What is the difference between celiac disease and wheat allergy
Coeliac UK is a UK charity for people with coeliac disease.
Its website has useful resources, including information about a gluten-free diet, local groups, volunteering and ongoing campaigns.
You can also call the Coeliac UK helpline 0333 332 2033, open Monday to Friday from 9am to 5pm.
Sheet final reviewed: 3 December 2019
Next review due: 3 December 2022
This article is about disorders related to gluten, a natural ingredient in numerous cereals.
It is not to be confused with sensitivities related to glutamate, a flavor-enhancing additive.
Gluten-related disorders is the term for the diseases triggered by gluten, including celiac disease (CD), non-celiac gluten sensitivity (NCGS), gluten ataxia, dermatitis herpetiformis (DH) and wheat allergy. The umbrella category has also been referred to as gluten intolerance, though a multi-disciplinary physician-led study, based in part on the 2011 International Coeliac Disease Symposium, concluded that the use of this term should be avoided due to a lack of specificity.
Gluten is a group of proteins, such as prolamins and glutelins, stored with starch in the endosperm of various cereal (grass) grains.
As of 2017[update], gluten-related disorders were increasing in frequency in diverse geographic areas. The increase might be explained by the popularity of the Western diet, the expanded reach of the Mediterranean diet (which also includes grains with gluten), the growing replacement of rice by wheat in numerous countries, the development in recent years of new types of wheat with a higher quantity of cytotoxic gluten peptides, and the higher content of gluten in bread and bakery products, due to the reduction of dough fermentation time.
Complications of coeliac disease
Complications of coeliac disease only tend to affect people who continue to eat gluten, or those who own not yet been diagnosed with the condition, which can be a common problem in milder cases.
Potential long-term complications include:
Less common and more serious complications include some types of cancers, such as bowel cancer, and problems affecting pregnancy, such as your baby having a low birth weight.
Find out more about the complications of coeliac disease
Treating coeliac disease
There’s no cure for coeliac disease, but following a gluten-free diet should assist control symptoms and prevent the long-term complications of the condition.
Even if you own mild symptoms, changing your diet is still recommended because continuing to eat gluten can lead to serious complications.
This may also be the case if tests show that you own some degree of coeliac disease even if you do not own noticeable symptoms.
It’s significant to ensure that your gluten-free diet is healthy and balanced.
An increase in the range of available gluten-free foods in recent years has made it possible to eat both a healthy and varied gluten-free diet.
Diagnosing coeliac disease
Routine testing for coeliac disease is not done in England.
Testing is generally only recommended for people who own an increased risk of developing coeliac disease, such as those with a family history of the condition.
First-degree relatives of people with coeliac disease should be tested.
See diagnosing coeliac disease for more information about when testing for coeliac disease should be done.
The following classification of gluten-related disorders was announced in 2011 by a panel of experts in London, and published in February 2012:
Main article: Wheat allergy
People can also experience adverse effects of wheat as result of a wheat allergy. Gastrointestinal symptoms of wheat allergy are similar to those of coeliac disease and non-celiac gluten sensitivity, but there is a diverse interval between exposure to wheat and onset of symptoms.
Wheat allergy has a quick onset (from minutes to hours) after the consumption of food containing wheat and could be anaphylaxis.
The treatment of wheat allergy consists of finish withdrawal of any food containing wheat and other gluten-containing cereals. Nevertheless, some people can tolerate barley, rye or oats.
Non-celiac gluten sensitivity (NCGS)
Main article: Non-celiac gluten sensitivity
Non-celiac gluten sensitivity (NCGS), or gluten sensitivity (GS), is a syndrome in which people develop a variety of intestinal and/or extraintestinal symptoms that improve when gluten is removed from the diet, after coeliac disease and wheat allergy are excluded. NCGS, which is possibly immune-mediated, now appears to be more common than coeliac disease, with a prevalence estimated to be 6–10 times higher.
Gastrointestinal symptoms, which resemble those of irritable bowel syndrome (IBS), may include any of the following: abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation),nausea, aerophagia, gastroesophageal reflux disease, and aphthous stomatitis.
Extra-intestinal symptoms, which can be the only manifestation of NCGS even in absence of gastrointestinal symptoms, may be any of the following: headache or migraine, “foggy mind”, fatigue,fibromyalgia, joint and muscle pain, leg or arm numbness,tingling of the extremities, dermatitis (eczema or skin rash),atopic disorders,allergy to one or more inhalants, foods or metals (such as mites, graminaceae, parietaria, cat or dog hair, shellfish, or nickel),depression,anxiety,anemia,iron-deficiency anemia, folate deficiency, asthma, rhinitis, eating disorders, or autoimmune diseases.
Among extra-intestinal manifestations, NCGS seems to be involved in some neuropsychiatric disorders, principally schizophrenia,autism and peripheral neuropathy, and also ataxia and attention deficit hyperactivity disorder (ADHD).
Gluten is likely responsible for the appearance of symptoms, but it has been suggested than in a subgroup of people with NCGS and symptoms love IBS, other components of wheat and related grains (oligosaccharides love fructans), or other plant proteins contained in gluten-containing cereals (agglutinins, lectins, and amylase trypsin inhibitors (ATIs)) may frolic a role in the development of gastrointestinal symptoms. ATIs are about 2–4% of the entire protein in modern wheat and 80–90% in gluten. In a review of May 2015 published in Gastroenterology, Fasanoet al. conclude that ATIs may be the inducers of innate immunity in people with coeliac disease or NCGS. As of 2019, reviews conclude that although FODMAPs present in wheat and related grains may frolic a role in non-celiac gluten sensitivity, they only explain certain gastrointestinal symptoms, such as bloating, but not the extra-digestive symptoms that people with non-celiac gluten sensitivity may develop, such as neurological disorders, fibromyalgia, psychological disturbances, and dermatitis. As occurs in people with coeliac disease, the treatment is a gluten-free diet (GFD) strict and maintained, without making any dietary transgression. Whereas coeliac disease requires adherence to a strict lifelong gluten-free diet, it is not yet known whether NCGS is a permanent, or a transient condition. The results of a 2017 study propose that NCGS may be a chronic disorder, as is the case with celiac disease. Theoretically, a trial of gluten reintroduction to observe reaction after 1–2 years of strict gluten-free diet might be advisable.
Approximately one third of personas with NCGS continue having symptoms despite gluten withdrawal.
This may be due to diagnostic error, poor dietary compliance, or other reasons. Those afflicted with NCGS may be under the impression that they don’t need to follow a strictly gluten free diet. However, the ingestion of even a little quantity of gluten may cause more immediate symptoms in people suffering from NCGS as compared with those afflicted with coeliac disease. People with NCGS should carefully read ingredient labels on food and be aware of potential cross contamination as a source of gluten in otherwise gluten-free foods. To discover out if there are unintended ingestions of gluten, an exhaustive evaluation with the advice of a coeliac disease specialized dietitian could be necessary.
In some cases, people can significantly improve with a low FODMAPs diet in addition to gluten withdrawal and/or a GFD with a low content of preservatives and additives. Furthermore, associated to gluten sensitivity, NCGS people may often present IgE-mediated allergies to one or more foods and it is estimated that around 35% of people suffer some food intolerances, mainly lactose intolerance.
Main articles: Celiac disease and Gluten-sensitive enteropathy-associated conditions
Autoimmune conditions related to gluten include celiac disease, dermatitis herpetiformis, and gluten ataxia.
There is research showing that in people with gluten ataxia early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. The population of people with gluten ataxia and other neurological conditions appears to own a diverse HLA distribution, in specific more HLA-DQ1, compared to most persons with celiac disease, who own HLA-DQ2 and HLA-DQ8.
Main article: Dermatitis herpetiformis
Dermatitis herpetiformis (DH), or Duhring-Brocq disease, is a chronicblisteringskinautoimmune condition, characterized by the presence of skin lesions that own an extensive and symmetrical distribution, predominating in areas of greater friction, and affecting mainly both elbows, knees, buttocks, ankles, and may also affect the scalp and other parts of the body, and non-symmetrical occasionally.
The lesions are vesicular-crusted and when flake off, they evolve to pigmented areas or achromic an intense burning, itchy and blistering rash. Despite its name, DH is neither related to nor caused by herpes virus: the name means that it is a skin inflammation having an appearance similar to herpes.
The age of onset is variable starting in children and adolescence but can also affect individuals of both sexes indistinctly at any age of their lives.
DH can relatively commonly present with atypical manifestations, which makes its diagnosis more hard.
Some people may show erythema or severe pruritus alone, wheals of chronic urticaria, purpuric lesions resembling petechiae on hands and feet, palmo-plantar keratosis, leukocytoclastic vasculitis-like appearance, and/or lesions mimicking prurigo pigmentosa. DH may be confused with numerous diverse cutaneous lesions, such as atopic dermatitis, eczema, urticaria, scabies, impetigo, polymorphic erythema and other autoimmune blistering diseases.
DH is considered to be the «coeliac disease of the skin». For this reason, the new guidelines of the European Society for Pediatric Gastroenterology, Hepatology and Nutrition for the diagnosis of coeliac disease conclude that a proven diagnosis of DH, by itself, confirms the diagnosis of coeliac disease.
Nevertheless, duodenalbiopsy is recommended in doubtful cases, or if there are suspected gastrointestinal complications, including lymphoma. People with DH own diverse degrees of intestinal involvement, ranging from milder mucosal lesions to the presence of villous atrophy.
The main and more efficacious treatment for DH is following a lifelong gluten-free diet, which produces the improvement of skin and gut lesions.
Nevertheless, the skin lesions may take several months or even years to vanish. To calm itching, dapsone is often recommended as a temporary treatment, during the time it takes for the diet to work, but it has no effect on the gastrointestinal changes and may own significant side effects.
Main article: Coeliac disease
Coeliac disease (American English: celiac) (CD) is one of the most common chronic, immune-mediated disorders, triggered by the eating of gluten, a mixture of proteins found in wheat, barley, rye, and oats and derivatives. Evidence has shown that this condition not only has an environmental component but a genetic one as well, due to strong associations of CD with the presence of HLA (Human leukocyte antigen) type II, specifically DQ2 and DQ8 alleles. These alleles can stimulate a T cell, mediated immune response against tissue transglutaminase (TTG), an enzyme in the extracellular matrix, leading to inflammation of the intestinal mucosa and eventually villous atrophy of the little intestine. This is where the innate and adaptive immune response systems collide.
CD is not only a gastrointestinal disease.
It may involve several organs and cause an extensive variety of non-gastrointestinal symptoms. Most importantly, it may often be completely asymptomatic. Added difficulties for diagnosis are the fact that serological markers (anti-tissue transglutaminase [TG2]) are not always present and numerous people may own minor mucosal lesions, without atrophy of the intestinal villi. Diagnosis of CD should be based on a combination of person’s familial history, genetics (i.e.
presence of HLA DQ2/DQ8) serology and intestinal histology.
CD affects approximately 1–2% of general population every over the world, but most cases remain unrecognized, undiagnosed and untreated, and exposed to the risk of long-term complications. People may suffer severe disease symptoms and be subjected to extensive investigations for numerous years, before a proper diagnosis is achieved. Untreated CD may result in the lack of absorption of nutrients, reduced quality of life, iron deficiency, osteoporosis, an increased risk of intestinal lymphomas and greater mortality. CD is associated with some autoimmune diseases, such as diabetes mellitus type 1,thyroiditis,gluten ataxia, psoriasis, vitiligo, autoimmune hepatitis, dermatitis herpetiformis, primary sclerosing cholangitis, and more.
CD with «classic symptoms», which include gastrointestinal manifestations such as chronic diarrhea and bloating, malabsorption of certain vitamins and minerals, loss of appetite, impaired growth and even bone pain, is currently the least common presentation form of the disease and affects predominantly to little children generally younger than two years of age.
CD with «non-classic symptoms» is the most common clinical found type and occurs in older children (over 2 years old), adolescents and adults. It is characterized by milder or even absent gastrointestinal symptoms and a wide spectrum of non-intestinal manifestations that can involve any organ of the body such as, cerebellar ataxia, hypertransaminasemia and peripheral neuropathy. As previously mentioned, CD extremely frequently may be completely asymptomatic both in children (at least in 43% of the cases) and adults.
To date, the only available medically accepted treatment for people with coeliac disease is to follow a lifelong gluten-free diet.
Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten. With gluten ataxia, damage takes put in the cerebellum, the balance middle of the brain that controls coordination and complicated movements love walking, speaking and swallowing, with loss of Purkinje cells.
People with gluten ataxia generally present gait abnormality or incoordination and tremor of the upper limbs. Gaze-evoked nystagmus and other ocular signs of cerebellar dysfunction are common. Myoclonus, palatal tremor, and opsoclonus-myoclonus may also appear.
Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible.
Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of every ataxias. Less than 10% of people with gluten ataxia present any gastrointestinal symptom, yet about 40% own intestinal damage.
Other conditions or risk factors
Antibodies to α-gliadin own been significantly increased in non-celiacs individuals with oral ulceration. Anti-α-gliadin antibodies are frequently found in celiac disease (CD), to a lesser degree subclinical CD, but are also found in a subset who do not own the disease.
Of people with pseudo-exfoliation syndrome, 25% showed increased levels of anti-gliadin IgA. Other people that are also at risk are those taking gluten despite having the disorder, or whose family members with CD. In addition people with autoimmune conditions are also at risk for CD. It has just been found that there is a risk of death in CD. Therefore gluten intake should be limited before or even after the diagnosis. One fourth of people with Sjögren’s syndrome had responses to gluten, of 5 that had positive response to gluten, only one could be confirmed as CD and another was potentially GSE[clarification needed], the remaining 3 appear to be gluten-sensitive.
Every were HLA-DQ2 and/or DQ8-positive.
Symptoms of coeliac disease
Eating foods that contain gluten can trigger a range of gut symptoms, such as:
Coeliac disease can also cause more general symptoms, including:
Children with coeliac disease may not grow at the expected rate and may own delayed puberty.
Coeliac disease is an autoimmune condition. This is where the immune system (the body’s defence against infection) mistakenly attacks healthy tissue.
In coeliac disease, the immune system mistakes substances found inside gluten as a threat to the body and attacks them.
This damages the surface of the little bowel (intestines), disrupting the body’s ability to take in nutrients from food.
It’s not entirely clear what causes the immune system to act this way, but a combination of genetics and the environment appear to play a part.
Coeliac disease is a condition that affects at least 1 in every 100 people in the UK.
But some experts ponder this may be underestimated because milder cases may go undiagnosed or be misdiagnosed as other digestive conditions, such as irritable bowel syndrome (IBS).
Reported cases of coeliac disease are around 3 times higher in women than men.
It can develop at any age, although symptoms are most likely to develop:
- during early childhood – between 8 and 12 months ancient, although it may take several years before a correct diagnosis is made
- in later adulthood – between 40 and 60 years of age
People with certain conditions, including type 1 diabetes, autoimmune thyroid disease, Down’s syndrome and Turner syndrome, own an increased risk of getting coeliac disease.
First-degree relatives (parents, brothers, sisters and children) of people with coeliac disease are also at increased risk of developing the condition.