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Coeliac disease
The term "coeliac" is from the Greek κοιλιακός (koiliakós, "abdominal“) Coeliac disease” is a long term autoimmune
disorder in people especially in children with the indigestion of Gluten leads to problems in the leg. It is also called gluten
sensitive enteropathy (small intestine disease and coeliac sprue during this disease cells inside the body attack the lining
of the intestine. This means that they cannot digest (eat) food properly, making them unable to have enough energy,
vitamins, or minerals.
Such disease usually effect children and duodenum and proximal jejunum that may be unable to grow taller or gain weight
properly. People with coeliac disease often lose weight and are also frequently tired. Coeliac disease was first described in
childhood; however, it may develop at any age. This often begins between six months and two years of age. It is
associated with other autoimmune diseases, such as diabetes mellitus type 1 and thyroiditis, among others.
What is gluten?
Gluten is a general name for the proteins found in wheat (wheat berries, oat, durum, emmer, semolina, spelt, farina, farro,
graham, rye, barley and triticale. Gluten helps foods maintain their shape, acting as glue that holds food together.
Gluten consist of two proteins i.e glutenin and gliadin
Glutien can cause three types of disease
1. Celiac disease
2. Grain allergies
3. Gluten tolerance
Signs and symptoms
People with coeliac disease often have bloating and pain in their abdominal (stomach) area, diarrhoea (watery stools) or
steatorrhea (fat in their stools) or pale, loose, and greasy stool and weight loss. These symptoms can lead to flatulence.
Their stomachs also start to hurt and they might suffer from joint pains, seizures, rashes, fatigue, slowness in growth and
puberty, loss of bone density and fertility issues.
1. IgA deficiency
2. Gastrointestinal area
During this stage chronic, pale, of large volume, and abnormally bad smelling stool (steatorrhea) . Abdominal pain and
cramping, bloatedness (when the gastrointestinal (bowel) tract is filled with air or gas by which the abdomen is also
swollen) the bowel becomes more damaged, a degree of lactose intolerance may develop
3. Malabsorption
The damages in the bowel make it less able to absorb nutrients, minerals, and the fat-soluble vitamins A, D, E, and K. The
inability to absorb carbohydrates and fats may cause weight loss and fatigue or lack of energy. Anaemia may develop in
several ways: iron malabsorption may cause iron deficiency anaemia, and folic acid and vitamin B12 malabsorption may
give rise to megaloblastic anaemia. Calcium and vitamin D malabsorption may cause osteopenia (decreased mineral
content of the bone) or osteoporosis (bone weakening and risk of fragility fractures). Copper and zinc deficiencies have
also been associated with coeliac disease.
4. Dermatitis herpetiformis
During coeliac disease when the patient eat gluten containing food then suddenly the rashes appear and blister forming on
their abdomen and arm which are extremely itch and this condition is called Dermatitis herpetiformis It effect 10%
people who have coeliac disease

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Causes
Coeliac disease is caused by a reaction to gluten i.e gliadins and glutenins. Sometimes celiac disease is triggered — or
becomes active for the first time — after surgery, pregnancy, childbirth, and viral infection or severe emotional stress.
1. Type 1 diabetes
2. Thyroid conditions
3. Ulcerative colitis – a digestive condition that causes inflammation of the colon (large bowel)
4. Neurological disorders (which affect the brain and nervous system) such as epilepsy
5. Down's syndrome and Turner syndrome
Epidemiology
Globally coeliac diseases affect between 1 in 100 and 1 in 170 people. Due to variable signs and symptoms it is believed
that about 85% of people affected are undiagnosed and only 1-2% people can be diagnosed.
Mechanisms of action in body or pathogenesis
Upon exposure to gluten, an abnormal immune response may lead to the production of several different autoantibodies
that can affect a number of different organ she disease is began when we take gluten food. During this disease when
glaiden is reach to bowel area then many antibodies are released against it and react with it. After that the lymphocytes
and some other WBC are released in a large number and the war is going on and finally the inflammation occur in the
small intestine and the wall of small intestine is damaged.
As the wall of small intestine is responsible for absorption so the absorption will be disrupted. Thus the following
compound or molecules are not absorb
1. Water that can lead to diarrhea
2. Fats that can lead to steatorrhea
3. Iron and vit B12 that can lead anemia
Risk factor
The eating of gluten early in a baby's life does not appear to increase the risk of CD but later introduction after 6 months
may increase it. Coeliac disease leads to an increased risk of both adenocarcinoma and lymphoma of the small bowel.
Long-standing and untreated disease may lead to other complications, such as ulcerative jejunitis (ulcer formation of the
small bowel) and stricturing (narrowing as a result of scarring with obstruction of the bowel). Pregnancy complications
including miscarriage, intrauterine growth restriction, low birth weight and preterm birth.
Reduction of risk factor
Breastfeeding
Prolonging breastfeeding until the introduction of gluten-containing grains into the diet appears to be associated with a
50% reduced risk of developing coeliac disease in infancy
Occurrence
It is more common in Down syndrome and genetically susceptible individual. Celiac disease is more commonly found
among white is more commonly found among white Europeans i.e American.
Coeliac disease is genetic and relatives (such as children, siblings, parents) with this disease have a 1 in 10 chance of
developing coeliac disease. This means that the person affected by it is born with genes that cause the immune system to
react poorly to gluten. However, coeliac disease is not always present during childhood. It can be triggered as an adult by
an event such as pregnancy (hormone shifts) or illness.

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Diagnosis
Diagnosis is often difficult and as of 2019, there continues to be a lack of awareness among physicians about the
variability of presentations of coeliac disease and the diagnostic criteria, such that most cases are diagnosed with great
delay. It can take up to 12 years to receive a diagnosis from the onset of symptoms and the majority of those affected in
most countries never receive it. To find out if a person has coeliac disease, doctors look in the blood to see if they have the
cells that attack the intestine when gluten is eaten. The protein that attacks the intestine is called an antibody. In the case
of coeliac disease, one of the antibodies thinks that gluten is something that will cause illness.
There are severaltests that can be used. The level of symptoms may determine the order of the tests, but all tests lose their
usefulness if the person is already eating a gluten-free diet.
1. Blood test
Serological blood tests are the first-line investigation required to make a diagnosis of coeliac disease. People who present
minor damage of the small intestine may have seronegative findings so many patients with coeliac disease often are
missed. In patients with villous atrophy, anti-endomysial (EMA) antibodies of the immunoglobulin A (IgA) type can
detect coeliac disease with a sensitivity and specificity of 90% and 99%, respectively. Both anti-transglutaminase and
anti-endomysial antibodies have high sensitivity to diagnose people with classic symptoms and complete villous atrophy,
but they are only found in 30–89% of the cases with partial villous atrophy and in less than 50% of the people who have
minor mucosal lesions (duodenal lymphocytosis) with normal villi.
Tissue transglutaminase modifies gluten peptides into a form that may stimulate the immune system more effectively.
These peptides are modified by tTG in two ways, deamidation or transamidation. tTG testing should be done first as it is
an easier test to perform. Guidelines recommend that a total serum IgA level is checked in parallel, as people with coeliac
with IgA deficiency may be unable to produce the antibodies on which these tests depend ("false negative"). In those
people, IgG antibodies against transglutaminase (IgG-tTG) may be diagnostic.
A negative serology test may still be followed by a recommendation for endoscopy and duodenal biopsy if clinical
suspicion remains high. Three other antibodies were measured: anti-reticulin (ARA), anti-gliadin (AGA) and anti-
endomysial (EMA) antibodies. ARA testing, however, is not accurate enough for routine diagnostic use. Serology may be
unreliable in young children, with anti-gliadin performing somewhat better than other tests in children under five.
Serology tests are based on indirect immunofluorescence (reticulin, gliadin and endomysium) or ELISA (gliadin or tissue
transglutaminase, tTG). Other antibodies such as anti–Saccharomyces cerevisiae antibodies occur in some people with
coeliac disease but also occur in other autoimmune disorders and about 5% of those who donate blood.
2. Endoscopy
An upper endoscopy with biopsy of the duodenum (beyond the duodenal bulb) or jejunum is performed to obtain multiple
samples (four to eight) from the duodenum. Not all areas may be equally affected; if biopsies are taken from healthy
bowel tissue, the result would be a false negative. Even in the same bioptic fragment, different degrees of damage may be
present. Most people with coeliac disease have a small intestine that appears to be normal on endoscopy before the
biopsies are examined.
Biopsies were obtained using metal capsules attached to a suction device. The capsule was swallowed and allowed to pass
into the small intestine. After x-ray verification of its position, suction was applied to collect part of the intestinal wall
inside the capsule. Often-utilised capsule systems were the Watson capsule and the Crosby–Kugler capsule. This method
has now been largely replaced by fibre-optic endoscopy, which carries a higher sensitivity and a lower frequency of
errors. Capsule endoscopy (CE) allows identification of typical mucosal changes observed in coeliac disease but has a
lower sensitivity compared to regular endoscopy and histology. CE is therefore not the primary diagnostic tool for coeliac
disease. However, CE can be used for diagnosing T-cell lymphoma, ulcerative jejunoileitis and adenocarcinoma in
refractory or complicated coeliac disease.

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3. Genetic test
People with ceolic disease carry both HLA DQ2 and DQ8 genes but 25-30% of the population with have the same genes
but it does not mean that such people will have coeliac disease. People (95%) with coeliac disease have either the variant
HLA-DQ2 allele or the HLA-DQ8 allele. Furthermore, around 5% of those people who do develop coeliac disease do not
have typical HLA-DQ2 or HLA-DQ8 alleles. Antibody testing may be combined with HLA testing if the diagnosis is
unclear. TGA and EMA testing are the most sensitive serum antibody tests, but as a negative HLA-DQ type excludes the
diagnosis of coeliac disease, testing also for HLA-DQ2 or DQ8 maximizes sensitivity and negative predictive values.
However, widespread use of HLA typing to rule out coeliac disease is not currently recommended.
4. Screening test
In the United Kingdom, the National Institute for Health and Clinical Excellence (NICE) recommend testing for coeliac
disease in first-degree relatives of those with the disease already confirmed, in people with persistent fatigue,
osteomalacia, peripheral neuropathy and ataxia, abdominal or gastrointestinal symptoms, faltering growth, unexplained
weight loss or iron, Down syndrome or Turner syndrome. vitamin B12 or folate deficiency, severe mouth ulcers, and with
diagnoses of type 1 diabetes, autoimmune thyroid disease, fertility problems and with newly diagnosed chronic fatigue
syndrome and irritable bowel syndrome.Dermatitis herpetiformis is included in other recommendations.
5. Other diagnostic tests
At the time of diagnosis, further investigations may be performed to identify complications, such as iron deficiency (by
full blood count and iron studies), folic acid and vitamin B12 deficiency and hypocalcaemia (low calcium levels, often
due to decreased vitamin D levels). Thyroid function tests may be requested during blood tests to identify hypothyroidism,
which is more common in people with coeliac disease.
Osteopenia and osteoporosis, mildly and severely reduced bone mineral density, are often present in people with coeliac
disease, and investigations to measure bone density may be performed at diagnosis, such as dual-energy X-ray
absorptiometry (DXA) scanning, to identify risk of fracture and need for bone protection medication.
Treatment or medication
To relieve the effects of coeliac disease, one must stop eating gluten. There are no medicines or cure that can stop coeliac
disease. To get fully better, it usually takes about two years of not eating gluten, during which time the previously
damaged intestine might recover. They must remain on a gluten-free diet for the rest of their life in order to treat this
condition. On the other hand we have 2nd opton i.e gene therpy during which we remove the defective genes