Intolerance of the proteins of wheat, rye, and barley; specifically, the gliadin fraction of the protein gluten. The villi of the small intestine are severely affected and absorption of food is poor. Stools are bulky and fermenting from unabsorbed carbohydrate, and contain a large amount of unabsorbed fat (steatorrhoea).
Around one in 100 people suffers from coeliac disease, a condition in which the small intestine fails to digest and absorb food, but many have no or few symptoms and remain undiagnosed. The intestinal lining is permanently sensitive to the protein gliadin (an insoluble and potentially toxic peptide protein in wheat, barley and rye) which is contained in gluten, a constituent of the germ of wheat, barley and rye. As bread or other grain-based foods are a regular part of most people’s diet, the constant presence of gluten in the intestine of sufferers of coeliac disease causes atrophy of the digestive and absorptive cells of the intestine. Children are usually diagnosed when they develop symptoms such as vomiting, diarrhoea, lethargy, anaemia, swollen abdomen and pale, frothy, foul-smelling faeces with failure to thrive. The diagnosis is usually made by a positive blood antibody test such as antiendomysial antibodies. However, because there may be an occasional false positive result, the gold standard’ is to obtain a biopsy of the jejunum through a tiny metal capsule that can be swallowed, a specimen taken, and the capsule retrieved. Though coeliac disease was long thought to occur in childhood, a second peak of the disorder has recently been identified among people in their 50s.
Celiac disease, also known as gluten-sensitive enteropathy, arises from an increased sensitivity to gluten, a protein present in wheat, rye, and certain other cereals. Consumption of gluten-containing foods triggers an abnormal immune response that damages the lining of the small intestine. This condition hampers proper nutrient absorption, leading to deficiencies in essential vitamins and minerals.
Coeliac disease has a tendency to occur within families and can exhibit a range of severity. The onset of the disorder can manifest during infancy or may not occur until adulthood.
In infants, symptoms of coeliac disease typically emerge within six months of introducing gluten into their diet. These symptoms may include irritability, listlessness, vomiting, diarrhea, dehydration, and severe illness. Infants and children may also experience stunted growth, failure to gain weight, and muscle wasting, particularly in the buttocks area. In adults, the development of symptoms such as fatigue, shortness of breath, abdominal pain, diarrhea, vomiting, and leg swelling may occur gradually over several months. Additionally, a chronic and distinct skin rash known as dermatitis herpetiformis may also be present.
The damage to the intestinal lining and impaired nutrient absorption in coeliac disease lead to weight loss and the production of bulky, malodorous stools. Consequently, deficiencies in essential vitamins and minerals can give rise to anemia and skin issues. It’s worth noting that certain individuals may experience intestinal lining damage without exhibiting symptoms of the disease.
Diagnosis of coeliac disease can be achieved through blood tests; however, in most cases, additional jejunal biopsies are conducted. During these procedures, small tissue samples are taken from the lining of the jejunum, which is the central portion of the small intestine, and examined for further evaluation and confirmation.
The primary treatment for coeliac disease involves adhering to a strict, lifelong gluten-free diet, which can bring relief from symptoms within a few weeks of its implementation. Specially manufactured gluten-free food items, such as flour and pasta, are readily accessible to support this dietary requirement. Failure to follow a gluten-free diet may pose a long-term risk of developing cancers in the small intestine.