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Celiac Disease

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Links to Articles

* Celiac Disease by Wikipedia.org

* Celiac Disease Cases Quadruple in U.S. Experts warn gluten intolerance becoming substantial public health concern by Reuters

* "Celiac 101"
A Helpful Guide
for the Newly Diagnosed by Janet Rinehart

* The Changing Face of Celiac Disease: Links with other autoimmune disorders by Spomenka Ljubic, et al.

* Endocrinological Disorders and Celiac Disease by Pekka Collin, et al.

* Biopsy-defined Adult Celiac Disease in Asian-Canadians by H J Freeman

* Development of a Vaccine for Celiac Disease by R.P. Anderson

 

 

 

Books on Celiac Disease

 

Celiac Disease: A hidden epidemic by Peter H.R. Green, Rory Jones

 

Gluten-Free Diet: A Comprehensive Resource Guide
by Shelley Case

 

Celiac Disease: A guide to living with gluten intolerance by Sylvia Bower, et al.

 

Let's Eat Out!: Your Passport to Living Gluten And Allergy Free by Kim Koeller, et al.

 

Frontiers in Celiac Disease by A. Fasano

 

 

 

Celiac Centers:

 

BIDMC Celiac Center, Harvard Medical School

 

 

Celiac Disease Center at Columbia University

 

 

Celiac Disease Center, the University of Chicago Mecial Center

 

 

Organizations:

 

Celiac Disease Awareness Campaign

 

Celiac Disease Foundation

 

Celiac.com

 

Celiac Sprue Association

 

Canadian Celiac Association

 

Coeliac UK

 

Association of European Celiac Societies

 

Spanish Celiac Associations

 

German Celiac Associaiton

 

Keliakialiito

 

Associazione Italiana Celiachia

 

Celiac Society of Australia

 

Turkish Celiac Association

 

Brazilian Celiac Society

 

Israeli Celiac Association

 

 

HLA Genetic Typing

* Questions and answers on HLA typing and Celiac Disease by Michael Jones, et al.

* Celiac Disease DNA Test by Health Check USA

* Celiac Disease DNA Test by Kimball Genetics

* Your DNA Results Indicate: Super Celiac! By Scott Adams

Most doctors assume that celiac desease is rare among Asians, but the celiac genes, DQ2 and DQ8, are not that uncommon in the Taiwanese population and in other Asian populations. Celiac disease is a hereditary intolerance to gluten, a protein found in wheat, barley and rye. It is a serious disease that can lead to autoimmune disorders and cancer. Celiac disease is associated with diabetes, thyroid disease, autoimmune liver disease, cardiomyopathy, rheumatoid arthritis, Addison's disease, osteoporosis, peripheral neuropathy, migraines, depression, and infertility. Patients with celiac disease are at high-risk for thyroid cancer, adenocarcinoma of the small intestine, lymphoma, esophageal cancer, melanoma, and malignancy in childhood. Strict avoidance of gluten is the only way to treat celiac disease.

 

Excerpts from Wikipedia.org

Coeliac disease, also spelled celiac disease, is an autoimmune disorder of the small bowel that occurs in genetically predisposed people of all ages from middle infancy. Symptoms include chronic diarrhoea, failure to thrive (in children) and fatigue, but these may be absent and symptoms in all other organ systems have been described. It is estimated to affect about 1% of Indo-European populations, although significantly underdiagnosed. A growing portion of diagnoses are being made in asymptomatic persons as a result of increasing screening.

Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat (and similar proteins of the tribe Triticeae which includes other cultivars such as barley and rye). Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the bowel tissue, causing an inflammatory reaction. That leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrients. The only effective treatment is a lifelong gluten-free diet.

 

Role of Other Grains

Wheat varieties or subspecies containing gluten such as spelt and Kamut®, and the rye/wheat hybrid triticale, also trigger symptoms.

Barley and rye also induce symptoms of coeliac disease.  A small minority of coeliac patients also react to oats.  It is most probable that oats produce symptoms due to cross contamination with other grains in the fields or in the distribution channels.  Other cereals, such as maize (corn), quinoa, millet, sorghum, rice are safe for a patient to consume. Other carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms.

 

Signs and Symptoms

Classic symptoms of coeliac disease include diarrhoea, weight loss (or stunted growth in children), and fatigue, but while coeliac disease is primarily a bowel disease, bowel symptoms may also be limited or even absent. Some patients are diagnosed with symptoms related to the decreased absorption of nutrients or with various symptoms which, although statistically linked, have no clear relationship with the malfunctioning bowel. Given this wide range of possible symptoms, the classic triad is no longer a requirement for diagnosis.

Children between 9 and 24 months tend to present with bowel symptoms and growth problems shortly after first exposure to gluten-containing products. Older children may have more malabsorption-related problems and psychosocial problems, while adults generally have malabsorptive problems.  Many adults with subtle disease only have fatigue or anaemia.

Coeliac disease has been linked with a number of conditions. In many cases it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.

• IgA deficiency is present in 2% of patients with coeliac disease, and in turn this condition features a tenfold increased risk of coeliac disease. Other features of this condition are an increased risk of infections and autoimmune disease.
• Dermatitis herpetiformis; this itchy cutaneous condition has been linked to a transglutaminase enzyme in the skin, features small bowel changes identical to those in coeliac disease and occurs more often (in 2%) in patients with coeliac disease.
• Neurological associations: epilepsy, ataxia (coordination problems), myelopathy, peripheral neuropathy and schizophrenia have all been linked with coeliac disease, but the strength of these associations and the causality are still subject to debate.
• Growth failure and/or pubertal delay in later childhood can occur even without obvious bowel symptoms or severe malnutrition. Evaluation of growth failure often includes coeliac screening.
• Miscarriage and infertility.
• Hyposplenism (a small and underactive spleen) - it is unclear whether this actually increases infection risk in the same way as in other people without a functioning spleen.
• Other auto-immune disorders: diabetes mellitus type 1, autoimmune thyroiditis, primary biliary cirrhosis and microscopic colitis.

 

Antibody Testing

Four serological blood tests exist for coeliac disease. The most widely used ones detect an antibody of the IgA type against particular antigens in the small bowel. Older tests detected antibodies against reticulin (ARA) or gliadin (AGA), but recent evidence supports the use of the more modern tests, namely those detecting IgA antibodies against endomysium (EMA) or tissue transglutaminase (TTG). Generally, serology may be unreliable in young children, with anti-gliadin performing somewhat better than other tests in children under five.

Guidelines recommend that a total serum IgA level is checked in parallel, as coeliac patients with IgA deficiency may be unable to produce the antibodies on which these tests depend ("false negative"). In those patients, IgG antibodies against transglutaminase (IgG-TTG) may be diagnostic.

 

HLA Genetic Typing

Antibody testing and HLA testing have similar accuracies.

 

Endoscopy

An upper endoscopy with biopsy of the duodenum (beyond the duodenal bulb) or jejunum is performed. It is important for the physician to obtain multiple samples (four to eight) from the duodenum. Not all areas may be equally affected; if biopsies are taken from healthy bowel, it would result in false negative results.

Most patients with coeliac disease have a small bowel that appears normal on endoscopy; however, five endoscopic findings have been associated with a high specificity for coeliac disease when all are found: scalloping of the small bowel folds (pictured), paucity in the folds, a mosaic pattern to the mucosa (described as a cracked-mud appearance), prominence of the submucosal blood vessels and a nodular pattern to the mucosa.

Until the 1970s, biopsies were obtained using metal capsules attached to a suction device. The capsule was swallowed and allowed to pass into the small intestine. After X-ray verification of its position, suction was applied to collect part of the intestinal wall inside the capsule. One much utilized capsule system is the Watson capsule. This method has now been largely replaced by fiberoptic endoscopy, which carries a higher sensitivity rate and a lower error frequency.

 

HLA DR3-DQ2

HLA DR3-DQ2 is double serotype that specifically recognizes cells from individuals who carry a multigene HLA DR, DQ haplotype. Certain HLA DR and DQ genes have known involvement in autoimmune diseases. DR3-DQ2, a multigene haplotype, stands out in prominence because it is a factor in several prominent diseases, namely coeliac disease and 'juvenile diabetes' (T1D type 1 diabetes, diabetes mellitus type 1). In coeliac disease, DR3-DQ2 haplotype is associated with highest risk for disease in first degree relatives, the majority of the risk is conferred by the DQA1*0501 DQB1*0201 haplotype that encodes DQ2.5cis isoform of HLA-DQ. In T1D both DR3 and DQ2 appear to confer risk to disease.

The frequency of both diseases changes with respect to both the environment (diet) and the frequency of the DR3-DQ2. With coeliac disease risk is increased with the consumption of Triticeae glutens, and this also increases risk in juvenile diabetes whereas other cereals also appear to play a role. More importantly the risk of disease is greatest in homozygotes and linear increases in haplotype resulting in several fold increases of disease risk. This increased risk is most prominent in a rare cancer, enteropathy associated T-cell lymphoma.

 

Distribution

HLA DR3-DQ2 is not spread evenly among humans. It is has a substantially higher frequency in the Western world, except indigenous Native American. It is virtually absent in some Asian populations. The current world distribution suggests that it spread from Africa with a wave that spread late in human evolution which reached central Asia more recently, a possibility is that it spread with agrarian cultures that migrated from Africa. [Note some population test DR3 or DQA1:DQB1, the DR3-DQ2 serotype is generally synonymous in frequency with DQ2.5]

DR3-DQ2 probably originated from Central or West Africa. DQ2.5cis haplotype is the second highest frequency haplotype in the Aka (N. Congo) and several other surrounding groups it is virtually absent in the !Kung. DQ2.5 primarily spread to the northwest and appears to have spread late in global spread of anatomically modern humans. The !Kung (San Bushmen; videos 2, 3, from the Journey of Man: A Genetic Odyssey by Spencer Wells) and Austronesians are reasonable marker populations of the earliest (eatward) spread out of Africa and those that spread rapidly, since the ancestors of the !Kung appear to have come from East Africa and share many Cw_B types in common with Austronesians and Northern Eurasians. DQ2.5 is at low frequencies in both of these populations, and it did not spread to Japan or the New World in pre-Columbian times. There is the possibility it spread to Arabia, but through stepwise expansion of small groups was lost from the DQ genetic repertoire.

DQ2.5 appears to be derived from DQ2.2 by gene recombination. One haplotype DQA1*0501:DQB1*0202 can be found in Africa suggesting DQB1*0201 evolved from DQB1*0202. The regions of Africa where DQ2.5 is at its highest frequencies indicate potential sources for western European haplotypes (e.g. Bedoin) but also indicate recent dispersion making precise evolution difficult to interpret. Other evidence for a west African origin/expansion is seen with the probable origin of DQA1*0501 from DQA1*0505, which is at relatively high frequencies in west-central Africa.

 

Frequencies in Asia

Based on frequencies in Central and East Asia, DR3-DQ2 appears to have spread eastward recently. Of particular interest to the West African/Central Asian comparison, not only is DQ3-DQ2.5 elevated in both places, but a linked HLA A-B haplotype, A33-B58, is found in West Africans and both the A33 and B58 alleles show more allelic and haplotype diversity in West Africa. This similarity would be remarkable if this haplotype came with migrations 50,000 to 130,000 years ago, since considerable equilibration and long range migrations are expected over this time frame. Ironically, there is no convincing route of travel between West Africa and Central Asia suggested by gene frequencies in the peoples between the two. This recent migation hypothesis is supported by HLA-A36 which shows a similar African/Central Asian bimodal distribution. One population that might have been related to this migration are non-caucasians of northern Africa.

DR3-DQ2 is notably higher in W. Mongolia, Kazahkstan and W. China. One eastern haplotype is "A33-B58" and has some punctuated distribution in Western Europe at relatively low levels, and is also in extreme disequilibrium where it is found, elsewhere. In Thailand it is elevated, particularly in the Thai Chinese, but in the south and most parts of Indonesia its frequency is zero. Elevated DR3-DQ2 levels in the Muong suggest a similar North to South spread.

DR3-DQ2 presence in the Koreans and lack thereof in the Japanese suggest a recent spread into Western Pacific Rim of Asia. By HLA, Y chromosome, or mitochondrial DNA the Japanese are about 60-85% of post-Jōmon period Korean origin, and the level of DR3-DQ2 in Japanese is about 1/10th that of Koreans suggesting that DR3-DQ2 did not spread in the Yayoi and that it spread recently with Mongol spread in Eastern Asia, it is rare both east and south of China (except in regions with strong historic migrations of Chinese), rare in Indigenous Austronesians, and isolated Indigeonous American groups.

 

The Importance of the Estimates

Currently, in assessing diseases like Coeliac disease a definite diagnosis is often not possible and statistical considerations are relied upon. The knowledge of frequencies in populations, particularly among ancestors of immigrants can aid patient and physician as to the potential risks. An example, one publication states that the western regions of Ireland have the highest coeliac disease rate in the world. Plotting the frequency of DQ2.5 from any part of Western Europe to the Irish one sees the frequency gradient progressing toward the north and west of Ireland; therefore, a high rate of coeliac disease is not unexpected in Western Ireland. People with many common ancestors from Ireland share similar risks of disease.

In the case of juvenile diabetes a clear distinction of DR3-DQ2 from DR7-DQ2 is necessary because both DR3 and DQ2 confer risk of disease. And DR3-DQ2/DR4-DQ8 individuals who have type 1 diabetes (late onset) are often mistaken for type-2 diabetes.

 

Associated Diseases

DR3-DQ2 is associated with probably the greatest frequency of autoimmune occurrence relative to any other haplotype. The DQA1*0501:DQB1*0201 (DQ2.5) locus confers susceptibility to Gluten Sensitive Enteropathy (GSE)and (Type 1 Diabetes ) but has also been linked to other rarer autoimmune diseases like myasthenia gravis.

 

Type 1 diabetes

In type 1 diabetes both DR3 and DQ2 appear to play a role.

 

 

HLA-DQ8

HLA-DQ8 (DQ8) is an HLA-DQ serotype that recognizes the common HLA DRB1*0302 and the less common HLA DRB1*0304 gene products. DQ8 is a form of 'split antigen' of the broad antigen group DQ3 which also contains DQ7 and DQ9. DQA1*0301 : DQB1*0302 is the most common DQ8 type but other alpha (DQA1*0302, *0303, *0401 and *0503) and beta (DQB1*0304 and *0305) may be recognized as part of the DQ8 antigen.

Certain HLA-DQ isoforms are more commonly associated with certain autoimmune diseases. DQ8 stands out because of its association with juvenile diabetes, coeliac disease. It is also linked to HLA-DR alleles that are implicated in rheumatoid arthritis and may increase risk. HLA-DQ is not spread uniformly and certain populations are at increased risk; however that risk is often dependent on environment (e.g. Triticeae glutens consumption).

DQ8.1 is found almost ubiquitously in every human regional population, but because of its unique distribution it becomes an object of molecular anthropology. There are 3 places where haplotype frequency is elevated, Central and South America, NE Pacific Rim, and Northern Europe.

 

Abundance in Asia

Hiatus of DQ8 in the NE Siberian Arctic, Elevated Levels in Amur Region and Eastern Turks The levels of DQ8 in SW to West Pacific Rim are at variable haplotype frequencies, from 2 to 30%, and level off around 10% for Ryūkyūan, Japanese, Koreans, Amur Regions and in the NW Pacific Rim drop to less than 1% in the Nivkh. There is a modern hiatus of DQ8 in the Alaska-Eastern Siberian region and it is unclear whether this is due to replacement, selection, or the mode in which first Americans arrived (i.e strictly maritime route). The DR types associated with DQ8 are DRB1*0403, *0404, *0406, *0407, *0408, and *0401 is split between many DQA1:B1 haplotypes. DQB1*0405 is commonly associated with DQA1*0303:DQB1*04 and so it is not included in DRB1*0401 in high resolution assessments. The Cook Island DQ8 had only one associated DR haplotype suggesting diversity limiting introduction into the region, either via the Taiwan-(Japan/Korea/China) route or through the west, for example the Bunun have high DRB1*0403. The majority of DRB1*04 appear to have redistributed from Eastern Asia from an unknown source, possibly in Central Asia or India. The distribution can be compared with native groups such as South Americans. Three groups with high levels, the Kogui, Sikuni, and Yucpa, have about 75% DQ8, the dominant DRB1* allele in 2 of 3 is the *0411 (N. China = 0), but *0407 (Ryūkyū, Japanese, Mansi-Eastern Ural, Naxi Chinese) and *0403 (Nganasan, Buryat, Negidal, Tunisians, Ryūkyū, Korea, Ainu) are also found. In North America DRB1*0404 and *0407 are more common than *0403 and, in the Lakota Souix, B1*0411 is rare. The DRB1*0404-DQ8 haplotype is more common in North Western Asia, and Northern Europe.

High Frequencies in the Americas

The global node for DQ8 is in Central America and northern South America where it reaches the highest frequency for any single DQ serotype, close to 90% phenotype frequency (77% haplotype frequency), and is at relatively high frequency in the indigenous North American population, and the coastal regions of the Gulf of Mexico and up the Mississippi Valley. The high freqeuncy of DQ8 in South America's northeastern regions and low frequency in Indigenous Americans of more recent Asian ancestry or Siberian origin suggest that DQ8 was at high frequency in the earliest Amerinds. The pattern of distribution is consistent with recent mtDNA results suggesting the first migrants to the New World settled in the lowland coastal regions, river valleys and moved slowly inland, subsequent settlers moved into the highland regions. DQ8 and DQ2.5 have many analogous functional similarities, and this first settler bias may be a reason for the similarity. Studies on Epstein Barr Virus and other proteins suggest both proteins are acidic (meaning peptides with increased negative charge) peptide presenters and may have been adaptive for certain hunting and gathering lifestyles, possibly coastal foragers.

 

High Levels of DQ8 in Northern Europe

DQ8 is also abundant in Northern Europe and is found at high frequencies in the German-Scandinavian-Uralic population north of Switzerland. HLA A-B haplotypes suggest that a migration from people east of the Urals is responsible for DQ8, possibly from as far east as the West Pacific Rim. The high level of DQ8 and DQ2.5 is something of great interest for DQ mediated diseases of Scandinavia and Northern Europe. DQ8 is also found in Iberia and places where east to west gene flow by other genetic markers cannot be substantiated, and the levels within the African or Middle Eastern population are possible sources, Iberia has considerable A1/B1 equilbration suggesting independent sources from Africa.

 

Global Spread of DQ8

DQ8 along with a few other Haplotypes appears to be split NW/SE in Eurasia and with the evidence for DQ2.5 and other haplotypes suggest an ancient Central Asian population was displaced by a more recent African migration. There are many common markers found in French, Germans, Danes, Swedes, Tibetans, Amur River, Japanese and Koreans that are potential indicators of this bilateral spread. The DQ8 haplotypes is found at high frequencies in the !kung, albeit one expects more DQ8 in Austronesia it is ubiquitously spread if at some times low frequencies, other times higher frequencies (Thai). The path of DQ8 spread to the New World is enigmatic, certainly Japan and Amur River are potent sources, but other displaced populations cannot be ruled out. If the mode of travel was through the Beringia corridor as proposed by archaeologist, the very low frequency of DQ8 at present is a very unusual find with regard to evidence for complete displacement elsewhere in the World. Markers that are shared between Japanese, TW-aboriginals tend to decline in frequency as one approaches Siberia, mtDNA markers decline in the Kuril chain. During the Jōmon period of Japan it appears there would have been displacement by Ninhvet/Ainu ancestors and depression of DQ8 throughout northern Japan, but the decline throughout the region is somewhat inexplicable outside of a catastrophic climate event between the settling of the New World and the current time. An alternative model is that there were multiple sources of DQ8 in the peopling of NE Asia, some sources were from Central Asia and some from the Indochinese region, some of the DQ8 found in NW Eurasia could be from an admixture of West Pacific Rim and Central Asian sources, and were displaced from the more central regions but not from the more Eastern regions.

 

DQ8 and Selection

Like DQ2.5, DQ8 might have been under selection for maritime, coastal foraging peoples and in particular for peoples adapted to the climate/habitat situation on the northern end of the habitable West Pacific Rim at the Last Glacial Maximum. Triticeae cultivation may apply negative selection on DQ8. While there were numerous members of Triticeae species similar to Mid Eastern wild Triticeae in the Americas, and a great number of domesticated plants in the new world, no single species of Triticeae appears to have been domesticated in the New World, and no clear examples in closely related tribes of grasses. Among new world grass species in post Columbian times, one species of Elymus has been domesticated for human consumption and another as a pastoral cultivar. This could be interpreted in 2 ways. First, that levels of DQ8, negatively, inhibited the domestication of Triticeae strains. Second, that the absence of such cultivars more suitable than already developed cultivars allowed DQ8 to rise or remain high, while DQ2.5 levels in NW under much longer term selection have fallen, or a little of both. Most of American cultivars were domesticated south of the Rio Grande river (exceptions are Caddo rice and Texas varigated squash, etc.). Wheat, particularly Barley and Rye are preferential cultivars in cooler climate, whereas Zea (maize) is more adaptive in tropical climates and some cultivars are relatively drought tolerant, Zea however lacks certain amino acids that must be supplimented by other foods to prevent malnutrition. The proximity of neolithization to the Equator in the New World may have much to do with the unapparent negative selection of DQ8 relative to the neolithization of Western Eurasia.

 

DQ8 and Disease

In Europe, DQ8 is associated with Type 1 diabetes and to a lessor degree Coeliac disease. The highest risk factor for type 1 diabetes is the HLA DQ8/DQ2.5 phenotype. In parts of eastern Scandinavia both DQ2.5 and DQ8 are high increases frequencies of late onset Type I and ambiguous Type I/II diabetes. DQ8 is also found in many indigeonous peoples of Asia, it was detected early on in the Bedoin population of Arabia where DQ2.5 is frequently absent, and in these instances DQ8 is solely associated HLA in Coeliac Disease.

In the United States, however there appears to be shift in autoimmune disease risk for immigrants from Mexico. Increased immunoreactivity of Hispanics in Houston appear to be associated with DR4-DQ8. The haplotype may incur the highest risk for rheumatoid arthritis.

In Japan DQ3 (DQ7, DQ8, DQ9) is associated with Myasthenia gravis in the early onset female population, though it does not appear DQ8 has the greater role, there are similarities between myastenia gravis in Japan and that detected in the Houston hispanic population, with DQ8 associated with younger females relative to the associations of all other HLA DQ types. Coeliac Disease is on the rise in Japan, and it is clear that dietary shifts are the reason, but, also there is no DQ2.5 in Japan and therefore it is not a risk factor. Diabetes, which was once considered a problem of the wealthy in Japan, but is also on the rise in the general population. The similarities with the Indigeonous Americans cannot be dismissed, because both wheat consumption, beef consumption and milk consumption are on the rise in Japan, but since there is no DQ2.5 the increased risk of late onset and Type I/II is almost eliminated from consideration.

The DR4 Linkage

Many disease associated with DQ8 have dual linkage with DR4, and certain DR4 (*0405) have independent and dependent risk association with DQ8, for example with Juvenile diabetes.

 

 

DQ8/DQ2.5 Heterozygotes

The distribution of this phenotype is largely the result of admixtures between peoples of eastern or central Asian origin and peoples of western or central Asian origin. The highest frequencies, by random mating, are expected in Sweden, but pockets of high levels also occur in Mexico, and a larger range risk exists in Central Asia.

Diseases that appear to be increased in Heterozygotes are Type 1 Diabetes. New evidence is showing an increased risk for late onset Type 1 diabetes in Heterozygotes (which includes ambiguous Type I/Type II diabetes. Celiac Disease may have a slightly increased risk with a more severe course of disease.

 

	DQ2.5	DQ8	DQ2.5/DQ8
Sweden	15.9	18.7	5.9
Jalisco	11.4	22.8	5.2
England	12.4	16.8	4.2
Kazakh	13.1	11	2.9
Uygur	12.6	11.4	2.9
Finland	9	15.7	2.8
Poland	10.7	9.9	2.1

 

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HLA Gene Frenquencies from the Origin of Minnan and Hakka, the So-Called "Taiwanese", Inferred by HLA Study by M. Lin, et al.

HLA	Minnan	Hakka
DQB1*02	8.8	10.6
DRB1*03	7.4	8.6
DQB1*0302c	19.4	7.6
DQB1*0302d	7.4	7.6

*0301c:0311-012/04/09/10, *0302d:0302/05/07-08

 

____________________________________________________________________________________________

 

* Is Adult Celiac Disease Really Uncommon in Chinese? by Ling-ling Jiang

Abstract: Celiac disease (CD) is a type of intestinal malabsorption syndrome, in which the patients are intolerant to the gliadin in dietary gluten, resulting in chronic diarrhea and secondary malnutrition. The disease is common in Europe and the United States, but only sporadic reports are found in East Asia including China. Is CD really rare in China? We examined 62 patients by capsule endoscopy for chronic diarrhea from June 2003 to March 2008. Four patients with chronic diarrhea and weight loss were diagnosed to have CD. Under the capsule endoscopy, we observed that the villi of the proximal small bowel became short, and that the mucous membrane became atrophied in these four patients. Duodenal biopsies were performed during gastroscopy and the pathological changes of mucosa were confirmed to be Marsh 3 stage of CD. A gluten free diet significantly improved the conditions of the four patients. We suspect that in China, especially in the northern area where wheat is the main food, CD might not be uncommon, and its under-diagnosis could be caused by its clinical manifestations that could be easily covered by the symptoms from other clinical situations, particularly when it came to subclinical patients without obvious symptom or to patients with extraintestinal symptoms as the initial manifestations.