Autoimmune Diseases & Gluten Sensitivity
Disorders & Gluten
Autoimmune conditions related to gluten include celiac disease, dermatitis herpetiformis, and gluten ataxia. There is research showing that in certain patients with gluten ataxia early diagnosis and treatment with a gluten-free diet (download PDF bottom of page) can improve ataxia and prevent its progression. The population of patients with gluten ataxia and other neurological conditions appears to have a different HLA distribution, in particular more HLA-DQ1, compared to the population of typical celiac disease patients who have HLA-DQ2 and HLA-DQ8.
If a person already has an autoimmune disease, it means that the body was attacking the body’s tissues. This process happens over the years. Inflammation is a natural response of the immune system when something seems dangerous to the body (virus, a cut or gluten). A shocking fact is that “one percent of the population has Celiac disease and one in 30 people have a gluten sensitivity–and eating gluten causes inflammation every time they eat it.” The immune system desperately attacks, including also body’s tissues that at the end can lead to autoimmune 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 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 small intestine. This is where the innate and adaptive immune response systems collide.
CD is not only a gastrointestinal disease, because it may involve to several organs and cause an extensive variety of non-gastrointestinal symptoms, and 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 many patients may have minor mucosal lesions, without atrophy of the intestinal villi. Diagnosis of CD should be based on a combination of patient’s familial history, genetics (i.e. presence of HLA DQ2/DQ8) serology and intestinal histology.
CD affects approximately 1–2% of general population all over the world, but most cases remain unrecognized, undiagnosed and untreated, and exposed to the risk of long-term complications. Patients may suffer severe disease symptoms and be subjected to extensive investigations for many 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, mal-absorption of certain vitamins and minerals, lose of appetite, impaired growth and even bone pain, is currently the least common presentation form of the disease and affects predominantly to small 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 although very 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.
Dermatitis herpetiformis (DH), or Duhring-Brocq disease, is a chronic blistering skin autoimmune condition, characterized by the presence of skin lesions that have 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.
A fact that difficults its diagnosis is the relatively common presentation with atypical manifestations. Some patients 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 many different cutaneous lesions, such as atopic dermatitis, eczema, urticaria, scabies, impetigo, polymorphic erythema and other autoimmune blistering diseases.
DH is considered to be as "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 its proven presence, by itself, confirms the diagnosis of coeliac disease. Nevertheless, duodenal biopsy is recommended in doubtful DH cases, or if there are suspected gastrointestinal complications, including lymphoma. People with DH have different 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 disappear. 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 have important side effects.
Gluten ataxia is a gluten-related disorder, a wide spectrum of disorders marked by an abnormal immunological response to gluten. Like celiac disease, it is an autoimmune disease. With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing. Gluten ataxia is the single most common cause of sporadic idiopathic ataxia.
Gluten ataxia is an immune-mediated disease triggered by the ingestion of gluten in genetically susceptible individuals. It should be considered in the differential diagnosis of all patients with idiopathic sporadic ataxia. Early diagnosis and treatment with a gluten free diet can improve ataxia and prevent its progression. Readily available and sensitive markers of gluten ataxia include anti-gliadin antibodies. Immunoglobulin A (IgA) deposits against transglutaminase 2 (TG2) in the small bowel and at extraintestinal sites are proving to be additionally reliable and perhaps more specific markers of the whole spectrum of gluten sensitivity. They may also hold the key to its pathogenesis.
Gluten ataxia is defined as sporadic cerebellar ataxia associated with the presence circulating antigliadin antibodies and in the absence of an alternative cause for ataxia.
Please seek professional help. Info on this page was last updated and verified on June 4th, 2017 P.S.T.