Celiac disease (gluten enteropathy) is a disease small intestine, which is caused by genetically determined intolerance to dietary gluten (a protein from cereal plants) and is characterized by the development of villous atrophy due to the exclusion of gluten (N.D. Parnell, P.J. Ciclitira, 1999).

Population-based screening studies conducted in recent years, showed that the frequency of this disease reaches 1%, and in most patients it is asymptomatic or has mild or atypical (extraintestinal) clinical manifestations, and therefore for a long time remains undiagnosed. Thus, in adults, celiac disease is usually diagnosed no earlier than 10 years from the appearance of the first clinical signs of the disease, and in Europe, for every case of established diagnosis of celiac disease, there are 5-13 undiagnosed cases. Meanwhile, the presence of celiac disease is associated with an increased risk of developing autoimmune pathology (up to 20%) and some oncological diseases(5-7 times increased risk of non-Hodgkin's lymphomas, 24-40 times increased risk of lymphomas of the gastrointestinal tract), and there is evidence that timely administration of a gluten-free diet can not only reduce the severity of the manifestations of celiac disease itself, but also prevent the development of diseases associated with it . Thus, the diagnosis of celiac disease is a pressing problem of modern clinical medicine.

In the process of diagnosing celiac disease, three main components are distinguished: clinical, seroimmunological and morphological.

Clinical diagnosis of celiac disease

The classic manifestation of celiac disease is malabsorption syndrome (impaired absorption): chronic diarrhea, polyfecal matter, flatulence, weight loss, hypoproteinemia, signs of deficiency of vitamins and microelements. However, in many In some cases, intestinal symptoms may either be completely absent or fade into the background, giving way to extraintestinal manifestations that predominate in the clinical picture. The spectrum of the main typical and atypical manifestations of celiac disease is presented in table. 1. It is obvious that all of the listed symptoms are nonspecific, therefore neither individual manifestations nor their combinations can be regarded as independent diagnostic criteria diseases, but their presence suggests a diagnosis of celiac disease if there are no other pathological conditions, explaining the existing symptoms.

Typical manifestations
- malabsorption syndrome: - diarrhea; - bloating; - weight loss; - intolerance to dairy products; - steatorrhea
Atypical manifestations
non-specific:	chronic fatigue; weakness; fatigue
hematological:	anemia (iron deficiency, folate deficiency, B12 deficiency); bleeding, tendency to bruise; hyposplenism
neurological:	peripheral neuropathy; cerebellar ataxia; epilepsy
metabolic:	bone pain; osteoporosis, osteomalacia; short stature; signs of vitamin deficiency
gynecological:	delayed puberty; amenorrhea; infertility; recurrent miscarriages
gastrointestinal:	irritable bowel syndrome; dyspepsia; gastroesophageal reflux; hypertransaminasemia
psychiatric:	depression; schizophrenia
dermatological:	atopic dermatitis; alopecia; keratosis pilaris
	arthralgia; aphthous stomatitis

Table 1. Clinical manifestations of celiac disease

In addition, in the diagnosis of celiac disease, an important role is played by the formation of risk groups, which include individuals who have a higher probability of developing celiac disease than in the general population. The risk groups specified in the recommendations of the World Gastroenterological Organization (OMGE) are presented in table. 2.

Risk group	Frequency of celiac disease
First and second degree relatives
Down syndrome
Autoimmune thyroid diseases
Diabetes mellitus type 1
Lymphocytic colitis
Chronic fatigue syndrome Chronic active hepatitis Irritable bowel syndrome

Table 2. Risk groups for celiac disease according to OMGE recommendations

Patients who have clinical symptoms, allowing to suspect celiac disease, as well as for persons at risk, seroimmunological testing for markers of celiac disease is indicated.

Seroimmunological testing

Seroimmunological markers of celiac disease include:

Antigliadin antibodies (AGA-IgA, AGA-IgG);

Antibodies to connective tissue components:

reticulin (ARA-IgA);

endomysium (EMA-IgA, EMA-IgG);

tissue transglutaminase (anti-tTG-IgA, anti-tTG-IgG).

Antigliadin antibodies are a classic serological marker of celiac disease, but the use of this test is currently not recommended due to low sensitivity and specificity (70–80%). The antireticulin antibody test is also not widely used. Thus, modern serological diagnosis of celiac disease is based on the detection of antibodies to tissue transglutaminase and (or) endomysial antibodies, the antigen for which is also tissue transglutaminase.

As a rule, IgA antibodies are determined to diagnose celiac disease. EMA-IgA is detected by indirect immunofluorescence using monkey esophagus or human umbilical cord as a tissue substrate. Despite some degree of subjectivity in assessing the results of immunofluorescence studies, this particular test is considered the “gold standard” serological diagnostics celiac disease, since its specificity reaches 100% with a sensitivity of about 90%. Anti-tTG-IgA is determined by the method enzyme immunoassay(ELISA), and if in the first generation tests the antigen was tissue transglutaminase from the liver guinea pigs, then currently human or recombinant tissue transglutaminase is used for this purpose, which has improved the accuracy of the test. The sensitivity of anti-tTG-IgA in diagnosing celiac disease is 91-97%, specificity is close to 100%.

When conducting serological diagnostics special attention required by patients suffering from selective IgA deficiency. In them, even in the case of celiac disease, IgA class markers may not be detected, and therefore patients with low levels of total IgA are recommended to be tested for anti-tTG, EMA- or AGA-IgG.

False-negative results of EMA and anti-tTG tests can also be obtained in individuals with early morphological stages of celiac disease (Marsh I, II). It is known that the level of these markers in the blood serum increases with increasing degree of mucosal atrophy, therefore, negative results of a serological test in patients with clinical signs of celiac disease should not be a reason for refusing to perform a duodenojejunal biopsy.

False-positive test results for celiac disease markers are also possible, which are usually observed in the presence of autoimmune diseases.

Although EMA and anti-tTG react with the same antigen, the test results do not always match. This is explained by the difference in the sensitivity of the methods used. In addition, it is possible that EMAs can react not only with tissue transglutaminase, but also with other antigens, such as actin or the beta chain of ATP synthase.

Endoscopy in the diagnosis of celiac disease

Suspicion of celiac disease is the basis for prescribing esophagogastroduodenoscopy (EGD), which is performed primarily to obtain samples of the mucous membrane for subsequent morphological examination. As a rule, biopsies are taken from several (usually three) points of the descending branch 12- duodenum(DPK). However, in rare cases, changes characteristic of celiac disease can be detected only in the jejunum, therefore, in the case of positive results of seroimmunological testing and in the absence of changes in the mucous membrane of the distal parts of the duodenum, it is advisable to repeat the biopsy distal to the ligament of Treitz. Immediately after removal from the forceps, the resulting material is placed on filter paper with the epithelial layer up and only then placed in a formaldehyde solution (along with a piece of filter paper to which it is fixed). Such fixation of biopsy specimens subsequently facilitates the orientation of the histological specimen, which is important for its correct assessment.

In some patients suffering from celiac disease, routine endoscopic examination of the duodenum may reveal characteristic changes in the mucous membrane, which include:

Reduction in the number or disappearance of folds;

Scalloping of folds;

Mosaic pattern of the mucous membrane;

Visible vascular pattern;

Nodularity.

As a rule, these changes are determined in the descending part of the duodenum, but can also be observed in the bulb. The specificity of these signs in relation to atrophy of the mucous membrane of the small intestine is very high and reaches 92-99%, however, the sensitivity, according to various sources, is only 9-88% and depends on the degree of atrophy. Thus, with partial atrophy (Marsh IIIA), these endoscopic markers are detected less frequently than with subtotal (Marsh IIIB) or total (Marsh IIIC) atrophy. There are no data on the endoscopic picture of the small intestinal mucosa in individuals with non-atrophic stages of celiac disease (Marsh I-II), however, it can be assumed that at these stages endoscopic examination does not reveal any changes, since the height of the villi of the small intestine is not changed. Thus, a normal endoscopic picture does not exclude the diagnosis of celiac disease and should not be a reason for refusing to perform a distal duodenal biopsy prescribed on the basis of clinical and laboratory data. If, during gastroduodenoscopy, endoscopic markers of celiac disease are established, a biopsy should be performed regardless of the indications for which the patient was sent for examination. The use of techniques such as capsule endoscopy and zoom endoscopy will improve sensitivity endoscopic examination in the diagnosis of celiac disease.

Morphological diagnosis of celiac disease

Morphological diagnosis of celiac disease is based on the detection of signs of two parallel processes occurring in the mucous membrane of the small intestine: atrophy and inflammation.

Atrophy of the mucous membrane in celiac disease is of a hyperregenerative nature and manifests itself, along with shortening and thickening of the villi, elongation (hyperplasia) of the crypts. For the diagnosis of celiac disease important has a change in the ratio of villus height to crypt depth, which is normally at least 2:1. This ratio can only be assessed if the histological specimen is correctly oriented, the representativeness criterion of which is the presence of at least three adjacent, longitudinally cut villi and crypts.

Inflammatory infiltration of the mucous membrane includes two components: infiltration of the surface epithelium by lymphocytes and lymphoplasmacytic infiltration of the lamina propria of the mucous membrane. The normal content of interepithelial lymphocytes (IEL) in the epithelium of the villi of the small intestine does not exceed 30 per 100 epithelial cells. Increased MEL content in the villi, or intraepithelial lymphocytosis, is a typical histological manifestation of celiac disease. Increased infiltration of the lamina propria of the mucous membrane with plasma cells and lymphocytes, although characteristic of celiac disease, does not have an independent diagnostic value and can only be taken into account in the presence of other histological signs of the disease. Among the cells infiltrating both the lamina propria and the epithelium, neutrophils can be found in fairly large numbers.

Depending on the presence and combination of signs, the histological picture of celiac disease is classified in accordance with the modified Marsh system, presented in table. 3.

Stage	Histological changes
	Increased infiltration of the villous epithelium of the MEL
	Increased infiltration of the villous epithelium MEL + hyperplasia (elongation) of the crypts (ratio of villous height to crypt depth less than 2:1)
	Partial villous atrophy + crypt hyperplasia
	Subtotal villous atrophy + crypt hyperplasia
	Total villous atrophy + crypt hyperplasia

Table 3. Histological classification of celiac disease

Marsh I. Infiltration of the villous epithelium by lymphocytes is the earliest histological manifestation of celiac enteropathy. Infiltration of the epithelium by lymphocytes persists at all stages of celiac disease, however, at late (atrophic) stages (Marsh IIIB-C), it can be quite difficult to assess the MEL content in the epithelium due to the pronounced regenerative-dystrophic pseudostratification of the epithelium.

March II . The first manifestation of hyperregenerative atrophy of the mucous membrane of the small intestine is elongation of the crypts (hyperplastic stage of celiac disease). At this stage, the ratio of villus length to crypt depth decreases to 1:1. In parallel with the elongation of the crypts, some expansion of the villi occurs. Infiltration of the epithelium by lymphocytes persists. Estimated The relationship between the length of the villus and the depth of the crypt should be determined only in a correctly oriented preparation.

March III. In subsequent (atrophic) stages of celiac disease, gradual shortening and expansion of the villi occurs in parallel with the deepening of the crypts (Marsh IIIA) until the complete disappearance of the villi (Marsh IIIC). In such cases, the structure of the mucous membrane of the small intestine resembles the large intestine. This stage is also characterized by changes in the surface epithelium associated with its damage and an attempt at regeneration: an increase in cell size, basophilia of the cytoplasm, an increase in the size of the nucleus, clearing of nuclear chromatin, loss of basal orientation by the nuclei (pseudostratification of the epithelium), blurriness and indistinctness of the brush border (may disappear altogether ).

Diagnostic criteria and clinical forms of celiac disease

As already indicated, the clinical manifestations of celiac disease are very nonspecific and only allow one to suspect the possible presence of this disease. Morphological changes small intestinal mucosa, characteristic of celiac disease (intraepithelial lymphocytosis, hyperregenerative atrophy), can be observed in a number of other diseases. However, there is a sign specific to celiac disease - the body’s reaction to the exclusion of gluten from the diet or, conversely, to its introduction into the diet. Confirmation of this reaction is key point establishing a definite diagnosis of celiac enteropathy. In 1970, the European Society of Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) developed guidelines for a three-stage diagnosis of celiac disease, which were used in both children and adults. At the first stage, in the presence of gastrointestinal manifestations characteristic of celiac disease (diarrhea, bloating, low weight) and abnormal results of nonspecific screening tests (eg, D-xylose test, fat malabsorption test), a biopsy of the small intestinal mucosa was performed and, if atrophy was detected, a gluten-free diet was prescribed. At the second stage, after 12 months of following a gluten-free diet, a repeat biopsy was performed and, if the histological picture was normalized, as well as the disappearance of clinical manifestations and screening test abnormalities, the patient was again transferred to a gluten-containing diet. The third stage consisted of assessing the reaction to the introduction of gluten after 3 months - the resumption of clinical symptoms, pathological results of screening tests and atrophy phenomena were in favor of celiac disease. If all three components were present, a definite diagnosis of celiac disease was established. After the introduction of seroimmunological screening tests, which have high sensitivity and specificity, into clinical practice, in most cases there was no need to re-study the response of the mucous membrane to the introduction (exclusion) of gluten. Currently, OMGE calls the “gold standard” for diagnosing celiac disease the identification of characteristic histological changes in combination with positive results of seroimmunological tests (anti-tTG-IgA or EMA-IgA).

ESPGHAN in 1990 revised the criteria for establishing a specific diagnosis of celiac disease, which became as follows:

1)history and clinical manifestations consistent with celiac disease;

2)results of serological screening tests consistent with celiac disease;

3)histological findings consistent with celiac disease (mucosal atrophy);

4)clear clinical and serological response to a gluten-free diet;

5)patient age more than 2 years;

6)other clinical conditions that may simulate celiac disease were excluded.

Thus, with serological and histological data typical for celiac disease, and in the presence of a clear clinical response to a gluten-free diet, a repeat biopsy can be refrained. However, the British Gastroenterological Society continues to recommend repeat histological examination 4-6 months after starting a gluten-free diet, since such confirmation of the diagnosis is more reliable. Histological examination over time remains mandatory for asymptomatic or minimally symptomatic patients, when clinical response cannot be assessed, as well as in cases of seronegative disease.

In persons with questionable morphological data or negative results serological tests, it is advisable to carry out typing for the presence of haplotypes HLA-DQ2 and HLA-DQ8 of the major histocompatibility complex. The expression of these molecules is prerequisite for the development of celiac disease, therefore, their absence excludes this diagnosis.

In cases where the previously made diagnosis of celiac disease appears doubtful, and the patient is on a gluten-free diet, a provocative test with a gluten load is used to clarify the presence of celiac disease. Typically, this may be required in cases where adherence to a gluten-free diet was started empirically before morphological examination of the small intestine and (or) obtaining the results of serological testing for markers of celiac disease, or if the diagnosis was made in childhood on the basis of morphological data without serological confirmation (in children transient enteropathies simulating celiac disease are possible: protein-induced enteropathies caused by intolerance to cow's milk, soy, etc., transient gluten intolerance, postenteritis syndrome). Before starting a provocative test, it is necessary to perform a serological determination of celiac disease markers and a morphological examination of the small intestinal mucosa. The patient is then asked to consume at least 10 g of gluten daily, which is equivalent to 4 slices of bread. After 4-6 weeks, serological and morphological studies are repeated. The appearance of changes characteristic of celiac disease is considered as confirmation of the diagnosis.

Depending on the combination of clinical, seroimmunological and histological characteristics, several main clinical forms of the disease are distinguished: obvious (classical, typical), atypical, erased (asymptomatic, hidden), latent (potential) and refractory (Table 4).

Explicit/classical (overt, classical, typical)	enteropathy clinic hyperregenerative atrophy (Marsh II-III)
Atypical	· Manifestations of enteropathy are absent or minimal Atypical manifestations predominate · positive serological tests hyperregenerative atrophy (Marsh II-III)
Erased/asymptomatic (silent, asymptomatic)	· no clinical manifestations positive serological tests · hyperregenerative atrophy (Marsh II-III)
Latent/potential	· no clinical manifestations positive serological tests positive genetic markers (HLA DO2/DQ8) · the architectonics of the mucous membrane is not disturbed · increased number of MEL (Marsh I)
Refractory (usually associated with the development of complications of celiac disease - collagenous sprue, ulcerative jejunoileitis, intestinal lymphoma)	· there are convincing clinical Serological and histological signs of celiac disease · no response to gluten-free diet

Table 4. Clinical forms celiac disease

Thus, the diagnosis of celiac disease is based on the results special methods studies (distal duodenal biopsy, seroimmunological tests), the conduct of which requires the doctor to know various options for clinical presentation, as well as diseases and conditions associated with a high risk of developing celiac disease. Effective identification of people suffering from celiac disease is possible only if both clinicians and endoscopists are highly alert to the possible presence of this disease.

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Attention! The article is addressed to medical specialists. Reprinting this article or its fragments on the Internet without a hyperlink to the source is considered a violation of copyright.

Chronic epithelial disease small intestine, which is characterized by congenital protein intolerance, is called celiac disease. This protein is found in various cereal crops, such as barley, rye, as well as oats and wheat.

The disease is more often detected in women, but is also common in children and men. In children, symptoms are usually pronounced, which is associated with insufficient development of the digestive tract and enzymatic system, and in adolescents and adults it is usually almost asymptomatic. Treatment of the disease consists of prescribing a special diet.

Celiac disease is caused by a congenital genetic disorder in which the lining of the small intestine is damaged by eating gluten. Protein in pure form leads to the gluing of the villi and their damage, which subsequently prevents them from fully functioning.

Celiac disease in adults can be caused by the following reasons:

• Genetic predisposition;
• Down syndrome;
• Autoimmune thyroid diseases;
• Type 1 diabetes mellitus, which requires immediate treatment;
• An inflammatory process in the colon, leading to the accumulation of lymphocyte blood cells, the so-called lymphocytic colitis;
• Irritable bowel syndrome;
• Chronic hepatitis of active type.

Celiac disease in children can also be caused by the above reasons, but in a child it occurs with more severe symptoms. The disease in children is also caused by a deficiency of intestinal enzymatic cells, the main purpose of which is to break down the protein peptide.

Inflammation of the villi of the small intestine can be caused by other factors, including:

• Stress and nervous tension;
• Surgery (for example, when removing appendicitis);
• Regular consumption of foods rich in gluten;
• Intestinal infections caused by dangerous bacteria and viruses.

Today the most common intestinal disease is celiac disease. From the outside digestive system There may be the following signs:

• Impaired absorption of various microelements and vitamins in the intestines (diarrhea mixed with mucus and blood, flatulence, increased stool volume);
• Intolerance to consuming products containing milk;
• Decreased appetite;
• Painful sensations in the navel area.

In other organs, celiac disease is manifested by the following symptoms:

• Short stature;
• Osteoporosis;
• Painful sensations in the bones;
• Destruction of tooth enamel;
• Constant strong thirst;
• Softening of bones as a result of impaired absorption of calcium in the intestine;
• Pale skin.

Celiac disease in children under two years of age has pronounced symptoms, and their appearance is caused by eating foods rich in gluten. These include:

• Nausea, weight loss and extreme thinness;
• Bloating and flatulence;
• Diarrhea with a strong unpleasant odor;
• Development of rickets;
• Excitement and crying.

In addition to the above symptoms, celiac disease in adults can also cause nonspecific signs, namely a feeling of lack of air, increased fatigue, migraine, and atopic dermatitis. In addition, it can lead to changes in behavior - insomnia, increased anxiety, sudden changes in mood.

Diagnosis of celiac disease is carried out based on the patient’s visit to the doctor and identification of complaints. After a visual examination and medical history, the gastroenterologist can perform a preliminary analysis, which requires further clarification.

A gastroenterologist also diagnoses celiac disease during an examination. To do this, the doctor palpates the abdominal area to identify painful sensations, measuring abdominal circumference, and also schedules a consultation with an allergist.

TO laboratory methods diagnostics include:

• A blood test performed to determine hemoglobin, the level of red blood cells, platelets and white blood cells, which allows us to determine the inflammatory process in the body.
• Biochemical blood test to determine high levels of immunoglobulin. This analysis is most informative only during the period active stage diseases.
• A stool test for celiac disease to determine occult blood, which is a sure symptom of intestinal dysfunction.
• Examination of stool to detect fragments undigested food.

Celiac disease in adults can also be detected through instrumental examination methods:

• Fibrogastroduodenoscopy is a procedure in which a specialist examines the internal cavity of the stomach and intestines using a special endoscope. During the FGDS process, the doctor also takes a biopsy of the duodenum to identify the structure of the surface epithelium;
• Evaluation of biopsy results using special technology;
• Studying bone tissue and determination of its density;
• Ultrasound of organs in the abdominal cavity to identify the location of damage to the walls of the small intestine.

Receiving positive biopsy results confirms the diagnosis of inflammation and villi adhesions in the small intestinal mucosa. However, if a blood test was used as a diagnostic method, then re-examination is required to confirm the results.

Treatment for this disease does not require the use of drug therapy or surgical treatment. It involves mainly a diet that includes foods with low content gluten, namely the complete exclusion of grains from the diet - wheat, rye, oats, and barley.

A gluten-free diet includes:

• Limiting the consumption of processed meats, canned foods, chocolate, as well as fatty sauces and mayonnaise, coffee and cocoa;
• Refusal of spicy, salty and fatty foods;
• Excluding flour from the diet, as well as eating baked goods made from gluten-free flour;
• Avoid beer and malt drinks as they contain gluten;
• It is possible to consume flour from rice, soy and corn, as well as meat and fish dishes, potatoes and fruits.

This diet gives noticeable results after just three weeks, and after a year the mucous membrane is completely restored. Treatment of the disease also involves eliminating associated symptoms.

Such therapy includes taking anti-diarrhea drugs, and in severe cases, treatment may include intravenous nutrient solutions, after which a gradual transition to regular food is required.

In addition to diet, iron deficiency anemia is treated, vitamins and microelements, calcium and vitamin D are taken. If not treated in a timely manner, the disease leads to various complications, including the development of ulcers, hypovitaminosis, the formation of malignant oncological tumors, as well as infertility and other consequences.

Treatment for this chronic disease You can also use folk remedies that can complement your diet. At the first signs of the disease, the following medicinal herbs and herbs will help improve the patient’s condition and relieve pain - honeydew, bedstraw, lungwort, swamp cudweed, meadowsweet, long-leaved speedwell, and bifolia.

To prepare the infusion, you need to mix all these herbs and pour boiling water over them, heat them in water for 30 minutes, and take 50 ml up to five times a day. However, such treatment must be coordinated with a gastroenterologist, since taking some herbs can lead to other adverse effects.

Folk remedies can complement a gluten-free diet and eliminate discomfort in the stomach. The patient can check the effectiveness of treatment with folk remedies by taking a blood test.

Disease prevention measures include:

• A gluten-free diet that helps prevent damage to the epithelium in the small intestine. This diet requires you to exclude from your diet those foods that contain grains.
• A thorough examination and blood test in patients at risk (diabetes mellitus, Down syndrome, autoimmune thyroid diseases, and lymphocytic colitis).

– a genetically determined dysfunction of the small intestine associated with a deficiency of enzymes that break down the gluten peptide. Malabsorption syndrome develops in celiac disease varying degrees severity, accompanied by foamy diarrhea, flatulence, weight loss, dry skin, and delayed physical development in children. To detect celiac disease, immunological methods are used (determination of antibodies to gliadin, endomysium, tissue transglutaminase), and small intestinal biopsy. Once the diagnosis is confirmed, a lifelong adherence to a gluten-free diet and correction of the deficiency of essential substances are required.

General information

Celiac disease in children usually begins to appear between 9 and 18 months. Appears frequently and loose stool with a large amount of fat and there is a decrease in body weight and stunted growth. In adults, the development of clinical symptoms of celiac disease can be triggered by pregnancy, previous surgical interventions, infection. Persons suffering from celiac disease often note a tendency to drowsiness, decreased performance, often rumbling in the stomach, flatulence, and stool instability (diarrhea followed by constipation). Elderly patients may experience pain and aches in the bones and muscles.

Stools are usually frequent (5 or more times a day), liquid, foamy with remnants of undigested food. With prolonged diarrhea, there is a possibility of developing signs of dehydration: dryness skin and mucous membranes.

The progression of malabsorption syndrome leads to the development of severe disorders of the body's internal homeostasis.

Celiac disease treatment

The goal of therapy for celiac disease is to restore intestinal function, normalize body weight and correct the deficiency of essential substances.

Pathogenetic treatment consists of following a gluten-free diet, that is, directly avoiding the action of the damaging factor. Following a gluten-free diet is necessary throughout your life. Most often (in 85% of cases) this measure leads to the subsidence of symptoms and the restoration of normal intestinal activity. As a rule, final recovery occurs no earlier than after 3-6 months, so adjust the content necessary for the body substances are required throughout the recovery period. If necessary, prescribe parenteral nutrition, administration of iron supplements and folic acid, saline solutions, calcium, vitamins.

Those patients who do not find a positive effect of the diet are prescribed hormonal drugs(prednisolone) for 6-8 weeks as anti-inflammatory therapy.

The lack of positive dynamics when excluding gluten from the diet for three months may indicate that the diet is not being fully followed, with violations, or there are concomitant diseases(disaccharidase deficiency, Addison's disease, small intestinal lymphoma, ulcerative jeunitis, giardiasis, lack of minerals in the diet: iron, calcium, magnesium).

In such cases, additional diagnostic measures are carried out to identify these conditions. By excluding everyone possible reasons If there is no improvement, hormonal therapy is prescribed. After three months of a course of prednisolone, a biopsy of the small intestine is performed.

Gluten-free diet

Gluten is found in the following products: bread and any products made from wheat, oatmeal, barley and rye flour, pasta, semolina. In small concentrations, gluten can be found in sausages and frankfurters, meat and canned fish, chocolate, ice cream, mayonnaise and ketchup, various sauces, instant coffee and cocoa powder, soy products, instant soups, bouillon cubes, products containing malt extract. As for drinks, you should avoid beer, kvass, and vodka.

People with celiac disease should often limit their consumption of whole milk because they may be lactose (milk sugar) intolerant. Currently, special dietary gluten-free products are available for sale (marked with a crossed out spike).

Prevention of celiac disease

There is no primary specific prevention for celiac disease. Secondary prevention of the development of clinical symptoms is to follow a gluten-free diet. If your closest relatives have celiac disease, it is advisable to conduct periodic examinations to identify specific antibodies.

Pregnant women with celiac disease are at risk for developing heart defects in the fetus. Pregnancy management in such women should be carried out with increased attention.

Prognosis and clinical examination

It is currently not possible to correct the sensitivity of epithelial cells to gluten, so patients with celiac disease must follow a gluten-free diet throughout their lives. Careful adherence to it leads to maintaining the quality and length of life. If the diet is not followed, survival rate drops sharply, cases fatal outcome Among patients with celiac disease, those who violate a gluten-free diet are 10-30%, while with strict adherence to the diet this figure does not exceed one percent.

All persons suffering from celiac disease should be registered with a gastroenterologist and undergo an annual examination. For patients who do not respond well to eliminating gluten from the diet, dispensary observation shown twice a year. The prognosis worsens markedly if this disease is complicated by the occurrence of small intestinal lymphoma.

ICD-10 code

Celiac disease is an autoimmune T-cell-mediated enteropathy that occurs in 80% of cases in girls under 10 years of age. The disease is induced by gluten in the presence of a genetic predisposition in the patient. The pathology causes damage and atrophy of the small intestine. Modern diagnostics celiac disease makes it possible to detect pathology even with an atypical and asymptomatic course. This helps prevent the development of fatal complications.

Diagnostic features

To make an accurate diagnosis, a doctor must follow the following algorithm:

• grade clinical picture diseases. The stage involves a careful study of the history and clinical picture;
• laboratory diagnostics, which involves determining the level of disease-specific antibodies;
• morphological examination - endoscopy and biopsy;
• assessment of the effect of a strict gluten-free diet for 6-12 months. This makes it possible to definitively confirm the presence of celiac disease if the diet leads to an improvement in the patient’s condition;
• examination of family members of a patient with celiac disease. In 10% of cases, the disease is found in first-degree relatives.

This algorithm can be supplemented by other modern research. To confirm the diagnosis, you can use HLA-DQ typing, identifying lymphocytes that are located between the cells of the mucosa. However, these studies are offered only by large and specialized laboratories.

It is worth considering each stage of the diagnostic algorithm in more detail.

Clinical manifestations

The main clinical sign is the development of malabsorption syndrome, which involves a violation of the absorption process in the intestine nutrients. This leads to the development of diarrhea, the appearance of foamy and foul-smelling stool. As the condition progresses, the child's abdomen enlarges along with weight loss. The disease can cause damage to other organs and systems of the body. The use of antibiotic therapy and enzymes does not eliminate symptoms.

The following symptoms are also identified:

• stomach ache;
• infrequent or daily vomiting;
• developmental delay in the child;
• delayed sexual development;
• frequent bone fractures;
• damage to teeth by caries;
• sleep disturbance;
• development of seizures or paresthesia;
• development of atopic or herpetiform dermatitis;
• in a series of coprograms the presence of fatty acids;
• anemia;
• frequent respiratory infections (more than 5 times a year).

During the examination and history taking, the doctor will need to identify children and adults who are at risk for developing celiac disease. These include:

• first degree relatives;
• patients with Down syndrome;
• patients with the development of autoimmune damage to the thyroid gland;
• patients with diabetes mellitus(mostly of the first type);
• patients with chronic fatigue syndrome.

If the patient is suspected of having autoimmune enteropathy, then additional laboratory and morphological diagnostics are necessary.

Laboratory research

Testing for celiac disease involves determining antibodies to gluten, which the body perceives as a dangerous protein compound. So when gluten food comes in, production begins large quantity antibodies to this protein.

Within laboratory diagnostics define:

• antibodies to tissue transglutaminase (TSG). This enzyme takes part in the breakdown of the gluten molecule. For celiac disease, determination of immunoglobulin A (IgA) and immunoglobulin G (IgG) is indicated;
• endomysium antibodies (EMA). The endomysium is a loose connective tissue that unites muscle fibers. These antibodies are also determined in 2 classes: IgA and IgG. This test can only be carried out in specialized laboratories;
• Anti-gliadin antibodies (AGA). This substance is a structural element of gluten. With an increase in the production of antibodies to it, one can reliably say about the development of celiac disease. This is the most specific diagnostic sign, the accuracy of which exceeds 95%.

When diagnosing celiac disease, the following combinations of laboratory tests are used:

1. Conducting screening, which involves determining AAG IgG and TSH IgA.
2. Serological study - determination of EMA and TSH IgA/IgG.
3. Carrying out complete serological diagnostics: EMA, TSH, AGA IgA.
4. HLADQ2/DQ8 genotyping – the test allows you to exclude the presence of celiac disease.

As part of laboratory diagnostics, stool is examined for occult blood and fragments of undigested food are determined.

Morphological study

Diagnostics allows us to establish the presence of an inflammatory process in the villi of the small intestine against the background of atrophy. For this purpose, fibrogastroduodenoscopy is performed. As part of the survey through oral cavity A special probe is inserted into the small intestine. It is equipped with a video camera, so the doctor can visually assess the condition of the intestines.

As part of the procedure, a biopsy sample is taken from the mucous membrane of the organ using special attachments for subsequent histological examination. The sample is stained and examined under a microscope. The laboratory technician evaluates the size and structure of the villi and the presence of lymphocytes. If they are small in size and contain an insufficient number of glandular cells, then this indicates the development of celiac disease. The danger of the disease lies precisely in the irreversible degeneration of the villi, which leads to the inability to absorb nutrients in the intestine.

The results obtained during biopsy and histological examination should be accompanied by an improvement in the clinical picture of the disease on the background of a gluten-free diet.

As additional diagnostic methods, it is possible to conduct an ultrasound examination of the digestive organs, computed tomography, MRI angiography of mesenteric vessels, contrast fluoroscopy of the intestine.

Difficulties of diagnostic measures

With celiac disease, diagnosis can be difficult, so doctors often make erroneous diagnoses. Difficulties arise with the development of an erased or atypical form of the disease, when the severity of symptoms varies widely. For example, diarrhea, which is the main symptom of the disease, may be absent.

This leads to patients being in critical condition 2-3 months after the onset of celiac disease. In some cases, children managed to live 6-7 years without lack of therapy and diet. However, at the same time, secondary metabolic disorders, which masked the signs of the underlying pathology.

In atypical cases, histological and serological examination is necessary. Patients are prescribed an MEL lymphogram (determination of interepithelial lymphocytes), which allows differential diagnosis with other intestinal pathologies with high sensitivity.

Celiac disease is a dangerous autoimmune pathology that leads to the development of severe secondary disorders. Therefore, patients need timely, comprehensive and accurate diagnostic measures. This allows you to stop the degradation of intestinal villi and normalize the absorption of nutrients.

Celiac disease- an immune-dependent disease that primarily affects gastrointestinal tract. It is characterized chronic inflammation mucous membrane of the small intestine, which can lead to intestinal villous atrophy, malabsorption and various clinical manifestations in childhood and adults. Intestinal symptoms may include diarrhea, abdominal cramps, pain and tension. Untreated celiac disease can lead to vitamin and mineral deficiencies, osteoporosis and other extraintestinal problems.

Currently, some progress has been made in understanding the essence of celiac disease, preventing and treating its manifestations through dietary interventions. There is a strong genetic predisposition to celiac disease, the greatest risk is associated with specific genetic markers known as HLA-DQ2 and HLA-DQ8, which are present in those affected by celiac disease individuals. Dietary proteins present in wheat, barley, and rye, commonly known as glutens Dietary proteins are present in wheat, barley, and rye in the form of a substrate known as gluten. They interact with HLA molecules and activate the pathological immune response of the mucous membrane and induce tissue damage. Even the most affected individuals experience remission after eliminating the diet from their diet.

Until now, celiac disease was considered a disease that was rare in the United States. However, studies that were carried out first in Europe and then in the USA showed that the real prevalence of celiac disease is much higher. Celiac disease probably affects three million Americans (approximately 1 percent of the US population), indicating that the condition is underdiagnosed.

The recent identification of autoantigens involved in the pathogenesis of celiac disease has led to the development of new serological diagnostic tests, but the strategy for using these new testing methods has not yet been determined. These tests have identified many individuals with non-classical gastrointestinal and extraintestinal symptoms.

1. How to diagnose celiac disease?
In order to take the first important step in diagnosing celiac disease, it is necessary to pay attention to its many varied clinical manifestations. There is no test that can confirm or rule out celiac disease in every individual. Just as there is a wide range of clinical manifestations of celiac disease, there are many laboratory and histopathological manifestations of this disease. The combination of clinical and laboratory findings leads to the diagnosis of celiac disease.

All diagnostic tests should be performed while the patient is on a gluten-containing diet. The first step towards diagnosing celiac disease is serological tests. They are highly sensitive and specific, the best available tests are IgA antihuman tissue transglutaminase (TTG) and IgA endomysial antibody immunofluorescence (EMA). Apparently these tests have the same diagnostic accuracy (TTG is a specific protein identified by IgA-EMA). The Antigliadin antibody (AGA) test is no longer recommended due to its low sensitivity and specificity. Serological tests for celiac disease in children less than 5 years of age are less reliable and may be less appropriate.

Biopsy of the proximal small intestine indicated for individuals with a positive antibody test, except for those with biopsy-proven dermatitis herpetiformis. Endoscopic confirmation without biopsy is not enough to confirm or exclude the diagnosis. Endoscopic findings are not sensitive enough to diagnose celiac disease since the changes are focal in nature and therefore multiple biopsies must be performed. Biopsy material should be obtained from the second part of the duodenum and beyond. The pathological report should indicate the degree of crypt hyperplasia and villous atrophy, as well as the number of intraepithelial lymphocytes.

Some degree of villous atrophy is necessary to confirm the diagnosis of celiac disease. The presence of intraepithelial lymphocytes in combination with crypt hyperplasia without villous blunting is less specific. Standardization of pathological findings for celiac disease is possible by applying published criteria (Marsh criteria, 1999). Collaboration between the pathologist and the treating physician can help correlate clinical data with laboratory results and clinical features. A second opinion when interpreting a biopsy may be required if the biopsy results are inconsistent with serological markers and clinical findings.

With concordant positive serology and biopsy results, a presumptive diagnosis of celiac disease can be made. The final diagnosis is made based on the disappearance of symptoms with the agliadine diet. Normalization of histological data on the background of the agliadine diet is currently not necessary for the definitive diagnosis of celiac disease.
In that case If there are clinical symptoms and a negative serological test, three scenarios are possible:

• First, the individual has a selective IgA deficiency. If IgA deficiency is identified, IgG-TTG and IgG-EMA tests should be performed.
• Secondly, the serological test may be “false negative” and should be repeated or an alternative serological test and/or small intestinal biopsy should be performed.
• Thirdly, the patient may not have celiac disease

When the diagnosis of celiac disease is in doubt due to uncertainty in the results, determination of genetic markers (HLA haplotypes) can categorize individuals into high- and low-risk groups for celiac disease. More than 97 percent of people with celiac disease have DQ2 and/or DQ8 markers, compared with 40 percent in the general population. Therefore, it is very unlikely that an individual negative for DQ2 and DQ8 has celiac disease (very high predictive value).

Great patience must be exercised when making recommendations in the event of positive serology for celiac disease and normal results biopsies. A single best approach may be recommended. Choices include additional small bowel biopsy, periodic monitoring of serological tests for celiac disease, or a trial of a gluten-free diet.

2. What is the prevalence of celiac disease?
Advances in understanding the multisystem nature of celiac disease and the development of effective serological tests have led to the understanding that celiac disease is much more common than generally believed.

Population-based studies in the United States using various combinations of serological tests and small intestinal biopsies suggest that the prevalence of celiac disease ranges from 0.5 to 1.0 percent (similar rates have been reported in Europe). This prevalence includes individuals with and without clinical symptoms. In some ethnic groups, the prevalence may be lower than in Caucasians. In the United States, there are very few data on the prevalence of celiac disease among different ethnic groups. This issue requires further research.

Typically, the incidence of celiac disease in populations is increasing. First-degree relatives of individuals with histologically confirmed celiac disease have 4 to 12 percent of cases of villous atrophy on biopsy. Second-degree relatives also have an increased prevalence, which can only be determined serologically. People with type 1 diabetes have biopsy-proven celiac disease in 3 to 8 percent of cases. The prevalence of celiac disease in Down syndrome ranges from 5 to 12 percent. Celiac disease is also associated with Turner and Williams syndrome, selective IgA deficiency and autoimmune diseases.

3. What are the manifestations and long-term consequences of celiac disease?
Celiac disease is traditionally defined as a gastrointestinal malabsorptive disorder that appears in early childhood after the introduction of gluten. It is now known that clinical manifestations are highly variable, can occur at any age, and involve multiple organ systems. Delay in diagnosis is common.

Since celiac disease is a multisystem disorder, its clinical manifestations are very diverse.

Gastrointestinal disorders may include diarrhea, weight loss, growth failure, vomiting, abdominal pain, flatulence, bloating, anorexia and constipation. The presence of obesity does not exclude the diagnosis.

It is very common for celiac disease to have extraintestinal manifestations in combination with minimal (or no) intestinal symptoms. A distinctive example is dermatitis herpetiformis(dermatitis herpetiformis) with an intense pruritic rash on the surfaces of the extensor muscles of the limbs. Iron deficiency anemia is common and may be the only symptom. Other manifestations may include unexplained short stature, delayed puberty, infertility, recurrent miscarriages, osteoporosis, hypovitaminosis, weakness, protein and calorie malnutrition, recurrent aphthous stomatitis, increased transaminases and hypoplasia of tooth enamel.

Celiac disease may be associated with autoimmune endocrinological disorders such as thyroiditis. In addition, let us mention various neuropsychiatric disorders such as depression, anxiety, peripheral neuropathy, ataxia, epilepsy with or without cerebral calcification, migraine headaches have been reported in individuals with celiac disease.

There is a classification of subphenotypes of celiac disease. It is useful for the clinic to identify them. These include the following:

• Classic celiac disease. The symptoms and consequences of gastrointestinal malabsorption dominate. Diagnosis is based on serological tests, biopsy evidence of villous atrophy, and improvement of symptoms with a gluten-free diet.
• Celiac disease with atypical symptoms. Characteristic is the dominance of extraintestinal symptoms over gastrointestinal ones. Recognition of atypical features of the course of celiac disease has become possible due to new data on its prevalence. As with classical celiac disease, the diagnosis is made on the basis of serological tests, biopsy evidence of villous atrophy and improvement of symptoms on a gluten-free diet.
• Silent (asymptomatic) celiac disease It is indicated for individuals who are asymptomatic but have positive serological tests and villous atrophy on biopsy. These individuals are identified during screening of high-risk groups, and villous atrophy may be incidentally discovered during endoscopy or biopsy performed for other reasons.
• Latent celiac disease determined by positive serological tests in the absence of villous atrophy on biopsy. These individuals do not have clinical manifestations, but they may appear in combination with or without histological changes.

Complications of celiac disease

Complications of celiac disease usually appear many years after the onset of the disease and are usually seen in adults. Refractory celiac disease is said to occur when symptoms persist and intestinal inflammation despite being on a gluten-free diet. It may occur in the context of ulcerative jejunitis and may be early manifestation intestinal lymphoma.

Many studies report an increased risk of non-Hodgkin's lymphoma in celiac disease, but there is often no difference between classic celiac disease-associated lymphoma (EATL) and other subtypes. EATL occurs in people diagnosed in childhood. Despite the increased risk, lymphoma remains very rare complication. Some studies suggest that a gluten-free diet reduces the risk of lymphoma.

In addition, the risk of adenocarcinoma of the small intestine is increased, and there is some evidence that the risk of carcinoma in any part of the gastrointestinal tract increases. The incidence of all causes of death in clinically diagnosed celiac disease is twice as high as in the control population.

4. Who should be tested for celiac disease?
Individuals with gastrointestinal symptoms such as diarrhea, malabsorption, weight loss, and abdominal bloating should be evaluated for celiac disease. Because celiac disease is a multisystem disorder, physicians should be familiar with the conditions when they need to be tested for this disease.

Patients who, for unknown reasons, have persistently elevated transaminases, growth retardation, delayed puberty, iron deficiency anemia, recurrent weight loss and infertility should be evaluated.

Other conditions that may require evaluation include irritable bowel syndrome, persistent aphthous stomatitis, autoimmune diseases, peripheral neuropathy, cerebral ataxia, and dental enamel hypoplasia. Although osteoporosis is common in patients with celiac disease, there is no evidence that the incidence of celiac disease is increased among patients with osteoporosis. There are many other associated systemic symptoms that are not specific to celiac disease, but for which evaluation for this pathology may be recommended.

There are many populations with increased risk celiac disease. These include individuals with type 1 diabetes, other autoimmune endocrinopathies, first- and second-degree relatives of people with celiac disease, and individuals with Turner syndrome. Individuals and clinicians should be aware of the increased prevalence of celiac disease in these groups of people.

People with symptoms in these populations should be tested for celiac disease; for example, individuals with type 1 diabetes and unexplained hypoglycemia. Since current data does not allow us to benefit from early detection and treatment of asymptomatic individuals, routine screening cannot be recommended at this time, but if such individuals are identified they should be interviewed. Another population at increased risk includes individuals with Down and Williams syndrome. When individuals from these groups cannot explain symptoms, screening is an appropriate option and should be recommended.

Persons for whom a gluten-free diet does not allow a diagnostic assessment should undergo a gluten challenge. For those who refuse to undergo a gluten challenge, the absence of DQ2 and DQ8 may help rule out the diagnosis. Reduction of symptoms on a gluten-free diet is not sufficient for a diagnosis of celiac disease. It should be noted that an adequately planned gluten-free diet does not affect nutritional status.

5. What is the management of patients with celiac disease?
Treatment for celiac disease should begin only after verification of the diagnosis, including serology and biopsy.

Treatment for celiac disease involves a lifelong gluten-free diet. A gluten-free diet involves excluding wheat, rye and barley. These food grains contain peptides from gluten, which causes celiac disease. Even small amounts of gluten can be harmful. Oats are probably safe for most patients with celiac disease, but their use is limited due to possible gluten contamination during food preparation. The strict definition of a gluten-free diet remains controversial due to the lack of an accurate method for determining gluten in foods and the lack of scientific data on which food components contain safe amounts of gluten.

Below are the following six key elements treatment of patients with celiac disease:

• Consultation with a skilled dietitian
• Education about the disease
• Lifelong adherence to a gluten-free diet
• Diagnosis and treatment of malnutrition ( Identification and treatment of nutritional deficiencies)
• Access to an advocacy group
• Continuous long-term followup by a multidisciplinary team

Knowledge of the nature of celiac disease, combined with experience in identifying gluten-containing foods, improves the quality of self-treatment. Participation in support groups is also effective in strengthening adherence to the gluten-free diet and can provide emotional and social support. Health care providers should be aware of and treat vitamin and mineral deficiencies, including deficiencies of iron, calcium, phosphorus, folate, vitamin B12 and fat-soluble vitamins. Individuals with newly diagnosed celiac disease should undergo screening for osteoporosis as the likelihood of osteoporosis is higher than in the general population. It is very important to have a “team” approach to treatment. In addition to treatment with a doctor and participation in a local support group, consultation with an experienced nutritionist is necessary.

After going through the initial diagnosis and treatment process, patients should make repeat visits with their doctor and dietitian to evaluate symptoms and the adequacy of the diet, and monitor for complications.

During these visits, health care providers may emphasize the benefits of adherence to a strict gluten-free diet throughout life.

Repeated serological tests may be used to monitor response to therapy (their usefulness has not been proven). These tests may remain positive for a long time (up to 1 year) before normalizing, especially in adults, and may not correlate with improvement in histology.

Persistently elevated serologic tests may indicate lack of adherence to the gluten-free diet or unintentional gluten ingestion. Currently, screening methods for complications of celiac disease, including lymphoma and adenocarcinoma of the small intestine, have not been developed.

• Conduct a cohort study to study the natural history of untreated celiac disease, particularly silent celiac disease.
• To determine the response to gluten peptides in DQ2+/DQ8+ individuals without celiac disease. Identify factors preventing the disease.
• To determine the factors involved in the occurrence of celiac disease in genetically sensitive individuals.
• To develop an animal model(s) of celiac disease, which will allow us to identify pathogenetic mechanisms.
• To determine the prevalence of celiac disease in US ethnic groups.
• Develop methods for preventing celiac disease. For example, timing the introduction of cereals to children in combination with the immune response (B-cells and T-cells) to glutens.
• To determine the relationship between celiac disease and autoimmune and neuropsychiatric diseases.
• To identify non-HLA genetic modifiers that influence the severity of the celiac disease phenotype.
• To develop non-invasive methods for determining and assessing the activity of celiac disease.
• Determine the minimum safe dose gluten for celiac disease.
• Develop an alternative to the gluten-free diet.
• To analyze the effectiveness and efficiency of serological tests in the general population.
• Conduct research on screening methods for diagnosing adenocarcinoma and lymphoma.
• Analyze the benefits of screening high-risk groups with clinically important implications.
• Research economic consequences health changes with celiac disease
• Identify and verify serological tests for the diagnosis of celiac disease in children.
• To investigate the quality of life of individuals with celiac disease.

Conclusions
Celiac disease is an immunopathological disease of the intestine with various manifestations. Celiac disease is a common disease, affecting 0.5 to 1.0 percent of the general population in the United States, but often underdiagnosed.

Currently, there are no specific and sensitive serological tests that are suitable for widespread diagnostic testing.

The main treatment for celiac disease is a lifelong gluten-free diet, which results in remission in most individuals.

Classic manifestations of diarrhea and malabsorption are less frequent and the number of atypical (asymptomatic) forms is increasing. Most patients are observed medical workers first link and wide range specialists. In this regard, increased vigilance against this disease is urgently needed.

Education of physicians, registered dietitians, and other health care professionals is necessary.

• Education of doctors, nutritionists, nurses and the public regarding celiac disease is carried out through an initiative of the trans-National Institutes of Health (NIH) led by the national Institute of Diabetes, Digestive and Kidney Diseases (NIDDK)) in association with the Center for Disease Control and Prevention diseases (Centers for Disease Control and Prevention).
• Standardization of serological tests and pathological criteria for the diagnosis of celiac disease.
• Adopting a standard definition of a gluten-free diet based on objective evidence such as those developed by the American Dietetic Association.
• Developing adequate tests for gluten in food and defining standards for gluten-free products in the United States based on standard food labeling.
• Establishment of the Federal Celiac Disease Societies, a group of individuals interested in celiac disease, individuals with celiac disease and their families, physicians, nutritionists and other health professionals to promote education, research and support for patients with celiac disease.