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A 25-year-old female presented herself to her family doctor complaining of tiredness and breathlessness on exertion, saying that it became worse over the last six months. At time of admittance, a physical examination was carried out. She was classed of medium height at 1.65m, had a low weight of 50kg. She had some pale mucous membranes. Her doctor had noted some bruising over her shins but the patient did not recall any injuries, however stated that she bruised quite easily over recent months. Clinical examinations showed a low haemoglobin count of 9.6g/dL, a mean cell volume of 86fL, white cell count of 3.8 x 109/L and platelet count of 330 x 1012/L. Vitamins levels were measured showing low levels of B12 at 68hg/L and slightly low levels of iron at 13mmol/L.
The patient was referred to the gastroenterology clinical at her local hospital for further clinical investigations. The results showed that the serology for antigliadin and other antibodies were positive. A bone-density scan showed early signs of osteoporosis. An upper gastrointestinal biopsy and duodenal biopsy was carried out being macroscopically normal but showing an increased amount of intraepithelial lymphocytes. A diagnosis of coeliac disease was confirmed and she was advised to go on a gluten-free diet.
Coeliac disease can be defined as an autoimmune disorder that affects the small intestine. It occurs by a sensitivity to the glycoprotein gliadin; a gluten, which is found in wheat, cereals and barley. Gliadin has similar characteristics to the enzyme tissue transglutaminase, which is found in the small intestine. The bowel of the small intestine also has small projections known as the villi. These villi are important in the absorption of food as they provide a large surface area to absorb vital nutrients like vitamins, minerals and folic acid. However when gliadin is consumed in the form of wheat, bodyâ€™s immune system mistakes the gluten molecule for an unfriendly organism such as a virus. The immune system begins to attack the molecule whilst at the same time causing damage to the enzyme tissue and the villi of the small intestine. It triggers the production of IgA antibodies that attack the mucosal lining of the bowel. This causes epithelial damage and villous atrophy resulting in malabsorption [1-3]. Food leaves the body without being absorbed resulting in lack of nutrients and diarrhoea.
Although the originality of coeliac disease is unknown it is known to be associated with genetic and environmental factors, therefore being known as a genetically predisposed disease. People are more susceptible to the disease if it recurrent in present generations of their families. Most patients diagnosed with coeliac disease would be carriers of one of two types of the HLA-DQ gene, which is part of the human leukocyte antigen system (HLA). Carriers can either possess the isoform of DQ2 or DQ8. These genes produce an increased risk of coeliac disease by receptors formed by these genes binding to gliadin peptides more tightly than other forms of the antigen-presenting receptor. These forms of the receptor are more prone to activating T-lymphocytes and starting the autoimmune process. The occurrence of the genes varies greatly around the world with higher rates of occurrence in Western Europe and parts of Africa and much lower rates in areas like Japan and China.
More than thirty years ago, where there were not enough facilities or an advanced technology to test for coeliac disease, the disease was wrongly taken to be rare. However currently it is declared that at least 1 out of every 100 people are diagnosed with coeliac disease and that women are two to three times more vulnerable to the disease than men. It is also confirmed that there is no age barrier to the occurrence of this disease and that it can be presented to small children as well as grown people.
A wide spectrum of symptoms are presented with coeliac disease and these symptoms can differ vastly in children and adults. Most children are less likely to show any symptoms until a diet rich in gluten is introduced to them. They will have episodes of diarrhoea (characteristically pale in colour, large and strong smelling). This is accompanied by vomiting which often leads to misdiagnosis of gastroenteritis rather than coeliac disease. Children will show signs of a swollen, irritable stomach with a loss of appetite. They will become malnourished and show signs of weight loss even though they may be ingesting a large appetite. Adults will experience all the above symptoms including lack of energy, severe abdominal pain, signs of mouth ulcers. There are also many malabsorption- related symptoms that they will experience. As iron is not absorbed by the bowel properly it may result in iron deficiency anaemia. Folic acid and vitamin B12 malabsorption may cause megaloblastic anaemia. As vitamin D and calcium are not being absorbed they cause a decrease in mineral content of the bone and therefore result in early stages of osteoporosis occurring. This is the weakening of the bones. Another symptom that adults may experience is a condition called dermatitis herpetiformis . This is a skin condition of coeliac disease characterised by blisters, and extremely itchy skin. It is frequently found on the face, elbows and buttocks. Sufferers of coeliac disease can suffer long time complications such as infertility due to a poor diet and lack of nutrients.
Initial symptoms can only be diagnosed by the GP asking questions to the patient on changes in their appetite, body physique and changes in their bowel motion. The GP will need to examine for mouth ulcers and unusual blisters on the skin. These will confirm an initial diagnosis of coeliac disease which can then be confirmed with a further two stages. The first stage is to have a blood test done which can distinguish people suspected with coeliac disease. The blood test screens for antibodies that is present in coeliac disease. The main antibody that will be tested for is the anti-endomysial antibody. If it is positive then the second stage of diagnosis, which is a biopsy of the gut, can be carried out. This will be done at a local hospital to help confirm the presence of disease. A local anesthetic will be given to numb your throat and make the patient feel relaxed. An endoscope tube that has a tiny camera and a very small cutting tool on the end will be inserted via the mouth, down to the small intestine and a little piece of the tissue will be cut away from the intestine. This sample will then be sent away for testing in a laboratory for any signs of coeliac disease.
Coeliac disease is a disease that cannot be prevented or easily eradicated but the symptoms that occur can disappear eventually if the patient decides to follow a strict gluten-free diet. This will allow the body to repair the damage done to the small intestine by the gluten molecules. Gluten-free diets consist of eating food items like fruit, salads, vegetables, potatoes, rice and maize, nuts and red meat, chicken, fish, eggs and dairy products. Patients will need to avoid foods like bread, pasta, breakfast cereals and some tinned soups and sauces. Beer and whiskey are made from grains containing gluten, but other alcoholic drinks such as wine and cider are gluten-free. Some medicines also contain gluten, so they must be checked with the doctor or pharmacist before consumption. Treatment will also include the restoration of minerals that were not absorbed in the small intestine. Folic acid supplements and iron tablets will need to be taken along with the gluten-free diet.
Although coeliac disease cannot be eradicated completely, avoiding gluten food products can ensure that a healthy life is led free from symptoms and long lasting complications.