Coeliac disease

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Coeliac disease
Classifications and external resources
Biopsy of small bowel showing coeliac disease manifested by blunting of villi, crypt 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 radio/652

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

Coeliac disease is caused by an abnormal 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 body's immune system cross-reacts with the enzyme tissue transglutaminase, 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 diet, lifelong in principle, from which gluten is absent.

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

Contents

[edit] Signs and symptoms

Classic symptoms of coeliac disease include diarrhoea, weight loss (or stunted growth in children) and fatigue, but while coeliac disease is a disease of the bowel, it may present with limited bowel symptoms. Some patients are diagnosed with symptoms related to the decreased absorption of nutrients or with symptoms which, although statistically linked, have no clear relationship with the malfunctioning bowel. Classically, weight loss, fat malabsorption (steatorrhea) and iron deficiency anemia were the cardinal signs of coeliac diseae. Given the wide range of presentations that are now recognized 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.[3] Many adults with subtle disease only have fatigue or anaemia.[1]

[edit] Gastrointestinal symptoms

The diarrhoea characteristic of coeliac disease is pale, voluminous and malodorous. Abdominal pain and cramping, bloatedness and abdominal distention (thought to be due to fermentative production of bowel gas) and mouth ulcers[4] may be present. As the bowel is more damaged, a degree of lactose intolerance may develop. However, the variety of gastrointertinal symptoms that may be present in patients with coeliac disease is great, and even Constipation is seen, in some series comprising up to a third of patients. Frequently the symptoms are ascribed to Irritable Bowel Syndrome, only later to be recognized as coeliac disease. Approximately 5% of patients initially thought to have Irritable Bowel Syndrome are found to have coeliac disease.

Coeliac disease leads to an increased risk of both adenocarcinoma and lymphoma of the small bowel, which returns to baseline with diet. Longstanding disease may lead to other complications, such as ulcerative jejunitis (ulcer formation of the small bowel) and stricturing (narrowing as a result of scarring).[5]

[edit] Malabsorption-related symptoms

The changes in the bowel make it less able to absorb nutrients, minerals and fat-soluble vitamins.[3]

  • The inability to absorb carbohydrates and fats may cause weight loss (or failure to thrive/stunted growth in children) and fatigue or lack of energy.
  • Anaemia may develop in several ways: iron malabsorption may cause iron deficiency anaemia, and folic acid and vitamin B12 malabsorption may give rise to megaloblastic anaemia. The inflammation of coeliac disease causes microscopic blood loss from the small intestine, also.
  • Calcium and vitamin D malabsorbtion (and compensatory secondary hyperparathyroidism) may cause osteopenia (decreased mineral content of the bone) or osteoporosis (bone weakening and risk of fragility fractures). Malabsorption of vitamin D may lead to vitamin D deficiency rickets or even hypocalcemic tetany, especially if patients with coeliac disease are treated with a biphosphonate drug before calcium absorption has a chance to normalize on a gluten-free diet. While patients with coeliac disease have an increased risk of osteopenia and osteoporosis, the actual risk of bone fracture is either unchanged or little increased compared to age-matched controls. Thus there is controversy regarding whether dietary treatment alone is adequate, or whether biphosphonate drugs should be administered to patients after initial dietary treatment.
  • A small proportion have abnormal coagulation due to deficiency of vitamin K, and are slightly at risk for abnormal bleeding.
  • Coeliac disease is also associated with bacterial overgrowth of the small intestine, which can worsen malabsorption, or cause malabsorption after treatment.[6]

[edit] Miscellaneous symptoms

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.

[edit] The role of other grains

Wheat varieties or subspecies containing gluten such as spelt and Kamut®, and the rye/wheat hybrid triticale, also trigger symptoms.[15]

Barley and rye also induce symptoms of coeliac disease.[15] A small minority of coeliac patients also react to oats.[16][17] Most probably oats produced symptoms due to cross contamination with other grains in the fields or in the distribution channels. There is at least one oat vendor (McCann's) which, while not claiming to be gluten-free, points out that the risk of contamination is low due to the processes they use.[18] Other cereals, such as maize (corn), 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.

[edit] Diagnosis

The condition is frequently misdiagnosed or overlooked as it can exhibit multiple symptoms and often the patient or medical staff may not link seemingly unconnected conditions. It is most frequently misdiagnosed when the sufferer complains of persistent indigestion, or symptoms other than diarrhea. Irritable bowel syndrome (IBS) is often the initial diagnosis due to the similarity of symptoms and the greater prevalence of IBS in the population. About 5% of patients initially diagnosed with IBS actually have coeliac disease. Unfortunately, the delay in diagnosis of coeliac disease can be great, in some cases measured in years.

There are several tests that can be used to assist in diagnosis. The level of symptoms may determine the order of the tests, but all tests must be done while the person is on a gluten containing diet. Antibodies level begin to decline and intestinal damage begins to heal when gluten is removed from the diet, so the risk of misdiagnosis is increased if the person is not eating gluten. Biopsies can normalize over the course of weeks, and antibody levels drop over the course of months. For those who have already commenced themselves on a gluten-free diet, a re-challenge of 2-6 weeks with 10 g of gluten (four slices of bread) per day before repeating the investigations. Those who experience severe symptoms earlier can be regarded as sufficiently challenged and can be tested earlier.[3]

[edit] Blood tests

Serology by blood test is both good at diagnosing coeliac disease (high sensitivity of 98%, i.e. it misses 2 in 100 cases) and excluding it (high specificity of >95%, i.e. a positive test is most likely confirmative of coeliac disease rather than another condition) except for the IgG anti-gliadin antibody, which has a false positive rate of approximately 50%. Because of the major implications of a diagnosis of coeliac disease, many recommend that a positive blood test is still followed by an endoscopy. A negative test may still prompt a biopsy if the suspicion is very high; this would pick up the remaining 2% undiagnosed cases. Due to the few limitations of blood tests, endoscopy and biopsy is still considered the gold standard in the diagnosis of coeliac disease.[3][5]

Due to its high sensitivity, serology has been proposed as a screening measure, because the presence of antibodies would detect previously undiagnosed cases of coeliac disease and prevent its complications in those patients.

Serology may also be used to monitor adherence to diet.[3][5]

Four serological blood tests exist for coeliac disease:

  • IgA and IgG anti-tissue transglutaminase antibody (anti-tTG). This test is sometimes used alone. If this test is positive it is highly likely that the patient has coeliac disease. It is not reliable in children before the age of 2.
  • IgA and IgG anti-gliadin antibodies (AGA), IgG and IgA. These tests are often useful when testing young symptomatic children, but they are found in fewer coeliacs than anti-tTG, and their presence does not automatically indicate coeliac disease because they are found in some other disorders. Both IgA and IgG anti-gliadin antibodies (AGA) may be detected in sera of patients with gluten sensitive enteropathy (coeliac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results.
  • IgA anti-endomysial antibodies (EMA). This test is being replaced by the anti-tTG test because both tests measure the autoantibodies that cause the tissue damage associated with coeliac disease. Many physicians still order this test. This test as tTG test is also not reliable in children before the age of 2.
  • An older test, the IgA anti-reticulin antibodies (ARA). IgA anti-ARA is not ordered as frequently as it once was, because it is less sensitive and less specific than the other tests. It is found in about 60% of people with coeliac disease and 25% of those with dermatitis herpetiformis.

For those based on IgA, a total IgA level is checked in parallel, as patients with IgA deficiency may have a normal result while still having coeliac disease ("false negative"). In those patients, IgG antibodies may be diagnostic.[19]

Features seen in patients with coeliac disease are characteristic symptoms, abnormal serologic tests, abnormal biopsies, resolution of symptoms on a gluten free diet, healing of intestinal lesions on a gluten free diet, and normalization of serologic tests on a gluten free diet. Ideally, at least two features of healing are found on follow-up of coeliac patients. Thus, even when a biopsy is used to diagnose coeliac disease, serologic testing needs to be done so that normalization of antibody levels may be used in confirmatory testing in follow-up.

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

[edit] Endoscopy

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

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 (eight or more) from the duodenum. Not all areas may be equally affected, which is why even upper endoscopy carries a small risk of false negative results.[5] 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. [20]

[edit] Pathology

The classic pathology changes of coeliac disease in the small bowel are categorized by the "Marsh classification":[21]

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

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

[edit] Other diagnostic tests

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

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

[edit] Screening and case finding

There is significant debate as to the benefits of screening. Some studies suggest that early detection would decrease the risk of osteoporosis and anaemia. In contrast, a cohort studied in Cambridge suggested that people with undetected coeliac disease had a beneficial risk profile for cardiovascular disease (less overweight, lower cholesterol levels).[1] This is essentially due to the malnutrition that malabsorbtion causes. Patients who are treated for coeliac disease often find that obesity and the developement of elevated cholesterol levels are new problems that need to be treated.

Clinical scenarios in which screening may be justified include type 1 diabetes, unexplained iron-deficiency anemia, Down's syndrome, Turner's syndrome, irritable bowel syndrome, lupus, and autoimmune thyroid disease.[citation needed]

[edit] Pathophysiology

[edit] Genetics

Coeliac disease is linked to the CELIAC1 locus (HLA DQ) and occurs almost exclusively (over 95%) in patients with human leukocyte antigen types DQ2 (DQA1*0501:DQB1*0201 or DQ2.5) and DQ8 (DQA1*0301:DQB1*0302), which is inherited in families. Over 95% of coeliac patients carry one or two of the DQ2 or DQ8 genes.

Every person carries two HLA-DQ genes, one from their mother and one from their father. About 20-30% of people carry HLA-DQ2 but do not have coeliac disease. Furthermore, about 5% of those people to develop coeliac disease do not have the DQ2 gene.[1] The frequency of these genes vary greatly, DQ2.5 is at high frequencies in Sardinians,[22] Basque, Ireland,[23]and Scandinavia. DQ8 is at high frequencies in the South and Central America (up to 90% phenotype frequency),[24] Mexico, and Sweden.

DQ α5-β2 peptide-binding cleft with deamidated gliadin peptide, modified from PDB 1S9V
DQ α5-β2 peptide-binding cleft with deamidated gliadin peptide, modified from PDB 1S9V [25]

DQ2 and DQ8 are serotypes defined by immunological reactivity where as DQA1:DQB1 are two-locus haplotypes that are commonly found that result in the serotypes, and any given person can produce 4 DQ molecules, 2 in the cis-haplotype dimer pairing and 2 in the transhaplotype dimer pairing. DQ2.5 and DQ8 produce susceptibility in the cis-haplotype pairing configuration. There is a third pairing of haplotypes, DQA1*0201:DQB1*0202(DQ2.2) / DQA1*0505:DQB1*0301 (DQ7.55) that, when both are found in a single patient, can produce susceptibility to coeliac disease via a trans-pairing of the DQA1*0505-DQB1*0202 gene products (DQ α5-β2 heterodimer) [26]. While DQ2.2/DQ2.5 may have increased susceptibility (capable of producing twice the number of DQ α5-β2)[27], without DQ7.55 and DQ2.5, DQ2.2 is atypically associated with coeliac disease[28].

It appears that DQ α5-β2 heterodimer is more avid in presenting gliadin peptides to T lymphocytes, which then initiate the autoimmune process.[1]

In addition to the HLA locus on chromosome 6q21.3, several other regions have been linked (especially 19p13.3 and 4p14).[29] 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.

[edit] 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 response in some sufferers of coeliac disease.

[edit] Tissue transglutaminase

Antibodies to the enzyme tissue transglutaminase (tTG) are found in an overwhelming majority of cases, and cross-react to gluten.[30] 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 coeliac patients has revealed that autoantibody deposits in the subclinical coeliacs 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.[31] 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 coeliac disease diagnosis. However, a recent study has shown that EMA negative coeliac patients tend to be older, more typically male with more severe abdominal symptoms and a lower frequency of "atypical" symptoms including autoimmune disease.[32] 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,[33] suggests that gliadin may be more responsible for the primary manifestations of coeliac disease whereas as tTG is a bigger factor in secondary effects such as allegic responses and secondary autoimmune diseases. In a large percentage of coeliac patients, a link between anti-tTG antibodies to rotaviral VP7 and antibodies to toll-like receptors has been described. These antibodies stimulate monocytes proliferation and could explain some early steps in the cascade of immune cell proliferation[34]. Earlier studies of rotavirus damage in the gut reveal a villous atrophy [35], viral proteins may take part in the initial flattening and stimulate self-crossreactive anti-VP7 production. Antibodies to VP7 may slow healing until the gliadin mediated tTG presentation provides a second source of crossreactive antibodies.

[edit] 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]

[edit] Triggers

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

  • Genetic risk factors and Triticeae glutens
  • An environmental agent, such as infection or a chemical substance
    • Viral infection
      • Rotavirus[34]
      • Human intestinal adenovirus[36]
  • 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 disease over those exposed at 4 to 6 months. Those exposed later had a slightly increased risk relative to those exposed at 4-6 months.[37]

Some research has suggested that smoking is protective against coeliac disease.[38] Results on this topic are however inconsistent, and smoking cannot be recommended as a means to avoid developing coeliac disease.

[edit] Treatment

[edit] Diet

Main article: Gluten-free diet

The only treatment is a life-long gluten-free diet.[39] 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.[40] Dietician input is generally requested to ensure the patient is aware which foods 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-related 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.[41]

[edit] 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]

[edit] 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.[42]
  • Inhibition of zonulin, a substance linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system.[43]
  • 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).

[edit] 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[44][45]) and 0.18-1.2% in adults.[1] People of African, Japanese, and Chinese descent are rarely diagnosed and reflects a decrease in the major susceptibility factor, DQ α5β2 isoform, or low wheat diets. 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.[46]

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]

[edit] Social and religious issues

[edit] 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.[47]

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]

[edit] 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]

[edit] 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).

[edit] 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. [48]

[edit] 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.[49] Dr Sydney V. Haas, an American paediatrician, reported positive effects of a diet of bananas in 1924.[50] 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.[51] 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.[52] The link with the gluten component of wheat was made in 1952 by a team from Birmingham, England.[53] Villous atrophy was described by British physician Paulley in 1954.[54] 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.[55]

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.[30]

[edit] References

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  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..
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[edit] External links

Wikibooks
Wikibooks Cookbook has an article on
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 | Malabsorption  (e.g. post-operative gastric bypass procedure, pernicious anemia, for B12)
Diseases of the liver - pancreas - gallbladder - biliary tree
Hepatitis | Cirrhosis | NASH | PBC | PSC | Budd-Chiari | Hepatocellular carcinoma | Acute pancreatitis | Chronic pancreatitis | Hereditary pancreatitis | Pancreatic cancer | Gallstones | Cholecystitis | Malabsorption  (eg. cystic fibrosis)
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
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