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Coeliac disease (celiac disease in North America) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy onward. Symptoms include pain and discomfort in the digestive tract, chronic constipation and diarrhoea, failure to thrive (in children), anaemia and fatigue, but these may be absent, and symptoms in other organ systems have been described. Vitamin deficiencies are often noted in people with coeliac disease owing to the reduced ability of the small intestine to properly absorb nutrients from food.
Increasingly, diagnoses are being made in asymptomatic persons as a result of increased screening; the condition is thought to affect between 1 in 1,750 in general and 1 in 105 people in the United States. Coeliac disease is caused by an immune reaction to gluten, a protein found in wheat, barley, rye and some oats, resulting in a damaged mucosa of the small intestine.
The only known effective treatment is a lifelong gluten-free diet.
The term coeliac is derived from the Greek koiliakůs (abdominal) 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.
Severe coeliac disease leads to the characteristic symptoms of pale, loose and greasy stool (steatorrhoea) and weight loss or failure to gain weight (in young children). People with milder coeliac disease may have symptoms that are much more subtle and occur in other organs than the bowel itself. It is also possible to have coeliac disease without any symptoms whatsoever. Many adults with subtle disease only have fatigue or anaemia.
As the bowel becomes more damaged, a degree of lactose intolerance may develop. Frequently, the symptoms are ascribed to irritable bowel syndrome (IBS), only later to be recognised as coeliac disease; a small proportion of people with symptoms of IBS have underlying coeliac disease, and screening for coeliac disease is recommended for those with IBS symptoms.
Calcium and vitamin D malabsorption may cause osteopenia (decreased mineral content of the bone) or osteoporosis (bone weakening and risk of fragility fractures). Growth failure and/or pubertal delay in later childhood.
Coeliac disease is caused by a reaction to gluten protein found in wheat, and similar proteins found in the crops of the tribe Triticeae (which includes other common grains such as barley and rye).
Wheat subspecies (such as spelt and durum) and related species (such as barley, rye, triticale and Kamut) also induce symptoms of coeliac disease. A small minority of people with coeliac also react to oats. It is most probable that oats produce symptoms due to cross-contamination (mixed) with other grains in the fields or in the distribution channels. Therefore, oats are generally not recommended. However, many companies assure the 'purity' of oats and are therefore still able to be consumed through these sources.
Other cereals such as maize, millet, sorghum, teff, rice, and wild rice are safe for people with coeliac to consume, as well as noncereals such as amaranth, quinoa, and buckwheat. Noncereal carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms.
There are various theories as to what determines whether a genetically susceptible individual will go on to develop coeliac disease. Major theories include infection by rotavirus or human intestinal adenovirus. Some research has suggested that smoking is protective against adult-onset coeliac disease.
People exposed to wheat, barley, or rye before the gut barrier has fully developed (within the first three months after birth) had five times the risk of developing coeliac disease relative to those exposed four to six months after birth. Breastfeeding may also reduce risk with prolonging breastfeeding until the introduction of gluten-containing grains into the diet associated with a 50% reduced risk of developing coeliac disease in infancy; whether this persists into adulthood is not clear. Factors that can trigger symptoms include: surgery, pregnancy, infection and emotional stress.
The prevalence of celiac disease (CD) genotypes in modern population is not completely understood. Given the characteristics of the disease and its apparent strong heritability, it would normally be expected that the genotypes would undergo negative selection and to be absent in societies where agriculture has been practised the longest (compare with a similar condition, Lactose intolerance, which has been negatively selected so strongly that its prevalence went from ~100% in ancestral populations to less than 5% in some European countries). By now, however, it is apparent that this is not the case; on the contrary, there is evidence of positive selection in CD genotypes. It is suspected that some of them may have been beneficial by providing protection against bacterial infections.
At present, the only effective treatment is a lifelong gluten-free diet. No medication exists that will prevent damage or prevent the body from attacking the gut when gluten is present. Strict adherence to the diet allows the intestines to heal, leading to resolution of all symptoms in most cases and, depending on how soon the diet is begun, can also eliminate the heightened risk of osteoporosis and intestinal cancer and in some cases sterility. Dietitian input is generally requested to ensure the person 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.
The diet can be cumbersome; failure to comply with the diet may cause relapse. The term gluten-free is generally used to indicate a supposed harmless level of gluten rather than a complete absence. The exact level at which gluten is harmless is uncertain and controversial. Some think that consumption of less than 10 mg of gluten per day is unlikely to cause histological (relating to tissue) abnormalities.
A tiny minority of people 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 on diet alone, or because the person is not adhering to the diet, or because the person is consuming foods that are inadvertently contaminated with gluten. If alternative causes have been eliminated, steroids or immunosuppressants (such as azathioprine) may be considered in this scenario.
Humans first started to cultivate grains in the Neolithic period (beginning about 9500 BCE) in the Fertile Crescent in Western Asia, and it is likely that coeliac disease did not occur before this time. Aretaeus of Cappadocia, living in the second century in the same area, recorded a malabsorptive syndrome with chronic diarrhoea. This gained the attention of Western medicine when Francis Adams presented a translation of Aretaeus's work at the Sydenham Society in 1856. The patient described in Aretaeus' work had stomach pain and was pale, feeble and incapable of work. The diarrhoea manifested as loose stools that were white, malodorous and flatulent, and the disease was intractable and liable to periodic return. The problem, Aretaeus believed, was a lack of heat in the stomach necessary to digest the food and a reduced ability to distribute the digestive products throughout the body, this incomplete digestion resulting in the diarrhoea. The cause, according to Aretaeus, was sometimes either another chronic disease or even consuming "a copious draught of cold water."
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