, Ramanan AV, Buchan I, Heller RF. Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies. Arch Dis Child 2006; 91: 39-43. Epub 2005.
  50. Kaukinen K, Partanen J, Mäki M, Collin P. HLA-DQ typing in the diagnosis of celiac disease. Am J Gastroenterol 2002; 97: 695-9.
  51. Molberg O, McAdam S, Lundin KE, et al. T cells from celiac disease lesions recognize gliadin epitopes deamidated in situ by endogenous tissue transglutaminase. Eur J Immunol 2001; 31: 1317-23.
  52. Dieterich W, Ehnis T, Bauer M, et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med 1997; 3: 797-801.
  53. Sakly W, Thomas V, Quash G, El Alaoui S. A role for tissue transglutaminase in alpha-gliadin peptide cytotoxicity. Clin Exp Immunol 2006; 146: 550-8.
  54. Liu E, Li M, Emery L, et al. Natural history of antibodies to deamidated gliadin peptides and transglutaminase in early childhood celiac disease. J Pediatr Gastroenterol Nutr 2007; 45: 293-300.
  55. Korponay-Szabó IR, Vecsei Z, Király R, et al. Deamidated gliadin peptides form epitopes that transglutaminase antibodies recognize. J Pediatr Gastroenterol Nutr 2008; 46: 253-61.
  56. Kurppa K, Lindfors K, Collin P, et al. Antibodies against deamidated gliadin peptides in early-stage celiac disease. J Clin Gastroenterol 2010 Nov 8. [Epub ahead of print]
  57. Volta U, Fabbri A, Parisi C, et al. Old and new serological tests for celiac disease screening. Expert Rev Gastroenterol Hepatol 2010; 4: 31-5.
  58. Kuloğlu Z, Doğancı T, Kansu A, et al. HLA types in Turkish children with celiac disease. Turk J Pediatr 2008; 50: 515-20.
  59. Sollid LM, Lie BA. Celiac disease genetics: current concepts and practical applications. Clin Gastroenterol Hepatol 2005; 3: 843-51.
  60. Bonamico M, Ferri M, Mariani P, et al. Serologic and genetic markers of celiac disease: a sequential study in the screening of first degree relatives. J Pediatr Gastroenterol Nutr 2006; 42: 150-4.
  61. Smyth DJ, Plagnol V, Walker NM, et al. Shared and distinct genetic variants in type 1 diabetes and celiac disease. N Engl J Med 2008; 359: 2767- 77.
  62. Al-Toma A, Goerres MS, Meijer JW, et al. Human leukocyte antigen-DQ2 homozygosity and the development of refractory celiac disease and enteropathy-associated T-cell lymphoma. Clin Gastroenterol Hepatol 2006; 4: 315-9.
  63. Cogulu O, Ozkinay F, Gunduz C, et al. Celiac disease in children with Down syndrome: importance of follow-up and serologic screening. Pediatr Int 2003; 45: 395-9.
  64. Alanay Y, Boduroğlu K, Tunçbilek E. Celiac disease screening in 100 Turkish children with Down syndrome. Turk J Pediatr 2005; 47: 138-40.
  65. Fasano A. Clinical presentation of celiac disease in the pediatric population. Gastroenterology 2005; 128 (4 Suppl 1): S68-73.
  66. Green PH. The many faces of celiac disease: clinical presentation of celiac disease in the adult population. Gastroenterology 2005; 128 (4 Suppl 1): S74-8.
  67. Jones S, D’Souza C, Haboubi NY. Patterns of clinical presentation of adult coeliac disease in a rural setting. Nutr J 2006; 5: 24.
  68. Mukherjee R, Egbuna I, Brar P, et al. Celiac disease: similar presentations in the elderly and young adults. Dig Dis Sci 2010; 55: 3147-53. Epub 2010.
  69. Ivarsson A, Persson LA, Juto P, et al. High prevalence of undiagnosed coeliac disease in adults: a Swedish population-based study. J Intern Med 1999; 245: 63-8.
  70. Richey R, Howdle P, Shaw E, Stokes T. Recognition and assesment of coeliac disease in children and adults: summary of NICE guidance. BMJ 2009; 338: b1684.
  71. Revised criteria for diagnosis of coeliac disease. Report of Working Group of European Society of Paediatric Gastroenterology and Nutrition. Arch Dis Child 1990; 65: 909-11.
  72. Basso D, Guariso G, Fasolo M, et al. A new indirect chemiluminescent immunoassay to measure anti-tissue transglutaminase antibodies. J Pediatr Gastroenterol Nutr 2006; 43: 613-8.
  73. Hill, ID. What are the sensitivity and specificity of serological tests for celiac disease? Do sensitivity and specificity vary in different populations?Gastroenterology 2005;128(4 Suppl 1):S25-32.
  74. Martin Stern; Working group on serologic screening for celiac disease. Comparative evaluation of serologic test for celiac disease: A European initiative toward standardization. J Pediatr Gastroenterol Nutr 2000; 31: 513-9.
  75. Horvath K, Hill ID. Anti- tissue transglutaminase antibody as the first line screening for celiac disease: Good-bye antigliadin test? Am J Gastroenterol 2002; 97: 2702-4.
  76. Ciclitira PJ, King AL, Fraser JS. AGA technical review on Celiac Sprue. American Gastroenterological Association. Gastroenterology 2001; 120: 1526-40.
  77. NIH Consensus Development Conference on Celiac Disease. NIH Consens State Sci Statements. 2004; 21: 1-23.
  78. Oberhuber G, Granditsch G, Vogelsang H. The histopathology of coeliac disease: time for standardized report schema for pathologists. Eur J Gastroenterol Hepatol 1999; 11: 1185-94.
  79. Ensari A. Gluten-sensitive Enteropathy (Celiac Disease) controversies in diagnosis and classification. Arch Pathol Lab Med 2010; 134: 826-36.
  80. Elsürer R, Tatar G, Şimşek H, et al. Celiac disease in Turkish population. Dig Dis Sci 2005; 50: 136-42.
  81. Korkut E, Bektas M, Oztas E, et al. The prevalence of celiac disease in patients fulfilling Rome III criteria for irritable bowel syndrome. Eur J Intern Med 2010; 21: 389-92. Epub 2010.
  82. Sanders DS. Celiac disease and IBS-type symptoms: the relationship exists in both directions. Am J Gastroenterol 2003; 98: 707-8.
  83. Anderson LA, McMillan SA, Watson RG, et al. Malignancy and mortality in a population-based cohort of patients with coeliac disease or “gluten sensitivity”. World J Gastroenterol 2007; 13: 146-51.
  84. Casella G, D’Incà R, Oliva L, et al; Italian Group – IBD. Prevalence of celiac disease in inflammatory bowel diseases: An IG-IBD multicentre study. Dig Liver Dis 2010; 42: 175-8. Epub 2009.
  85. Venkatasubramani N, Telega G, Werlin SL. Obesity in pediatric celiac disease. J Pediatr Gastroenterol Nutr 2010; 51: 295-7.
  86. Korponay-Szabó IR, Szabados K, Pusztai J, et al. Population screening for coeliac disease in primary care by district nurses using a rapid antibody test: diagnostic accuracy and feasibility study. BMJ 2007; 335: 1244-7. Epub 2007.
  87. Pyle GG, Paaso B, Anderson BE, et al. Effect of pretreatment of food gluten with prolyl endopeptidase on gluten-induced malabsorption in celiac sprue. Clin Gastroenterol Hepatol 2005; 3: 687-94.
  88. Sollid LM, Khosla C. Future therapeutic options for celiac disease. Nat Clin Pract Gastroenterol Hepatol 2005; 2: 140-7.
  89. Esposito C, Caputo I, Troncone R. New therapeutic strategies for coeliac disease: tissue transglutaminase as a target. Curr Med Chem 2007; 14: 2572-80.
  90. Schuppan D, Junker Y, Barisani D. Celiac disease: from pathogenesis to novel therapies. Gastroenterology 2009; 137: 1912-33. Epub 2009.
  91. Rodrigo L. Investigational therapies for celiac disease. Expert Opin Investig Drugs 2009; 18: 1865-73.