Coeliac disease (celiac sprue, nontropical sprue, endemic sprue, gluten enteropathy) is a chronic autoimmune disorder of the small intestine that results in an inability to tolerate gliadin, a prolamin found in wheat. Symptoms include pain, chronic constipation, chronic diarrhoea, failure to thrive and fatigue.
Diarrhea is the most common symptom in untreated celiac sprue and is present in 45-85% of all patients. Diarrhea caused by celiac disease is due to the maldigestion and malabsorption of ingested nutrients. The stools might be watery or semiformed, light tan or gray, and oily or frothy and have a characteristic foul odour. In infants and young children, extensive diarrhea often leads to severe dehydration, electrolyte depletion, and metabolic acidosis .
Malabsorption of ingested fat (steatorrhea) results in the delivery of excessive dietary fat to the large bowel. This results in the production of hydroxy fatty acids by bacteria, which causes secretion of fluids into the intestine. Flatulence (seen in 28% of patients) and borborygmus (seen in 35-72% of patients) results from the release of intestinal gas by the bacterial florae feasting on undigested and unabsorbed food materials and often becomes excessive and in some cases, explosive.
Weight loss (seen in 45% of all patients) is variable because some patients might compensate for the malabsorption by increasing food intake. In infants and young children with untreated celiac disease, failure to thrive and growth retardation are relatively common.
Anemia (seen in 10-15% of patients) is usually due to impaired absorption of iron or folate from the proximal small intestine. In severe celiac disease with ileal involvement, absorption of vitamin B-12 might be impaired. A bleeding diathesis is usually caused by prothrombin deficiency due to impaired absorption of fat-soluble vitamin K.
Osteopenia and osteoporosis might cause bone pain for several reasons, including defective calcium transport by the diseased small intestine, vitamin D deficiency, and binding of luminal calcium and magnesium to unabsorbed dietary fatty acids.
The diagnosis is focused on testing for specific antibodies. For instance, if excessively high levels of endomysial and anti-tissue transglutaminase antibodies are found, the individual most definitely has celiac disease.
High levels of another antibody, anti-gliadin, may also be detected, but this doesn’t always mean a person has celiac disease . However, anti-gliadin antibody levels are important when monitoring response to treatment, this is because they will usually begin to fall after a few months of successful treatment of celiac disease with a gluten-free diet.
People who test positive for celiac disease antibodies will be subjected to intestinal biopsy to confirm the diagnosis. A small intestinal biopsy is performed with an esophagogastroduodenoscopy (EGD). Loss of villi and other characteristics of celiac disease, such as an increased number of lymphocytes are present.
The primary management of celiac disease is dietary. Complete elimination of gluten-containing grain products (including wheat, rye, and barley) is essential to treatment. However, complete avoidance of gluten-containing grain products is often difficult for patients to achieve and maintain. This is because certain products like wheat flour are virtually ever present in the American diet .
A small percentage of patients with celiac disease fail to respond to a gluten-free diet. In some patients who are refractory, corticosteroids can prove very helpful. In patients who fail to respond to corticosteroids, other comorbid conditions, such as lymphomas of the small intestine, have to be ruled out  .
With early removal of gluten from the diet, it becomes less likely for health complications to develop. The body quickly returns to health, in many cases, after the individual begins strict gluten-free nutrition.
To achieve optimal health, the gluten free diet must be maintained for life .
Celiac disease is caused by a reaction to gliadin, a prolamin (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 (like spelt and durum) and related species (such as barley, rye, triticale and Kamut) also induce symptoms of celiac disease . A small minority of people with celiac disease also react to oats. It is most probable that oats produce symptoms due to cross-contamination 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 like maize, millet, sorghum, teff, rice, and wild rice are safe for individuals with coeliac to ingest, as well as non-cereals like amaranth, quinoa, and buckwheat. Non-cereal carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms of celiac disease.
Celiac disease isn’t common. Its prevalence is decreased among blacks and those of Hispanic or Asian ethnicity. The incidence of symptomatic celiac disease in adults is estimated at 2 to 13 per 100,000 per year .
Celiac disease has a strong hereditary connotation. The prevalence of the condition in first-degree relatives is 10% approximately.
A strong association exists between celiac disease and two human leukocyte antigen (HLA) haplotypes (DQ2 and DQ8). Damage to the intestinal mucosa is seen with the presentation of gluten-derived peptide gliadin, made up of 33 amino acids, by the HLA molecules to helper T cells. Helper T cells mediate the inflammatory response. Endogenous tissue transglutaminase deamidates gliadin into a negatively charged protein thereby increasing its immunogenicity. Absence of intestinal villi and lengthening of intestinal crypts characterize mucosal lesions in untreated celiac disease. More lymphocytes infiltrate the epithelium (intraepithelial lymphocytes). Destruction of the absorptive surface of the intestine leads to a maldigestive and malabsorption syndrome .
The disease cannot be prevented.
Also known as celiac sprue and gluten sensitive enteropathy, celiac disease is mostly a chronic disorder of the digestive tract which brings about an inability to tolerate gliadin which is the alcohol soluble fraction of gluten. The protein gluten is mostly found in rye, barley and wheat .
In patients with ciliac sprue, ingestion of giladin triggers an immunologically mediated inflammatory response which ends up damaging the mucosa of the intestines. This brings about maldigestion and malabsorption of food nutrients.
Celiac disease is reaction to eating gluten. Gluten is a protein that is seen in wheat, rye and barley.
In people that have celiac disease, consumption of this protein causes an immune response in your small intestine. Over a period of time the reaction damages the small intestine and this leads to malabsorption (inability to absorb other nutrients).
With this intestinal damage, weight loss, bloating and diarrhea in some cases sets in. After a while, the brain, nervous system, liver, and other organs end up getting deprived of important nutrients.
In children with this condition, malabsorption can affect development and growth. This intestinal irritation can lead to stomach pain especially after eating.
There is no total cure for this disease but it can be controlled by following a strict gluten free diet. The diet can also lead to gradual healing of the intestine.