What is the difference between celiac and wheat allergy

Compared to the pathophysiology of celiac disease, the pathophysiology of NCGS is far less understood.

What is the difference between celiac and wheat allergy

A literature review of 2014 found that people suffering from NCGS «are a heterogeneous group, composed of several subgroups, each characterized by diverse pathogenesis and clinical history, and, probably, clinical course».[64]


Celiac disease (CD) and NCGS are closely linked with human leukocyte antigen (HLA) class II genes, HLA-DQ2 and HLA-DQ8, located on chromosome 6p21.[2] Almost every CD people are HLA-DQ2/HLA-DQ8 positive, with 95% HLA-DQ2 and the relax generally HLA-DQ8 (which is carried by 30% of Caucasians).[2] However, the specificity of HLA-DQ2 and/or HLA-DQ8 for CD is low, with estimates ranging from 36% to 53%.

In persons with NCGS, the HLA-DQ2 and/or HLA-DQ8 alleles are present in only about 50%, which is still a greater proportion than in the general population.[2]


When enteropathy develops in early childhood, symptomatic disease is more rapidly evident. A survey of geriatrics with celiac disease in Finland revealed that the incidence of disease was much higher than the general population.[57] Allergic disease may rise or drop with age; certain evidence points to the increased or daily use of non-steroidal anti-inflammatory factors (aspirin, ibuprofen) as an increased risk factor for urticaria or anaphylaxis, and the sensitizing dose may include low-dose aspirin therapy used in the treatment of heart disease.

NCGS may be a late-onset condition: in a prospective study performed among adults of 18 to 80 years, the median age of disease onset was found to be 55 years, with a six times higher prevalence in females than in males.[5]

The pathogenesis of NCGS is not yet well understood. There is evidence that not only gliadin (the main cytotoxic antigen of gluten), but also other proteins named ATIs which are present in gluten-containing cereals (wheat, rye, barley, and their derivatives) may own a role in the development of symptoms. ATIs are potent activators of the innate immune system.[32][40]FODMAPs, especially fructans, are present in little amounts in gluten-containing grains and own been identified as a possible cause of some gastrointestinal symptoms in persons with NCGS.[32][5][40][58] As of 2019, reviews own concluded that although FODMAPs may frolic a role in NCGS, they only explain certain gastrointestinal symptoms, such as bloating, but not the extra-digestive symptoms that people with NCGS may develop, such as neurological disorders, fibromyalgia, psychological disturbances, and dermatitis.[40][41][32]

Immunochemistry of glutens

Main article: Gluten immunochemistry

Triticeae glutens are significant factors in several inflammatory diseases.

The immunochemistry can be subdivided into innate responses (direct stimulation of immune system), class II mediated presentation (HLA-DQ), class I mediated stimulation of killer cells, and antibody recognition. The responses to gluten proteins and polypeptide regions differs according to the type of gluten sensitivity. The response is also dependent on the genetic makeup of the human leukocyte antigen genes. In enteropathy, there are at least 3 types of recognition, innate immunity (a form of cellular immunity priming), HLA-DQ and antibody recognition of gliadin and transglutaminase.[59] In NCGS, there is high AGA IgG in more than half of the cases.[60] In wheat allergy, there appears to be an innate component and the response pathways are mediated through IgE against gliadin and other wheat proteins.[61][62][63]


More than 250 symptoms of gluten sensitivity own been reported, including bloating, abdominal discomfort or pain, constipation and diarrhea.[51] Sensitivity may also present with extraintestinal symptoms, including headache, «brain fog», tingling and/or numbness in hands and feet, fatigue, as well as muscular disturbances and bone or joint pain;[52][53][54] also neuropsychiatric manifestations («gluten-sensitive idiopathic neuropathies») own been reported on.[55]


Studies using anti-gliadin antibodies (AGA) reveal that diagnosed or untreated[clarification needed] individuals with AGA own an increasing risk for lymphoid cancers and decreased risk for other conditions associated with affluence.[56]


In the United States, fewer cases of CD own been found compared to other countries.[76] The incidence of celiac disease and of wheat allergy is estimated each to lie at around 1% of the population.

There has been a 6.4 increase in the case reports of celiac disease between 1990 and 2009.[49] The incidence of NCGS is unknown; some estimates range from 0.6% to 6%,[68] and a systematic review of 2015 reported on studies with NCGS prevalence rates between 0.5% and 13%.[77]

In Europe, the average consumption of gluten is 10g to 20g per day, with parts of the population reaching 50g or more per day.[2]


The following classification of gluten-related disorders was announced in 2011 by a panel of experts in London, and published in February 2012:[6][7]

Non-celiac gluten sensitivity (NCGS)

Main article: Non-celiac gluten sensitivity

Non-celiac gluten sensitivity (NCGS), or gluten sensitivity (GS),[1] is a syndrome in which people develop a variety of intestinal and/or extraintestinal symptoms that improve when gluten is removed from the diet,[31] after coeliac disease and wheat allergy are excluded.[32] NCGS, which is possibly immune-mediated, now appears to be more common than coeliac disease,[33] with a prevalence estimated to be 6–10 times higher.[34]

Gastrointestinal symptoms, which resemble those of irritable bowel syndrome (IBS),[31][35] may include any of the following: abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation),[35][36]nausea, aerophagia, gastroesophageal reflux disease, and aphthous stomatitis.[32][35]

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,[32][35][36]fibromyalgia,[36][37][38] joint and muscle pain,[32][35][36] leg or arm numbness,[32][35][36]tingling of the extremities,[32][35] dermatitis (eczema or skin rash),[32][35]atopic disorders,[32]allergy to one or more inhalants, foods or metals[32][36] (such as mites, graminaceae, parietaria, cat or dog hair, shellfish, or nickel),[36]depression,[32][35][36]anxiety,[36]anemia,[32][35]iron-deficiency anemia, folate deficiency, asthma, rhinitis, eating disorders,[36] or autoimmune diseases.[32]

Among extra-intestinal manifestations, NCGS seems to be involved in some neuropsychiatric disorders,[39] principally schizophrenia,[11][35]autism[11][35][36] and peripheral neuropathy,[11][35] and also ataxia[11] and attention deficit hyperactivity disorder (ADHD).[32]

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.[16] ATIs are about 2–4% of the entire protein in modern wheat and 80–90% in gluten.[32] 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.[32] 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.[40][41][32] As occurs in people with coeliac disease, the treatment is a gluten-free diet (GFD) strict and maintained, without making any dietary transgression.[36] 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.[21][36] The results of a 2017 study propose that NCGS may be a chronic disorder, as is the case with celiac disease.[41] Theoretically, a trial of gluten reintroduction to observe reaction after 1–2 years of strict gluten-free diet might be advisable.[36]

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.[36]

In some cases, people can significantly improve with a low FODMAPs diet in addition to gluten withdrawal[5] and/or a GFD with a low content of preservatives and additives.[42] Furthermore, associated to gluten sensitivity, NCGS people may often present IgE-mediated allergies to one or more foods[36] and it is estimated that around 35% of people suffer some food intolerances, mainly lactose intolerance.[43]

Autoimmune disorders

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.[8] 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.[9]

Dermatitis herpetiformis

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.[24][25] 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.[25][26]

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.[26]

DH is considered to be the «coeliac disease of the skin».

What is the difference between celiac and wheat allergy

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.[26] People with DH own diverse degrees of intestinal involvement, ranging from milder mucosal lesions to the presence of villous atrophy.[24]

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.[24][27]

Coeliac disease

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.[10][11] 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.[12] 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.[13] This is where the innate and adaptive immune response systems collide.

CD is not only a gastrointestinal disease.

What is the difference between celiac and wheat allergy

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[14] and numerous people may own minor mucosal lesions, without atrophy of the intestinal villi.[15] 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.[16]

CD affects approximately 1–2% of general population every over the world,[17] but most cases remain unrecognized, undiagnosed and untreated, and exposed to the risk of long-term complications.[16][18] People may suffer severe disease symptoms and be subjected to extensive investigations for numerous years, before a proper diagnosis is achieved.[19] 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.[11] CD is associated with some autoimmune diseases, such as diabetes mellitus type 1,[12]thyroiditis,[20]gluten ataxia, psoriasis, vitiligo, autoimmune hepatitis, dermatitis herpetiformis, primary sclerosing cholangitis, and more.[20]

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.[13][18][19]

CD with «non-classic symptoms» is the most common clinical found type[19] and occurs in older children (over 2 years old),[19] adolescents and adults.[19] 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.[16] As previously mentioned, CD extremely frequently may be completely asymptomatic[18] both in children (at least in 43% of the cases[21]) and adults.[18]

To date, the only available medically accepted treatment for people with coeliac disease is to follow a lifelong gluten-free diet.[16][22][23]

Gluten ataxia

Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten.[2] 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.

What is the difference between celiac and wheat allergy

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.[28]

Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression.

What is the difference between celiac and wheat allergy

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.[28][29]

Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of every ataxias.[28][30] Less than 10% of people with gluten ataxia present any gastrointestinal symptom, yet about 40% own intestinal damage.[28]

Wheat allergy

Main article: Wheat allergy

People can also experience adverse effects of wheat as result of a wheat allergy.[16] 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.[14][44]

The treatment of wheat allergy consists of finish withdrawal of any food containing wheat and other gluten-containing cereals.[44][45] Nevertheless, some people can tolerate barley, rye or oats.[46]

Other conditions or risk factors

Antibodies to α-gliadin own been significantly increased in non-celiacs individuals with oral ulceration.[47] 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.[48] 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.

What is the difference between celiac and wheat allergy

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.[49] 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.[50]


A literature review of 2014 found that non-coeliac gluten sensitivity diagnosis can be reached only by excluding celiac disease (CD) and wheat allergy.[64]

Persons suspected of having celiac disease may undergo serological testing for IgA anti-tissue transglutaminase antibodies (abbreviated anti-tTG antibodies or anti-TG2 antibodies) and anti-endomysial antibodies (abbreviated EMA) provided the IgA-level is high, and if IgA is low, testing for certain IgG antibodies; in case of positive serological indication, a duodenal biopsy may confirm athletic celiac disease.[65]

Eliminating the possibility of CD can generally also be done by adding HLA-DQ typing.

The absence of HLA-DQ2 and HLA-DQ8 has a extremely high negative predictive worth for CD,[2][66] and the predictive worth can be further enhanced by including HLA-DQ7.5 (HLA-DQ2 and HLA-DQ8 are found in coeliac disease 98% of the time in Caucasians, HLA-DQ7.5 present in the remaining 1.6% and only 0.4% of Caucasians are missed with the combination of these 3).[citation needed] Without serological or HLA-DQ2/8 positivity, celiac disease is likely not present.

HLA-DQ typing has a practical advantage in that it is the only diagnostic test that allows to exclude CD when a person is already on a gluten-free diet; however, as not only celiacs are HLA-DQ2/HLA-DQ8 positive, this method has a higher untrue positive rate than anti-TG2 and EMA antibody testing.

What is the difference between celiac and wheat allergy

A four-of-five law was proposed 2010 for confirming celiac disease, with the disease confirmed if at least four of the following five criteria are satisfied:[2][67]

  1. celiac enteropathy at the little bowel biopsy; and
  2. human leukocyte antigen (HLA)-DQ2 or DQ8 genotypes;
  3. typical symptoms of celiac disease;
  4. positivity of serum celiac disease immunoglobulin, A class autoantibodies at high titer;
  5. response to the gluten-free diet.

For diagnosis of wheat allergy, allergy tests are available.


Main article: Gluten-free diet

For people with celiac disease, a lifelong strict gluten-free diet is the only effective treatment to date;[22][68]

For people diagnosed with non-celiac gluten sensitivity, there are still open questions concerning for example the duration of such a diet. The results of a 2017 study propose that non-celica gluten sensitivity may be a chronic disorder, as is the case with celiac disease.[41]

For people with wheat allergy, the individual average is six years of gluten-free diet, excepting persons with anaphylaxis, for whom the diet is to be wheat-free for life.[68]

Preferably, newly diagnosed celiacs seek the assist of a dietician to get support for identifying hidden sources of gluten, planning balanced meals, reading labels, food shopping, dining out, and dining during travel.[69] Knowledge of hidden sources of gluten is significant for people with celiac disease as they need to be extremely strict regarding eating only gluten-free food.[70] The degree of gluten cross contamination tolerated by people with non-celica gluten sensitivity is not clear but there is some evidence that they can present with symptoms even after consumption of little amounts.[36] Sporadic accidental contaminations with gluten can reactivate movement disorders associated with non-celica gluten sensitivity.[71] A part of people with gluten-related neuropathy or gluten ataxia appears not to be capable to tolerate even the traces of gluten allowed in most foods labeled as «gluten-free».[72]

The inclusion of oats in gluten-free diets remains controversial.

Avenin present in oats may also be toxic for coeliac sufferers.[73] Its toxicity depends on the cultivar consumed.[74] Furthermore, oats are frequently cross-contaminated with gluten-containing cereals.[73]

Risks of non-medical and self-diagnosed adoption of a gluten-free diet

Withdrawing gluten from the diet without previously carrying out a finish medical examination can hamper the diagnosis of celiac disease.

Diagnostic tests (antibodies and duodenum biopsies) lose their usefulness if the person is already eating a gluten-free diet.[75]

Potential nutritional deficiencies

Gluten proteins own low nutritional and biological worth and replacing grains that contain gluten is simple from the nutritional point of view.[22] However, an unbalanced selection of food and an incorrect choice of gluten-free replacement products may lead to nutritional deficiencies. Replacing flour from wheat or other gluten-containing cereals with gluten-free flours in commercial products may lead to a lower intake of significant nutrients, such as iron and B vitamins.

Some gluten-free commercial replacement products are not enriched or fortified as their gluten-containing counterparts, and often own greater lipid/carbohydrate content.

What is the difference between celiac and wheat allergy

Children especially often over-consume these products, such as snacks and biscuits.[73]

Pseudocereals (quinoa, amaranth, and buckwheat) and some minor cereals are healthy alternatives to these prepared products and own high biological and nutritional value.[73][22] Furthermore, they contain protein of higher nutritional quality than those of wheat, and in greater quantities.[73]

Nutritional complications can be prevented by a correct dietary education.[73]