celiac disease
Resource Center




 

 

celiac disease in the news

Mayo Clinic discovers potential link between celiac disease and cognitive decline 

EurekAlert! - Oct 09 1:31 PM
ROCHESTER, Minn. -- Mayo Clinic researchers have uncovered a new link between celiac disease, a digestive condition triggered by consumption of gluten, and dementia or other forms of cognitive decline.

Study: Celiac Disease and Dementia Linked 
RedNova - Oct 09 3:17 PM
U.S. researchers say they have found a new link between celiac disease, a digestive condition triggered by consumption of gluten, and dementia. There has been very little known about this connection between celiac disease and cognitive decline until now, said Dr.

Mayo Clinic Discovers Potential Link Between Celiac Disease and Cognitive Decline 
[Press Release] U.S. Newswire via Yahoo! News - Oct 09 1:03 PM
Mayo Clinic researchers have uncovered a new link between celiac disease, a digestive condition triggered by consumption of gluten, and dementia or other forms of cognitive decline. The investigators' case series analysis an examination of medical histories of a group of patients with a common problem of 13 patients will be published in the October issue of "Archives of Neurology."

Study: Celiac disease and dementia linked 
UPI - Oct 09 12:41 PM
ROCHESTER, Minn., Oct. 9 (UPI) -- U.S. researchers say they have found a new link between celiac disease, a digestive condition triggered by consumption of gluten, and dementia.

celiac diease

 

 

- symptoms of celiac disease

- celiac disease

Coeliac disease
Biopsy of small bowel showing coeliac disease manifested by blunting of villi, crypt coliac disease hyperplasia, and lymphocyte infiltration of crypts.
ICD-10 K90.0
ICD-9 579.0
OMIM 212750
DiseasesDB 2922
MedlinePlus 000233
eMedicine med/308  ped/2146 celliac disease radio/652

Coeliac disease or celiac disease is an autoimmune disorder of celic disease the small bowel that occurs in genetically predisposed individuals in celiac disese all age groups after early infancy. Symptoms may include diarrhoea, failure to thrive (in children) and fatigue, but these may be celisc disease absent and associated symptoms in all other organ systems celiec disease have been described. It affects caliac disease approximately 1% of Caucasian populations, though it is significantly underdiagnosed. A growing celiacdisease portion of diagnoses are being made in asymptomatic persons as a result of increasing screening.[1]

Coeliac disease celiac dusease is caused by an abnormal reaction to gliadin, a celia disease gluten protein found in wheat (and similar proteins of the tribe Triticeae which celiac diseas includes other cultivars such as barley and rye). Upon celiac diseae exposure to gliadin, the body's immune system cross-reacts with the enzyme tissue transglutaminase, ceilac disease causing an inflammatory reaction that leads to flattening of the lining the small intestine, which celica disease interferes with the absorption of nutrients. The only effective treatment is a diet, lifelong in principle, from which gluten celaic disease is absent.

This condition has several other names, celiac disease including: cœliac disease (with ligature), c(o)eliac sprue, non-tropical sprue, endemic sprue, gluten enteropathy or symptoms of celiac disease gluten-sensitive enteropathy, and gluten intolerance. The term coeliac derives from the Greek κοιλια celiac disease symptoms (koilia, abdomen), and was introduced in diet for celiac disease the 19th century in a translation of what is generally regarded as an celiac sprue disease ancient Greek description of the disease by Aretaeus of Cappadocia.[2]

Contents

  • 1 Signs celiac disease diet celiac disease neurological symptoms and symptoms
    • 1.1 Gastrointestinal symptoms
    • 1.2 Malabsorption-related symptoms
    • 1.3 Miscellaneous mangosteen and celiac disease symptoms
    • 1.4 The role of other grains
  • 2 Diagnosis
    • 2.1 Blood celiac disease recipes tests
    • 2.2 Endoscopy
    • 2.3 Pathology
    • 2.4 Other celiac disease diagnosis diagnostic tests
    • 2.5 Screening and case finding
  • 3 Pathophysiology
    • 3.1 Genetics
    • 3.2 Prolamins
    • 3.3 Tissue celiac disease and alopecia malabsorption symptoms celiac disease transglutaminase
    • 3.4 Villous celiac disease and obesity atrophy and malabsorption
    • 3.5 Triggers
  • 4 Treatment
    • 4.1 Diet
    • 4.2 Refractory symptoms of celiac disease candida disease
    • 4.3 Experimental treatments
  • 5 Epidemiology
  • 6 Social genetic testing for celiac diseases and religious issues
    • 6.1 Roman symptons of celiac disease Catholic position
    • 6.2 Eastern Orthodox Position
    • 6.3 The celiac diet disease free gluten Church of Jesus Christ of Latter-day Saints
    • 6.4 Coeliacs and Passover
  • 7 History
  • 8 References
  • 9 External celiac disease + hives links

Signs and symptoms

Classic symptoms of coeliac celiac disease misdiagnosed disease include diarrhoea, weight loss (or stunted growth in celiac disease treatments children) and fatigue, but while coeliac disease is a disease of the bowel, it may present long term effects of celiac disease with limited bowel symptoms. Some patients are diagnosed with symptoms related to sjogrens disease and celiac the decreased absorption of nutrients or with symptoms which, although statistically linked, have what is celiac disease no clear antidepressant therapy and celiac disease relationship with the malfunctioning bowel.

Children between 9 and 24 months tend to present celiac disease cholestorol with bowel symptoms and growth problems shortly after first exposure neuropathy from celiac disease to gluten-containing products. Older children may have more malabsorption-related problems and psychosocial problems, while adults celiac disease alcoholic drinks generally have malabsorptive problems.[3] Many adults with subtle disease only have fatigue or anaemia.[1]

Gastrointestinal symptoms

The diarrhoea celiac disease canada characteristic of coeliac disease is pale, voluminous and malodorous. Abdominal pain and cramping, bloatedness and abdominal distention (thought to be due celiac disease cause death to fermentative production celiac disease help medicine relief stomach pain of bowel gas) and mouth ulcers[4] may be present. As the bowel is more damaged, a degree of lactose celiac disease support groups intolerance may develop. Constipation diabetes and celiac disease is rare, but may be a manifestation of coeliac disease.[3]

Coeliac disease leads to an increased information on celiac disease risk of both adenocarcinoma and lymphoma of the small bowel, which returns to morgellons disease celiac baseline with diet. Longstanding disease may lead natural skin care celiac disease to other complications, such as ulcerative jejunitis (ulcer formation of the small bowel) and stricturing (narrowing as a result what not to eat with celiac disease of scarring).[5]

Malabsorption-related symptoms

The changes alba celiac disease in the bowel make it less competent in absorbing nutrients, minerals and fat-soluble vitamins.[3]

  • The inability to alcoholism glutamine celiac disease absorb carbohydrates and lipids may cause weight loss (or b celiac b disease gluten free diet support center at failure to thrive/stunted growth in children) b-12 celiac disease and fatigue or lack of energy.
  • Anaemia may develop in baby with celiac disease several ways: iron malabsorption may cause iron deficiency anaemia, and folic acid and vitamin B12 malabsorption may give rise celiac disease and autism to megaloblastic anaemia.
  • Calcium and vitamin D (and compensatory secondary hyperparathyroidism) may cause osteopenia (decreased mineral content of celiac disease and children the bone) or osteoporosis (bone weakening and risk of celiac disease desserts fragility fractures). Malabsorption of vitamin celiac disease ethics D may lead to vitamin D deficiency rickets or even hypocalcemic tetany.
  • A small proportion have abnormal coagulation due to deficiency of celiac disease foundation vitamin K, and are slightly at risk for abnormal bleeding.
  • Coeliac disease celiac disease genetic testing is also celiac disease gluten free diet associated with bacterial overgrowth of the small intestine, which can worsen malabsorption, or cause malabsorption after treatment.[6]

Miscellaneous symptoms

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

  • IgA deficiency celiac disease symp is present in 2% of patients celiac disease symtoms onset with coeliac disease, and in turn this condition features a tenfold increased risk of coeliac disease.[7][8] Other features celiac disease test of this condition are an increased risk of infections and celiac disease test kits autoimmune disease.
  • Dermatitis herpetiformis; this itchy celiac disease versus irritable bowel disease table cutaneous condition has been linked to a transglutaminase in the skin, features college scholarships for celiac disease small bowel changes identical to those in coeliac disease[9] and occurs columbus ohio specializing in celiac disease more often (2%) in patients with coeliac disease.[3]
  • Neurological associations: depression caused by to celiac disease epilepsy, ataxia (coordination problems), myelopathy and peripheral neuropathy have all diagnosis of celiac disease been linked with coeliac disease, but the strength of these associations and the causality is still subject drperlmutter and celiac disease of debate.[10]
  • Growth failure and/or pubertal maltodextrin and celiac disease delay in later childhood can occur even without obvious bowel symptoms or severe malnutrition. mortality rate in celiac disease Evaluation of growth failure often includes celiac screening.
  • Miscarriage and infertility.
  • Hyposplenism (a national celiac disease small and underactive spleen) - it is unclear whether this actually increases infection risk in coeliacs.[11]
  • Other auto-immune disorders: signs and symptoms of celiac disease diabetes mellitus type 1, autoimmune thyroiditis,[12] primary apple belly celiac disease biliary cirrhosis[13] and microscopic colitis.[14]

The role of other grains

Wheat varieties are headaches are side affect of celiac disease or subspecies such as authrorities celiac disease medical more spelt and Kamut®, and the rye/wheat hybrid triticale, also trigger symptoms.[15]

Barley and rye can celiac disease cause insomnia also induce coeliac disease.[15] A small minority of coeliac patients also can celiac disease cause siezures react to oats.[16][17] Most probably oats produced celiac digestive disease govenment htm index niddk nih pub symptoms due to cross contamination with other grains in the fields or in celiac digestive disease govornment htm index niddk nih pub the distribution channels. There is at least celiac disease + blood in stool one oat vendor (McCann's) which, while not claiming to be gluten-free, points out that the celiac disease + ssri risk of contamination is low due to the processes they celiac disease - tooth malformity use.citation needed] Other cereals, celiac disease alcoholism such as maize (corn), sorghum, rice are safe for a patient celiac disease and appendicitis to consume. Other carbohydrate-rich foods, like potatoes and bananas, do not contain gluten and do not trigger the disease.

Diagnosis

The condition is frequently misdiagnosed celiac disease and fibromyalgia or overlooked as it can exhibit multiple symptoms and often the patient or medical staff may not link seemingly unconnected celiac disease and hair loss conditions. celiac disease and hemorrhoids It is most frequently misdiagnosed when the sufferer complains of diarrhea, persistent celiac disease and ms indigestion, an itchy rash (dermatitis herpetiformis), or irritable bowel syndrome.

There are several tests that can be celiac disease children stories used to assist in diagnosis. The level of symptoms may celiac disease free kid recipes determine the order of the tests, but all tests celiac disease las vegas nv must be done while the person is on a gluten containing diet. Antibodies celiac disease unicameral bone cyst are reduced and intestinal damage begins to heal immediately upon removing all gluten from the diet, celiac disease women's health problems so the risk of misdiagnosis is increased if the difference between ibd and celiac disease table person is not eating gluten. For those who have already commenced themselves on a gluten-free gluten intolerance celiac disease diet, professional guidelines recommend a re-challenge of 2-6 weeks with 10 g of gluten (four intestinal celiac disease dermatitis herpetiformis slices of bread) before repeating the intravenous and celiac disease investigations. Those who experience severe symptoms earlier can be regarded as sufficiently challenged and can be tested earlier.[3]

Blood tests

Serology by blood test is both good at marfan celiac disease diagnosing coeliac disease (high sensitivity of 98%, i.e. it natural treatment for celiac disease misses 2 in 100 cases) and excluding it (high specificity of >95%, i.e. a positive test is most non hodgkins lymphoma and celiac disease likely confirmative of coeliac disease ppt celiac disease rather than other condition). Because of the major implications of a diagnosis of coeliac disease, many recommend that a studies on treating celiac disease positive blood test is still followed by an endoscopy. A topical fluoride treatment and safety for celiac disease negative test may still prompt a biopsy if the suspicion addison's disease celiac disease auto immune dissorders is very high; this would pick up the remaining advanced celiac disease 2% undiagnosed cases. Due to the few limitations of blood tests, are headaches are symptom of celiac disease endoscopy and biopsy is still considered the gold standard in the diagnosis of coeliac disease.[3][5]

Due to its authoritiers celiac disease medical more high sensitivity, serology has been proposed as a screening measure, blood test celiac disease because the presence of antibodies would can celiac disease cause complex partial siezure activity detect previously undiagnosed cases of coeliac disease and prevent its complications in canada + celiac disease those patients.

Serology may also be used to monitor celiac condidtion disease more symptom adherence to diet.[3][5]

Four serological blood tests exist for coeliac disease:

  • IgA and IgG anti-tissue transglutaminase antibody (anti-tTG). celiac condition disease mroe symptom This test is sometimes used alone. If this test is positive celiac condition disease omre symptom it is highly likely that the patient has coeliac disease. It is not reliable in children before celiac digestive disease govenrment htm index niddk nih pub celiac digestive disease goverment htm index niddk nih pub the age of 2.
  • IgA and IgG anti-gliadin antibodies (AGA), IgG and IgA. These tests are often useful when celiac digestive disease government htm index niddk nih pub testing young symptomatic children, but they celiac digestive disease governmnet htm index niddk nih pub are found in fewer coeliacs than anti-tTG, and their presence does not automatically celiac digestive disease govorment htm index niddk nih pub indicate coeliac disease because they are found in some other disorders.
  • IgA anti-endomysial antibodies (EMA). This test is being replaced by the anti-tTG test celiac disease and blood tests because both tests measure celiac disease and candida the autoantibodies that cause the tissue damage associated with coeliac celiac disease and chrones disease. Many physicians still order this test. This test as tTG celiac disease and elevated crp test is also not reliable in children before the age of 2.
  • An older test, the IgA anti-reticulin antibodies (ARA). IgA anti-ARA celiac disease and emotional problems is not ordered as frequently as it celiac disease and epilepsy once was, because it is less sensitive and less specific than the other tests. celiac disease and heredity It is found in about 60% of people with coeliac celiac disease and hypogonadism disease and 25% of those with dermatitis herpetiformis.

For those based on IgA, a total IgA celiac disease and ibd differences level is checked in parallel, as patients with IgA deficiency celiac disease and immunizations may have a normal result while still celiac disease and minnesota physicians having coeliac disease ("false negative"). In those patients, IgG antibodies may be celiac disease and sleep disorder diagnostic.[18]

Many doctors consider coeliac disease to be diagnosed where the patient has positive blood celiac disease and sweating tests and shows improved symptoms after the adoption of a gluten-free diet, while celiac disease and wheat others require at least one upper celiac disease assco. of can. endoscopy with biopsy. The problem with not doing a biopsy at all is celiac disease child stories that patients later commonly want to know if they really have celiac disease constipation coeliac disease and need to remain gluten restricted. A diagnosis with biopsy confirmation at the time celiac disease cure of initial diagnosis eliminates this common clinical problem.

Endoscopy

Endoscopic still of duodenum celiac disease ethical issues of patient with coeliac disease showing scalloping of folds.
Schematic of the Marsh classification of upper jejunal pathology in coeliac disease

An upper endoscopy with biopsy of the duodenum celiac disease foods (beyond the duodenal bulb) or jejunum celiac disease genetic marker is performed. It is important for the physician to celiac disease gluten b free b diet support center at obtain multiple samples (three or more) from various places throughout the intestine. Not all areas may be celiac disease gluten intolerance equally affected, which is why even upper endoscopy carries a small risk of false negative results.[5] Most celiac disease in infants celiac disease information patients with coeliac disease have a normal appearing small bowel on endoscopy; however, five endoscopic findings have celiac disease ingredients been associated with a high specificity for coeliac disease when all are celiac disease message board and gluten free found: scalloping of the small bowel folds celiac disease monkeys (pictured), paucity in the folds, a mosaic pattern to the mucosa (described as a cracked-mud appearance), prominence of the celiac disease nutrient absorption submucosal blood vessels and a nodular pattern to the celiac disease self diagnosis mucosa. [19]

Pathology

The classic pathology changes of coeliac disease in celiac disease severe emotional distress the small bowel are categorized by the "Marsh classification":[20]

  • Marsh stage 0: normal mucosa
  • Marsh stage celiac disease signs and symptoms 1: increased number of intra-epithelial lymphocytes, usually exceeding 20 celiac disease sprue diagnosis per 100 enterocytes
  • Marsh stage 2: proliferation of the celiac disease sprue symptoms crypts of Lieberkuhn
  • Marsh stage 3: partial or complete villous atrophy
  • Marsh stage celiac disease symptoms and signs 4: hypoplasia of the small bowel architecture

The changes classically improve or celiac disease symtoms reverse after gluten is removed from the diet, so many official guidelines recommend a repeat biopsy several months after commencement celiac disease thrush of gluten exclusion.

In some cases a deliberate gluten challenge, followed by biopsy, may be celiac related diseases conducted to confirm or refute the diagnosis. A normal clinical treatment of celiac disease biopsy and normal serology after challenge indicates the diagnosis may have been incorrect.[3] Patients crohn's or celiac disease are warned that one does not "outgrow" coeliac disease in the same diagnosing celiac disease dr. green celiac disease way as childhood food intolerances.

Other diagnostic tests

Other tests that may assist in the diagnosis enzyme efficiently degrades gluten disease celiac koning are blood tests for a full blood count, electrolytes, calcium, renal function and liver enzymes. Coagulation testing may be useful ethical issues and celiac disease to identify ethical issues of celiac disease deficiency of vitamin K, which predisposes patients to hemorrhage. These tests should be repeated on fish oil for celiac disease follow-up, as well as anti-tTG titres.[3]

Some professional guidelines[3] recommend screening of all patients for osteoporosis by DXA/DEXA scanning.

Screening and case gastroparesis as a symptom of celiac disease finding

The is significant debate as to the benefits of screening. Some genetically positive for celiac disease studies suggest that early detection would decrease the risk of osteoporosis gluten intolerance without celiac disease and anaemia. In contrast, a cohort studied in Cambridge suggested that people hashimoto's thyroiditis and celiac disease symptoms with undetected coeliac disease had a beneficial risk profile for cardiovascular disease (less overweight, lower cholesterol levels).[1]

Clinical scenarios in which screening may be justified how to test for celiac disease include type 1 diabetes, unexplained iron-deficiency anemia, Down's syndrome, Turner's syndrome, irritable bowel syndrome, lupus, and iga and igg results in celiac disease autoimmune thyroid disease.citation needed]

Pathophysiology

Genetics

Coeliac disease is linked is celiac disease a disability to the CELIAC1 locus (HLA DQ) and occurs is celiac disease an allergy almost exclusively (over 95%) in patients with human leukocyte antigen types jewish genetic diseases celiac DQ2 (DQA1*0501:DQB1*0201) and DQ8 (DQA1*0301:DQB1*0302), which is inherited in families. Over 95% of coeliac patients carry one or two latent celiac disease of the DQ2 or DQ8 genes. DQ2 and DQ8 are serotypes defined by immunological maine celiac disease support group reactivity where as DQA1:DQB1 are two locus haplotypes management celiac disease that are commonly found that result in meal plan for celiac disease the serotypes, and any given person can produce 4 DQ molecules, 2 in the cis-haplotype dimer pairing and 2 medical card celiac disease in the transhaplotype dimer pairing. naspghan celiac disease DQA1*0501:DQB1*0201 and DQ8 produce susceptibility in the cis-haplotype pairing configuration. There is a third pairing of national celiac disease awareness day haplotypes, DQA1*0201:DQB1*0202 / DQA1*0505:DQB1*0301 (DQ7) national celiac disease awareness month that when both are found in a single patient can produce susceptibility to coeliac disease via a natural health celiac disease trans-pairing of the DQA1*0505-DQB1*0202 gene products. With this exception DQB1*0202 nauseated after eating carbohydrates celiac disease is atypically assocaited with coeliac disease.citation needed]

It appears that HLA-DQ2-(DQA1*05) neurological effects of celiac disease is niddk celiac disease more avid in presenting gliadin peptides to T lymphocytes, which then initiate the obstipation and celiac disease autoimmune process.[1]

Every person carries two HLA-DQ_ genes, one from their mother and one from their father. About 20% of osteoporosis celiac disease diet normal people places to go when having celiac disease in australia carry HLA-DQ2, which raises the question of what other factors cause a subgroup of about 5% of those seacoast celiac disease support group people to develop coeliac disease.[1]. The frequency of these genes vary greatly, DQ2(DQA1*05) speech on celiac disease is at high frequencies in the studies involving steroid therapy for celiac disease Sardinians, Basque, British Ilses, Scandinavia. DQ8 is at high frequencies in the South and Central America (up to 90% phenotype frequency), symptoms celiac disease test for celiac disease Mexico, and Sweden. HLA-DQ2(DQA1*05)/DQ8 heterozygotes are at slightly increased risk for coeliac disease versus homozygotes of either and may have more severe testing for celiac disease disease.citation needed]

In addition to the HLA locus on chromosome 6q21.3, several other regions have been linked (especially 19p13.3 and 4p14).[21] Mendelian Inheritance in Man designates five regions as CELIAC1-5 (6q21.3, 5q31-q33, 2q33, 19p13.1, 15q11-q13). For CELIAC3, the CTLA4 gene was found to be linked, and CELIAC4 the gene coding for myosin IXB. CELIAC2 and CELIAC5 have no suspected gene association.

Prolamins

The proteins responsible for the immunological reaction in coeliac disease are the prolamins, storage proteins rich in proline (prol-) and glutamine- (-amin) that dissolve in alcohols and are resistant to pepsin and chymotrypsin, two main digestive proteases. Apart from gliadin (from wheat) the main putative prolamins are hordein (from barley), and secalin (from rye). Recent research has identified a 33 amino acid-long homologous polypeptide in these species that may be responsible for its effects in coeliac disease.[1] There is ongoing controversy on the ability of avenin (from oats) to induce the coeliac response.

Tissue transglutaminase

Tissue transglutaminase, drawn from PDB 1FAU.

Antibodies to the enzyme tissue transglutaminase (tTG) are found in an overwhelming majority of cases, and cross-react to gluten.[22] Tissue transglutaminase participates in the modification of gluten peptides, the product of which may be more potent in stimulating the immune system.[1]

Stored biopsies from suspected celiac patients has revealed that autoantibody deposits in the subclinical celiacs are detected prior to clinical disease. These deposits are found in patients who present with other autoimmune diseases, anemia or maladsoption phenomena at a much increased rate over the normal population.[23]. Endomysial component of antibodies (EMA) to tTG are believed to be directed toward cell surface transglutaminase, and these antibodies are still used in confirming a celiac disease diagnosis. However, a recent study has shown that EMA negative celiac patients tend to be older, more typically male with more severe abdominal symptoms and a lower frequency of "atypical" symptoms including autoimmune disease.[24] In this study the anti-tTG antibody deposits did not correlate with the severity of villous destruction. These findings, coupled with recent work showing that gliadin has an innate response component,[25] suggests that gliadin may be more responsible for the primary manifestations of celiac disease whereas as tTG is a bigger factor in secondary effects such as allegic responses and secondary autoimmune diseases.

Villous atrophy and malabsorption

The inflammatory process, mediated by T cells, leads to disruption of the structure and function of the small bowel's mucosa, and causes malabsorption (it impairs the body's ability to absorb nutrients, minerals and fat-soluble vitamins A, D, E and K from food). Lactose intolerance may be present due to the decreased bowel surface and reduced production of lactase, but typically resolves once the condition is treated.

Some research suggests an alternative route mediated by interleukin 15 in which the innate immune system is induced by a shorter gluten peptide (p31-43/49) that causes killing of enterocytes by lymphocytes in the epithelium.[1]

The villous atrophy seen on biopsy may also be due to unrelated causes, such as tropical sprue, giardiasis, radiation enteritis and several rarer causes. While positive serology and typical biopsy are highly suggestive of coeliac disease, lack of response to diet may require these conditions to be considered.[5]

Triggers

There are various theories as to what determines whether a genetically susceptible individual will go on to develop coeliac disease. Major theories include:

  • An environmental agent, such as infection or a chemical substance
  • Stress
  • Timing of the exposure to gluten (before the gut barrier has developed fully): those exposed to wheat, barley, or rye at any time in the first three months had five times the risk of developing coeliac over those exposed at 4 to 6 months. Those exposed later had a slightly increased risk relative to those exposed at 4-6 months.[26]

Some research has suggested that smoking is protective against coeliac disease.[27] Results on this topic are however inconsistent, and smoking cannot be recommended as a means to avoid developing coeliac disease.

Treatment

Diet

Main article: Gluten-free diet

The only treatment is a life-long gluten-free diet.[28] At this time no medication will prevent damage, nor prevent the body from attacking the gut when gluten is present. The disease is controlled by strict adherence to a gluten-free diet, which allows the intestines to heal and resolves all symptoms in the vast majority of cases and, depending on how soon the diet is begun, can also eliminate the heightened risk of osteoporosis and intestinal cancer.[29] Dietician input is generally requested to ensure the patient is aware which food contain gluten, which foods are safe, and how to have a balanced diet despite the limitations. In many countries gluten-free products are available on prescription and may be reimbursed by health insurance plans. More manufacturers are producing gluten-free products, some of which are almost indistinguishable from their gluten-containing counterparts.

The diet can be cumbersome; while young children can be kept compliant by their parents, teenagers may wish to hide their problem or rebel against the dietary restrictions, risking relapse. Many food products contain traces of gluten even if apparently wheat-free. Gluten-free products are usually more expensive and harder to find than common wheat-containing foods.

Even while on a diet, health-realted quality of life (HRQOL) is decreased in people with coeliac disease. Some have persisting digestive symptoms or dermatitis herpetiformis, mouth ulcers, osteoporosis and fractures. Symptoms suggestive of irritable bowel syndrome may be present, and there is an increased rate of anxiety, fatigue, dyspeptic and musculoskeletal pain.[30]

Refractory disease

A tiny minority of patients suffer from refractory disease, which means they do not improve on a gluten-free diet. This may be because the disease has been present for so long that the intestines are no longer able to heal, or because the patient is not adhering to the diet. If alternative causes have been eliminated, steroids or immunomodulators (such as azathioprine) may be considered in this scenario.[5]

Experimental treatments

Various other approaches are being studied that would reduce the need of dieting. All are still under development, and are not expected to be available to the general public for a while:[1]

  • Genetically engineered wheat species, or wheat species that have been selectively bred to be minimally immunogenic. This, however, could interfere with the effects that gliadin has on the quality of dough.
  • A combination of enzymes (prolyl endopeptidase and a barley glutamine-specific cysteine endopeptidase (EP-B2)) that degrade the putative 33-mer peptide in the duodenum. This combination would enable coeliac disease patients to consume gluten-containing products.[31]
  • Inhibition of zonulin, a substance linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system.[32]
  • Other treatments aimed at other well-understood steps in the pathogenesis of coeliac disease, such as the action of HLA-DQ2 or tissue transglutaminase and the MICA/NKG2D interaction that may be involved in the killing of enterocytes (bowel lining cells).

Epidemiology

The prevalence of clinically diagnosed disease (symptoms prompting diagnostic testing) is 0.05-0.27% in various studies. However, population studies from Europe, South America, Australasia and the USA (using serology and biopsy) indicate that the prevalence may be between 0.33 and 1.06% in children (5.66% in one study of Saharawi children[33][34]) and 0.18-1.2% in adults.[1] People of African, Japanese, and Chinese descent are rarely diagnosed.citation needed] Risk is elevated in those with other autoimmune diseases.citation needed] A large multicentre study in the US found a prevalence of 0.75% in not-at-risk groups, rising to 1.8% in symptomatic patients, 2.6% in second-degree relatives of a patient with coeliac disease and 4.5% in first-degree relatives. This profile is similar to the prevalence in Europe.[35]

From the fact that prevalence seems to remain the same between childhood and adulthood one may deduce that the principal trigger occurs early in life.[1]

Social and religious issues

Roman Catholic position

Roman Catholic doctrine states that for a valid Eucharist the bread must be made from wheat. The Catholic Church has approved the use of low-gluten hosts, but even these are not gluten-free. Some Catholic coeliac sufferers have requested permission to use rice wafers; such petitions have always been denied.[36]

The issue is more complex for priests. Although a Catholic (lay or ordained) receiving under either form is considered to have received Christ "whole and entire", the priest, who is acting in persona Christi, is required to receive under both species when offering Mass — not for the validity of his Communion, but for the fullness of the sacrifice of the Mass. On August 22, 1994, the Congregation for the Doctrine of the Faith apparently barred coeliacs from ordination, stating, "Given the centrality of the celebration of the Eucharist in the life of the priest, candidates for the priesthood who are affected by coeliac disease or suffer from alcoholism or similar conditions may not be admitted to holy orders." After considerable debate, the congregation softened the ruling on July 24, 2003 to "Given the centrality of the celebration of the Eucharist in the life of a priest, one must proceed with great caution before admitting to Holy Orders those candidates unable to ingest gluten or alcohol without serious harm."citation needed]

Eastern Orthodox Position

The Orthodox Church also requires that the bread used at the Eucharist be made with wheat flour; here the bread is leavened with yeast. Orthodox Christians receive Communion under the species of bread and wine; both are given together from the chalice with a spoon. Some Orthodox coeliac sufferers have been able to receive communion simply by having the priest take only the consecrated wine in the spoon; others, more sensitive to wheat, have had to use a special chalice containing only the consecrated wine. This latter case is extremely unusual, and is strictly speaking only permissible with the permission of the diocesan bishop. While Orthodox Christians do not have such an explicit rationale as the Roman Catholic Church, their general understanding is that, in the case of exceptions made for the sake of Economy, the Holy Spirit makes up whatever is lacking.citation needed]

The Church of Jesus Christ of Latter-day Saints

The Sacrament of the Lord's Supper as observed by members of The Church of Jesus Christ of Latter-day Saints allows for some flexibility in adapting to the needs of coeliac congregants. Section 27 of the church's canonical Doctrine and Covenants reads:

"it mattereth not what ye shall eat or what ye shall drink when ye partake of the sacrament, if it so be that ye do it with an eye single to my glory—remembering unto the Father my body which was laid down for you, and my blood which was shed for the remission of your sins."

As awareness of coeliac disease has increased, many congregations have made allowance for Coeliac congregants where necessary by permitting gluten-free breadstuff to be used, sometimes alongside regular breads (where possible).

Coeliacs and Passover

The Jewish festival of Pesach (Passover) may present problems with its obligation to eat matzo. Matzo is normally made from wheat or other gluten-containing grains, so oat matzo is used. Many products prepared for Passover are free of wheat, barley, spelt, oats, and rye, as many Orthodox (especially Hasidic) Jews avoid wheat products altogether (gebroks) apart from matzo. Potato starch is the primary starch used to replace the grains. [37]

History

Aretaeus of Cappadocia, living in the second century, described a malabsorptive syndrome now widely perceived as an early description of coeliac disease. It gained the attention of Western medicine when Francis Adams presented a translation of Aretaeus' work at the Sydenham Society in 1856. Adams introduced the term "coeliac".[2] In 1888 Dr Samuel Gee, a paediatrician at Great Ormond Street Hospital in London gave the first modern-day description of the condition, as well as improvement on a diet of mussels.[38] Dr Sydney V. Haas, an American paediatrician, reported positive effects of a diet of bananas in 1924.[39] This diet remained in vogue until the actual cause of coeliac disease was determined.

While a role for carbohydrates had been suspected, the link with wheat was not made until 1950 by the Dutch paediatrician Dr Willem Dicke.[40] It is likely that clinical improvement of his patients during the Dutch famine of 1944 (during which flour was sparse) may have contributed to his discovery.[41] The link with the gluten component of wheat was made in 1952 by a team from Birmingham, England.[42] Villous atrophy was described by British physician Paulley in 1954.[43] Dr Margo Shiner, working on Prof Sheila Sherlock's team at the Postgraduate Medical School in London, described the principles of small bowel biopsy in 1956.[44]

Throughout the 1960s other features of coeliac disease were elucidated. In 1966 dermatitis herpetiformis was linked to gluten sensitivity,[9] and in 1970 features of hyposplenism (decreased activity of the spleen) were linked to coeliac disease.[11] The link with tissue transglutaminase was not made until 1997.[22]

References

  1. ^ a b c d e f g h i j k van Heel D, West J (2006). "Recent advances in coeliac disease.". Gut 55 (7): 1037-46. PMID 16766754..
  2. ^ a b Adams F, translator (1856). “On The Cœliac Affection”, The extant works of Aretaeus, The Cappadocian. London: Sydenham Society. Retrieved on 2006-09-04.
  3. ^ a b c d e f g h i j Ciclitira P. Interim Guidelines for the Management of Patients with Coeliac Disease. British Society of Gastroenterology, 2002. MS Word document.
  4. ^ Ferguson R, Basu M, Asquith P, Cooke W (1976). "Jejunal mucosal abnormalities in patients with recurrent aphthous ulceration.". Br Med J 1 (6000): 11-13. PMID 1247715..
  5. ^ a b c d e f (2001). "American Gastroenterological Association medical position statement: Celiac Sprue.". Gastroenterology 120 (6): 1522-5. PMID 11313323..
  6. ^ Tursi A, Brandimarte G, Giorgetti G (2003). "High prevalence of small intestinal bacterial overgrowth in celiac patients with persistence of gastrointestinal symptoms after gluten withdrawal.". Am J Gastroenterol 98 (4): 839-43. PMID 12738465.
  7. ^ Crabbé P, Heremans J (1967). "Selective IgA deficiency with steatorrhea. A new syndrome.". Am J Med 42 (2): 319-26. PMID 4959869..
  8. ^ Collin P, Mäki M, Keyriläinen O, Hällström O, Reunala T, Pasternack A (1992). "Selective IgA deficiency and coeliac disease.". Scand J Gastroenterol 27 (5): 367-71. PMID 1529270..
  9. ^ a b Marks J, Shuster S, Watson A (1966). "Small-bowel changes in dermatitis herpetiformis.". Lancet 2 (7476): 1280-2. PMID 4163419..
  10. ^ Pengiran Tengah D, Wills A, Holmes G (2002). "Neurological complications of coeliac disease.". Postgrad Med J 78 (921): 393-8. PMID 12151653..
  11. ^ a b Ferguson A, Hutton M, Maxwell J, Murray D (1970). "Adult coeliac disease in hyposplenic patients.". Lancet 1 (7639): 163-4. PMID 4189238..
  12. ^ Collin P, Kaukinen K, Välimäki M, Salmi J (2002). "Endocrinological disorders and celiac disease.". Endocr Rev 23 (4): 464-83. PMID 12202461..
  13. ^ Kingham J, Parker D (1998). "The association between primary biliary cirrhosis and coeliac disease: a study of relative prevalences.". Gut 42 (1): 120-2. PMID 9518232.
  14. ^ Matteoni C, Goldblum J, Wang N, Brzezinski A, Achkar E, Soffer E (2001). "Celiac disease is highly prevalent in lymphocytic colitis.". J Clin Gastroenterol 32 (3): 225-7. PMID 11246349.
  15. ^ a b Grain toxicity (RTF). The CELIAC list. Retrieved on 2006-08-27.
  16. ^ Lundin K, Nilsen E, Scott H, Løberg E, Gjøen A, Bratlie J, Skar V, Mendez E, Løvik A, Kett K (2003). "Oats induced villous atrophy in coeliac disease.". Gut 52 (11): 1649-52. PMID 14570737.
  17. ^ Størsrud S, Olsson M, Arvidsson Lenner R, Nilsson L, Nilsson O, Kilander A (2003). "Adult coeliac patients do tolerate large amounts of oats.". Eur J Clin Nutr 57 (1): 163-9. PMID 12548312..
  18. ^ Korponay-Szabó I, Dahlbom I, Laurila K, Koskinen S, Woolley N, Partanen J, Kovács J, Mäki M, Hansson T (2003). "Elevation of IgG antibodies against tissue transglutaminase as a diagnostic tool for coeliac disease in selective IgA deficiency.". Gut 52 (11): 1567-71. PMID 14570724..
  19. ^ Niveloni S, Fiorini A, Dezi R, Pedreira S, Smecuol E, Vazquez H, Cabanne A, Boerr LA, Valero J, Kogan Z, Maurino E, Bai JC. (1998). "Usefulness of videoduodenoscopy and vital dye staining as indicators of mucosal atrophy of celiac disease: assessment of interobserver agreement". Gastrointestinal Endoscopy 47 (3): 223-229. PMID 9580349.
  20. ^ Marsh M (1992). "Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity ('celiac sprue').". Gastroenterology 102 (1): 330-54. PMID 1727768..
  21. ^ Popat S, Bevan S, Braegger C, Busch A, O'Donoghue D, Falth-Magnusson K, Godkin A, Hogberg L, Holmes G, Hosie K, Howdle P, Jenkins H, Jewell D, Johnston S, Kennedy N, Kumar P, Logan R, Love A, Marsh M, Mulder C, Sjoberg K, Stenhammar L, Walker-Smith J, Houlston R (2002). "Genome screening of coeliac disease.". J Med Genet 39 (5): 328-31. PMID 12011149..
  22. ^ a b Dieterich W, Ehnis T, Bauer M, Donner P, Volta U, Riecken E, Schuppan D (1997). "Identification of tissue transglutaminase as the autoantigen of celiac disease.". Nat Med 3 (7): 797-801. PMID 9212111..
  23. ^ Kaukinen K, Peraaho M, Collin P, Partanen J, Woolley N, Kaartinen T, Nuuntinen T, Halttunen T, Maki M, Korponay-Szabo I (2005). "Small-bowel mucosal tranglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: A Prospective and radmonized clinical study.". Scand J Gastroenterology 40: 564-572. PMID 16036509.
  24. ^ Salmi TT, Collin P, Korponay-Szabo IR, Laurila K, Partanen J, Huhtala H, Kiraly R, Lorand L, Reunala T, Maki M, and Kaukinen K. (2006). "Endomysial antibody-negative coeliac disease: clinical characteristics and intestinal autoantibody deposits.". Gut 2006 Mar 29; [Epub ahead of print]. PMID 16571636.
  25. ^ Londei M, Ciacci C, Ricciardelli I, Vacca L, Quaratino S, and Maiuri L. (2005). "Gliadin as a stimulator of innate responses in celiac disease.". Mol Immunol 42 (8): 913-918. PMID 15829281.
  26. ^ Norris JM, Barriga K, Hoffenberg EJ, Taki I, Miao D, Haas JE, Emery LM, Sokol RJ, Erlich HA, Eisenbarth GS, Rewers M. (2005). "Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease.". JAMA 293 (19): 2343-2351. PMID 15900004..
  27. ^ Suman S, Williams E, Thomas P, Surgenor S, Snook J (2003). "Is the risk of adult coeliac disease causally related to cigarette exposure?". Eur J Gastroenterol Hepatol 15 (9): 995-1000. PMID 12923372..
  28. ^ Kupper C (2005). "Dietary guidelines and implementation for celiac disease.". Gastroenterology 128 (4 Suppl 1): S121-7. PMID 15825119.
  29. ^ Treem W (2004). "Emerging concepts in celiac disease.". Curr Opin Pediatr 16 (5): 552-9. PMID 15367850.
  30. ^ Häuser W, Gold J, Stein J, Caspary W, Stallmach A (2006). "Health-related quality of life in adult coeliac disease in Germany: results of a national survey.". Eur J Gastroenterol Hepatol 18 (7): 747-54. PMID 16772832..
  31. ^ Siegel M, Bethune M, Gass J, Ehren J, Xia J, Johannsen A, Stuge T, Gray G, Lee P, Khosla C (2006). "Rational design of combination enzyme therapy for celiac sprue.". Chem Biol 13 (6): 649-58. PMID 16793522..
  32. ^ Fasano A, Not T, Wang W, Uzzau S, Berti I, Tommasini A, Goldblum S (2000). "Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease.". Lancet 355 (9214): 1518-9. PMID 10801176..
  33. ^ Catassi C, Rätsch I, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L (1999). "Why is coeliac disease endemic in the people of the Sahara?". Lancet 354 (9179): 647-8. PMID 10466670.
  34. ^ Carlo Catassi (2002). Coeliac disease, an emerging problem in developing countries. Celiachia News Inglese 2002. Associazione Italiana Celiachia. Retrieved on 2006-09-04.
  35. ^ Fasano A, Berti I, Gerarduzzi T, Not T, Colletti R, Drago S, Elitsur Y, Green P, Guandalini S, Hill I, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman S, Murray J, Horvath K (2003). "Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study.". Archives of Internal Medicine 163 (3): 286-92. PMID 12578508.
  36. ^ Associated Press. "Girl with digestive disease denied Communion", MSNBC, Microsoft, December 8, 2004. Retrieved on 2006-05-30..
  37. ^ Rabbi Avraham Juravel. Gluten Intolerance, Celiac, Allergies And Pesach. Orthodox Union. Retrieved on 2006-09-03.
  38. ^ Gee SJ (1888). On the coeliac affection. St Bartholomew's Hospital Report 24 : 17-20.
  39. ^ Haas SV (1924). The value of the banana in the treatment of coeliac disease. Am J Dis Child 24: 421-37.
  40. ^ van Berge-Henegouwen G, Mulder C (1993). "Pioneer in the gluten free diet: Willem-Karel Dicke 1905-1962, over 50 years of gluten free diet.". Gut 34 (11): 1473-5. PMID 8244125..
  41. ^ Dicke WK. Coeliakie: een onderzoek naar de nadelige invloed van sommige graansoorten op de lijder aan coeliakie [PhD thesis]. Utrecht, the Netherlands: University of Utrecht, 1950.
  42. ^ Anderson C, French J, Sammons H, Frazer A, Gerrard J, Smellie J (1952). "Coeliac disease; gastrointestinal studies and the effect of dietary wheat flour.". Lancet 1 (17): 836-42. PMID 14918439..
  43. ^ Paulley J. "Observation on the aetiology of idiopathic steatorrhoea; jejunal and lymph-node biopsies.". Br Med J 4900: 1318-21. PMID 13209109..
  44. ^ Shiner M (1956). "Duodenal biopsy.". Lancet 270 (6906): 17-9. PMID 13279152..

External links

Wikibooks Cookbook has a recipe for
Gluten-Free
  • Coeliac UK (charity)
  • The Celiac Disease Foundation (U.S.)
  • National Digestive Diseases Clearinghouse - page on coeliac disease
  • National Foundation for Celiac Awareness (U.S.)
  • University of Maryland Center for Celiac Research
Health science - Medicine - Gastroenterology - edit
Diseases of the esophagus - stomach
Halitosis | Nausea | Vomiting | GERD | Achalasia | Esophageal cancer | Esophageal varices | Peptic ulcer | Abdominal pain | Stomach cancer | Functional dyspepsia | Gastroparesis | Abdominal angina 
Diseases of the liver - pancreas - gallbladder - biliary tree
Hepatitis | Cirrhosis | NASH | PBC | PSC | Budd-Chiari | Hepatocellular carcinoma | Acute pancreatitis | Chronic pancreatitis | Pancreatic cancer | Gallstones | Cholecystitis
Diseases of the small intestine
Peptic ulcer | Intussusception | Malabsorption (e.g. Coeliac, lactose intolerance, fructose malabsorption, Whipple's) | Lymphoma
Diseases of the colon
Diarrhea | Appendicitis | Diverticulitis | Diverticulosis | IBD (Crohn's, Ulcerative colitis) | IBS | Constipation | Colorectal cancer | Hirschsprung's | Pseudomembranous colitis
Search Term: "Coeliac_disease"

- celiac disease symptoms

coliac disease