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Celiac disease: life prognosis for this disease and effective treatment methods

Celiac disease – what is it? Celiac disease is an autoimmune disorder of the gastrointestinal tract, characterized by damage to the small intestine when food containing (gluten) is ingested. The process is accompanied by impaired absorption of nutrients in the small intestine, which leads the body to exhaustion.

The exact causes and pathogenesis are not fully understood.

Etiology and pathogenesis

There are several hypotheses for the occurrence of celiac disease.

According to one of them, the body determines the lack of enzymes capable of breaking down gluten contained in barley, wheat, rye and oats.

If you develop celiac disease, you must completely avoid eating foods containing gluten.

According to another version, the disease occurs due to the insensitivity of the intestinal mucosa to the effects of gluten. An allergization reaction occurs, in which undigested gluten destroys the villi of the small intestine.

During life, a malabsorption of nutrients occurs in the affected small intestine.

It is believed that the disease is inherited from relatives suffering from the pathology. May appear at an early age or during adult life. The process is reversible if you avoid taking foods containing gluten.

Risk factors

The danger of celiac disease is observed in the following situations:

hereditary predisposition, when close relatives or parents have a deficiency of these enzymes;
disease with rheumatoid arthritis;
diabetes;
SLE (systemic lupus erythematosus);
dermatitis herpetiformis;
Down syndrome can trigger the development of the disease;
acute hepatitis for more than 6 months;
long-term infectious processes of the intestine;
autoimmune lesions of the thyroid gland.

Persons with the listed diseases are at risk for developing celiac disease.

Type of disease

Highlight various shapes celiac disease:

typical - a form in which the disease manifests itself only in intestinal damage;
atypical – the disease is difficult to diagnose due to symptoms of damage to other organs and systems;
hidden - the development of pathology occurs without an obvious clinical picture;
latent – the pathological process is determined only by laboratory tests, symptoms are not determined;
refractory – combines signs of a typical and atypical form.

The difficulty of diagnosis lies in the difference distinctive features diseases from other lesions of the gastrointestinal tract. Diagnosis is possible only with laboratory detection of pathology.

Symptoms of the disease

The main signs of celiac disease are diarrhea (increased frequency of stools), steatorrhea (disruption of the processes of breakdown of nutrients, fats are detected in the stool), polyhypovitaminosis and sudden weight loss in the body. The manifestation of the disease in childhood and adulthood differs in clinical picture.

If celiac disease develops, barley, oatmeal, feather and semolina porridges are not acceptable for consumption, especially for babies and young children

Pediatric celiac disease

Childhood celiac disease appears between the ages of 9 and 18 months. Characterized by the following symptoms:

painful sensations in the abdomen;
nausea;
there is a decrease in appetite;
in severe cases of the disease, vomiting occurs;
loose, frequent stools with a foul odor;
increased tearfulness and irritability;
there is a lag in physical and mental development (short stature, underweight, delayed puberty);
the skin becomes pale;
with the development of hypovitaminosis, convulsions begin;
Small ulcers that heal poorly can be found in the corners of the mouth and oral cavity.

Progression of the disease leads to dysfunction internal organs and body systems, negatively affects homeostasis.

Symptoms of Celiac Disease in Adults

The development of symptoms of the disease in women is observed at the age of 30-40 years. For men, 40-50. In addition to the age category, the appearance of pathology can be triggered by pregnancy, surgical interventions on the digestive system or infectious intestinal diseases.

The developed clinical picture is characterized by the appearance of the following symptoms:

loose stools up to 5 times a day with an unpleasant odor;
constant flatulence;
loss of appetite and weight loss;
pain in the abdomen;
Chronic fatigue syndrome occurs (patients complain of constant drowsiness, apathy, decreased performance, dizziness and bad mood);
as signs of exhaustion increase, the mood changes towards increased aggressiveness, irritability, and anger;
Older people often experience pain in bones and muscles;
paresthesia (perversion of sensations in the limbs);
women reproductive age note disruption of menstruation, difficulties in conceiving and bearing a child;
migraines and a feeling of shortness of breath do not affect everyone;
with critical loss of body weight, increased sweating occurs;
With the development of hypovitaminosis, skin rashes often occur, teeth and hair begin to deteriorate, and the skin becomes pale.

Abdominal pain and frequent bowel movements are symptoms of exacerbation of celiac disease

During an exacerbation of the disease, mental disorders are possible:

patients often talk to themselves;
sleep disturbance, insomnia;
emergence or exacerbation of schizophrenia;
mental lability increases (the emotional background changes instantly);
anxiety and restlessness for no apparent reason.

In addition to the classic manifestation, celiac disease can manifest itself as iron deficiency anemia or osteoporosis (bone fragility is caused by tissue loss due to lack of minerals).

Important. Prolonged or severe diarrhea leads to dehydration.

Complication

Celiac disease is a serious disease that requires constant diet control. The lack of timely and complete treatment, as well as poor diet, provokes the development of the following pathologies:

development of erosions and ulcers of the small intestine;
progression of the disease, in severe cases following a diet does not lead to restoration of intestinal functions;
infertility;
lack of vitamins and minerals leads to disruption of the functioning of all organs and systems of the body;
increased traumatism and frequent fractures with the development of osteoporosis;
malignancy is an oncological lesion of the gastrointestinal tract and bladder.

With the development of celiac disease in children, the above symptoms are supplemented by a lag in mental and psychomotor development. For children under 2 years of age, the risk of death is high.

Foods that do not contain gluten

If the disease manifests itself during pregnancy, bearing a fetus is almost impossible.

Important. if a woman with celiac disease decides to have a child. The entire pregnancy must be spent in a sanatorium or hospital treatment under the supervision of doctors. Repeated births contraindicated.

Diagnostics

A reliable diagnostic method is a biopsy of the mucous membrane of the small intestine followed by examination of the condition of the villi. With celiac disease, the villi are atrophied; after 6 months of following the diet, they are restored to healthy condition. In addition to changes in the intestinal mucosa, an accumulation of lymphocytes is detected in the mucous membrane of the digestive tract.

A biopsy is performed during intestinal endoscopy. In addition to a biopsy, a test with gliadin (a protein found in gluten) has a high degree of accuracy. The subject is given 400 ml of gliadin per 1 kg of body weight. Such a load in case of celiac disease entails multiple stools with severe steatorrhea. Also, with pathology, the level of glidinin in samples increases by 100% (in healthy person by 50%).

Less reliable methods for studying the gastrointestinal tract, which allow one to suspect or clarify pathology: ultrasound of the abdominal organs, CTG (computed tomography), MRI angiography (magnetic resonance imaging of blood vessels), X-ray of the intestine with contrast.

Of the symptoms that allow one to suspect the disease in childhood One can highlight developmental delays in infants, stunted growth in preschool and school children, and malnutrition in adults (with normal food intake and no diets).

Treatment

When diagnosing celiac disease, the patient should clearly understand the need for constant adherence to the diet. There are no other effective treatments for celiac disease. Everything should be excluded from the diet:

bread made from rye and wheat;
cereals and confectionery products made from flour;
boiled sausage;
sausages;
canned meat;
mayonnaise;
mustard;
various sauces;
ice cream;
chocolate;
alcohol.

This is not a complete list. requires careful food selection.

Products containing:

If the breakdown of gluten is impaired, preference should be given to a vegetable and fruit diet. The question of the possibility of eating meat is decided on an individual basis, taking into account personal tolerance

... coeliakia (from Greek: koilikos): intestinal, suffering from intestinal dysfunction... the diagnosis of celiac celiac disease is very responsible, as it requires lifelong adherence to a gluten-free diet.

Celiac disease(celiac enteropathy, celiac disease, non-tropical sprue) is a genetically determined disease of the small intestine associated with hypersensitivity to gliadin - a fraction of the vegetable gluten protein - and is characterized by atrophy of the villous epithelium of the small intestine with clinical manifestations of malabsorption syndrome of varying severity.

Gluten is a high molecular weight protein found mainly in wheat, rye and barley. Its alcohol-soluble fraction, gliadin, can be divided into subgroups alpha, beta, gamma and delta. In celiac disease, all these glutamine-rich proteins have a damaging effect on the lining of the small intestine.

Epidemiology. Mass serological studies followed by histological examination of duodenal biopsies in individuals with positive serological tests have shown that the frequency of celiac disease reaches 1:200–1:100. In Europe, celiac disease occurs with a frequency of 1:152 - 1:300 people, in the United States - 1:250 people. Typical celiac disease with severe malabsorption is indeed rare. The mortality rate among patients with untreated celiac disease is 10-30%, while with adequate treatment - a strict gluten-free diet - it drops to 0.4%.

Etiology. Celiac disease is a genetically determined disease associated with HLA-DQ2 and HLA-DQ8. Genetic predisposition is clearly visible in the families of patients; among the patient’s relatives, the incidence of celiac disease is 10%, and the concordance of identical twins for this disease is 70%. Genetic information is realized only when gliadin is taken orally.

Pathogenesis. Due to a deficiency (genetically determined) of specific enzymes, in particular aminopeptidases, the intestines do not completely break down gluten, which includes gliadin. Gliadin is a toxic substance. The pathogenic effect of gliadin in persons predisposed to celiac disease is a damaging effect on the mucous membrane of the small intestine, which leads to atrophy and severe malabsorption.

Moreover, the damaging effect of gliadin is not realized directly, but through interepithelial T-lymphocytes and T-lymphocytes of the lamina propria of the small intestinal mucosa. T-lymphocytes of the mucous membrane recognize only those gliadin peptides that have antigen properties. Recognition of the antigen leads to an increase in the production of cytokines and antibodies, which, through a series of intermediate reactions and the formation of immune complexes, cause damage and then atrophy of the mucous membrane of the small intestine with shortening of the villi and significant elongation of the crypts. The epithelium lining the villi is flattened and abundantly infiltrated with intraepithelial lymphocytes. A strong pronounced infiltration of the lamina propria of the small intestinal mucosa by lymphocytes is also determined. Damaged mature enterocytes are replaced by poorly differentiated ones, which leads to a decrease in the absorption surface of the small intestine and, as a consequence, to impaired absorption of nutrients with all the ensuing clinical consequences.

Clinical picture. The disease begins to manifest itself in infancy, when the diet includes products made from wheat, rye, barley, oats (for example, semolina, oatmeal and etc.). Further, in the absence of treatment, the symptoms of gluten enteropathy intensify during childhood, and decrease in adolescence, but at the age of 30-40 they resume again. In many patients, the symptoms of the disease may be very mild (options clinical manifestations for gluten enteropathy, see

lee). Therefore, the disease in childhood and adolescence is not recognized, and the diagnosis is first made only in middle or old age. The most characteristic clinical symptoms of celiac enteropathy are diarrhea and flatulence. Diarrhea with significant intestinal damage (especially in severe cases of the disease) is manifested by frequent, up to 10 or more times a day, and abundant watery or semi-formed, light brown stools. Quite often, the stool is foamy or ointment-like and contains a large amount of undigested fat with a foul odor. Flatulence is accompanied by a feeling of fullness, bloating and is accompanied by the release of a large amount of foul-smelling gas. In many patients, flatulence does not decrease even after defecation. Symptoms due to the development of malabsorption syndrome: weight loss, growth retardation and physical development children, protein metabolism disorders (up to hypoproteinemic edema), lipid and carbohydrate metabolism, calcium metabolism disorders, anemia (iron deficiency and B12 deficiency), dysfunction of the endocrine glands, polyhypovitaminosis, myocardial damage (myocardial dystrophy), etc.

Adult patients are characterized by a hidden atypical course of the disease. There are usually no specific physical symptoms. There is short stature, decreased appetite, muscle atrophy, dry and pale skin, aphthous stomatitis, manifestations of dermatitis herpetiformis - a papulovesicular rash with severe itching, which is observed mainly on the extensor surface of the limbs, trunk, neck, and scalp.

The desire for etiological diagnosis of nervous diseases led to the identification of cases of celiac disease among neurological patients. In 10% of patients with celiac disease (mostly we're talking about on identifying atypical forms of celiac disease) are observed neurological symptoms, which can be like initial manifestations, and complications of celiac enteropathy. Possible development of cerebral ataxia, neuropathy (most often in patients with celiac disease develops chronic distal symmetrical neuropathy with a predominance of sensory impairments, however, there are reports of the development of purely motor neuropathy with mononeuritis), epilepsy, headache (headache is qualified as the most common neurological pathology in patients with gluten celiac disease diagnosed in childhood, with cessation or reduction of headaches against the background of strict adherence to an anti-gluten diet). Also, against the background of celiac enteropathy, the risk of developing depression is high (occurs in approximately every third patient with celiac disease).

!!! Wide range of different neurological symptoms in patients with celiac disease provides grounds for recommending the use of serological screening for celiac disease among patients with neurological diseases. However, the presence of celiac disease in a neurological patient cannot serve as a basis for concluding an etiological connection between these diseases.

Celiac disease is often combined with such autoimmune diseases as diabetes mellitus type 2 (2-16% of cases), thyroiditis (3-5%), primary biliary cirrhosis (6-7%), Addison's disease (1%), selective IgA deficiency (8-19%), syndrome Sjögren (15%).

It should be noted that typical celiac disease with severe malabsorption is generally rare. In the vast majority, diarrhea and symptoms of malabsorption are absent, but extraintestinal manifestations are detected: iron deficiency anemia, aphthous stomatitis, Dühring's dermatitis, osteoporosis, short stature, delayed sexual development, infertility, insulin-dependent diabetes, etc. Such latent and subclinical forms occur in approximately an order of magnitude more often than typical classical celiac disease.

Celiac enteropathy may have the following clinical options course of the pathological process: typical form (development of the disease in early childhood with diarrhea with polyfecalia and steatorrhea, anemia, metabolic disorders inherent in malabsorption syndrome of 2 or 3 severity); torpid (refractory) form (severe course, lack of effect from usual treatment, in connection with which the use of glucocorticoid hormones is necessary); latent form (subcl.

The tissue is thin, the only manifestations may be extraintestinal manifestations of genetic and autoimmune origin; antiendomysial antibodies are detected in the blood serum - precursors of the possible evolution of the development of severe celiac enteropathy).

Diagnostics. An accurate diagnosis of celiac disease can only be made with a biopsy of the small intestine. Characteristic morphological changes are observed not only in the jejunum, but also in the distal part duodenum. Therefore, you can use both the data from the study of biopsy samples obtained from the jejunum during intestinoscopy, and the data from the assessment of biopsy samples from the subbulb of the duodenum obtained using a conventional duodenoscope. For active detection of celiac disease in groups increased risk apply immunological methods. Antibodies to gliadin (AGA), autoantibodies to endomysium (AEMA) and tissue transglutaminase (ATTG) are determined in the blood. All patients in whom elevated concentrations of antibodies are detected undergo a morphological study of the mucous membrane of the small intestine.

Mandatory laboratory research : enzyme immunoassay determination of serological markers of celiac disease - antigliadin antibodies (AGA IgA and IgG), endomysial antibodies (EMA IgA), antibodies to tissue transglutaminase (tTG); general blood analysis; general urine analysis; total protein and protein fractions; blood sugar; immunogram; liver and kidney tests; blood type and Rh factor; coprogram; stool test for elastase 1; repeated stool cultures pathogenic microflora and examination of worm eggs; blood electrolytes.

Mandatory instrumental diagnostic methods: Endoscopy with morphological examination of biopsies taken from the descending duodenum - the “golden” diagnostic standard - should be carried out in all cases to verify the diagnosis; video capsule endoscopy is the second “gold” diagnostic standard; passage of barium through the small intestine (enteroclysis); irrigoscopy; Ultrasound of the abdominal organs and thyroid gland.

Differential diagnosis carried out with tropical sprue, intolerance to milk and soy proteins, with hypogammaglobulinemic and collagen sprue, as well as with unclassified celiac disease, with lymphoma of the small intestine and Mediterranean lymphoma (heavy a-chain disease).

The main treatment for celiac disease is strict lifelong adherence to a gluten-free diet.. It should be noted that with celiac disease there is no direct relationship between the consumption of bread and cereals and the nature of the stool, so patients never associate the development of the disease with bread intolerance. The damaging effect of gluten can only be detected by the degree of atrophy of the villi of the small intestinal mucosa and their restoration with careful adherence to a gluten-free diet.

Gluten free diet. The patient is prohibited from eating wheat, rye, barley and all products that may contain these grains even in negligible doses. The basis of the diet is rice, buckwheat, potatoes, soybeans, and corn. Oats and products made from it are allowed; their use is limited in many recommendations due to the fact that when preparing flour and products made from it using standard industrial methods, contamination with wheat gluten occurs. The patient should be well informed that even a minor and single error in the diet leads to the progression of the disease, which does not have clear clinical manifestations. Particular attention should be paid to the so-called hidden gluten, which may be part of various biological additives, medicines. If a patient with celiac disease is lactose intolerant, he should limit his intake of dairy products.

Symptomatic (drug) therapy. Antidiarrheal drugs are used. Treatment of diarrhea should be comprehensive, affecting all major pathogenetic mechanisms its occurrence and the main etiological cause of the disease.

tibacterial therapy is prescribed to restore intestinal eubiosis. Preference is given to drugs that do not disturb the balance of microbial flora in the intestine. According to indications, iron and folic acid supplements are used, enzyme deficiency Replacement therapy (enzyme preparations) is indicated. To prevent osteoporosis, calcium and vitamin D supplements are prescribed, and, if indicated, bisphosphonates and calcitonin are prescribed. In severe cases of the disease or in the absence of clinical and morphological changes against the background of a strict gluten-free diet for more than 6 months, the use of glucocorticosteroids is indicated (the average therapeutic dose is 7.5-20 mg of prednisolone per day). According to indications, parenteral nutrition, correction of water and electrolyte balance, intravenous administration of albumin, etc. are also used.

Symptoms of Celiac Enteropathy

Symptoms of celiac disease in adults are often subtle. Disease long time may be limited to vague abdominal pain, bloating, occasional diarrhea, and fatigue. In typical cases, celiac enteropathy is characterized by diarrhea with polyfecal matter and steatorrhea, and the development of severe malabsorption syndrome.

Clinical signs of enteropathy

Diarrhea as constant symptoms of celiac enteropathy. The frequency of stool can be from 2 to 10 times a day or more, both during the day and at night. Even with a low frequency of bowel movements, significant polyfecal volume occurs. In most cases, the stool is clayey, putty-like, light, liquid, and foamy.

Common symptom when diagnosed with celiac enteropathy - bloating that increases in the evening hours. May be observed dull pain diffuse in all parts of the abdomen, associated with bloating. Clinically, malabsorption syndrome is characterized by a violation of the general condition and the following symptoms: weakness, decreased performance up to its permanent loss, progressive weight loss. Body weight loss can range from 5 to 30 kg.

If celiac disease begins in childhood, patients are stunted in growth and physical development.

Forms of the disease celiac enteropathy

There are several clinical forms or variants of the disease.

Typical celiac enteropathy characterized by:

development of the disease in early childhood,
diarrhea with polyfecal and steatorrhea,
anemia,
metabolic disorders inherent in severe malabsorption syndrome.

Latent gluten enteropathy The disease has a long-term subclinical course and first appears in adulthood or even in old age. A careful study of the anamnesis can reveal that in childhood patients were lagging behind in physical development, often their hemoglobin was reduced or mild signs of hypovitaminosis were observed (cracks in the corners of the mouth, glossitis, etc.). From the moment the first symptoms of the disease appear, the clinical picture may be similar to that of the typical or asymptomatic form.

Torpid (refractory) gluten enteropathy The disease is characterized by a severe course, lack of effect from conventional treatment, and therefore there is a need to use glucocorticoid hormones.

Atypical celiac enteropathy. Clinical syndromes observed with it are relatively rare, and the clinical picture of the disease is dominated by extraintestinal symptoms caused by malabsorption (anemia, hemorrhages, osteoporosis) or immune disorders (allergies, autoimmune thyroiditis, diabetes mellitus type 1, Sjögren's syndrome - dryness of all mucous membranes - etc.).

Asymptomatic celiac enteropathy the disease is characterized by the absence clinical symptoms diseases. It is diagnosed through extensive epidemiological surveys of risk groups and can have two options:

hidden gluten enteropathy: there are no symptoms of malabsorption, but the intestinal mucosa has characteristic signs of hyperregenerative atrophy and (or) an increased number of interepithelial lymphocytes (IEL);

potential (probable) celiac enteropathy.

The second form of pre-disease is characteristic of those who have a normal intestinal mucosa, there are no symptoms of impaired absorption, but the risk of GEP disease is very high.

Complications when diagnosed with celiac enteropathy

Currently, a number of diseases are identified that are genetically and autoimmunely associated with celiac enteropathy.

Diseases genetically associated with enteropathy: Dühring's dermatitis herpetiformis, recurrent aphthous stomatitis and hypogammaglobulinemia, Down syndrome, autism, schizophrenia.

Autoimmune diseases associated with gluten enteropathy: insulin-dependent diabetes mellitus, autoimmune thyroiditis, primary biliary cirrhosis, autoimmune hepatitis, Sjogren's syndrome, rheumatoid arthritis, vasculitis, systemic lupus erythematosus, recurrent pericarditis, fibrous alveolitis, polymyositis, dementia, etc.

Diagnosis of the disease celiac enteropathy

The problem is of general medical significance. Active detection of celiac disease not only makes it possible to cure these patients, but also aims to primary prevention osteoporosis, anemia, infertility, type 1 diabetes mellitus, autoimmune and oncological diseases.

Implementation in clinical practice Immunological methods for diagnosing the disease have changed traditional ideas about it as a rare disease. Epidemiological screening (rapid) studies based on the determination of antibodies to gliadin, endomysium and tissue transglutaminase show that in risk groups, symptoms of celiac enteropathy are hundreds of times more common than in the general population. This prevalence is explained by an increase in the proportion of latent, asymptomatic forms. At the same time, obvious symptoms of gluten enteropathy (diarrhea, steatorrhea, exhaustion, anemia, hypoproteinemia, etc.) may be absent for a long time. As a result, patients are deprived of the opportunity to receive adequate treatment for celiac enteropathy for many years, and often their entire lives.

It should be noted that with this disease there is no direct relationship between the consumption of bread and cereals and the nature of the stool, so patients never associate the development of the disease with bread intolerance. The damaging effect of gluten can only be detected by the degree of atrophy of the mucous membrane of the small intestine and its reduction with careful adherence to the diet.

In recent decades, the study of the disease has stepped forward. Very significant changes have taken place. Immunological diagnostic methods have been introduced into clinical practice, which has changed traditional performance about the disease celiac enteropathy as a rare disease. According to epidemiological studies conducted in major scientific centers in Europe and the USA, it was found that from 1 to 3% of the population have antibodies to gluten fractions (cereal protein), as well as to the own tissues of the small intestine (endomysium) and the enzyme (tissue transglutaminase), which are markers of gluten enteropathy. In the vast majority of patients, the presence of symptoms of celiac enteropathy is confirmed by histological examination of the small intestinal mucosa. However, their disease, as a rule, occurs without exhaustion, diarrhea, other intestinal symptoms and a detailed picture of malabsorption syndrome, and in a low-symptomatic erased or asymptomatic form it manifests itself as selective malabsorption disorders (anemia, osteoporosis, amenorrhea, etc.) or autoimmune disorders (thyroiditis, diabetes, infertility).

The Scientific Society of Gastroenterologists of Russia, at its regular V Congress on February 6, 2005, adopted the following resolution on this issue on active detection of the disease.

Patients with chronic diarrhea, exhaustion and other clinical symptoms of gluten enteropathy, it is necessary to prescribe a biopsy of the mucous membrane of the duodenum subbulb.

Patients suffering from systemic osteoporosis complicated by bone pain and fractures, iron deficiency anemia of unknown etiology, primary infertility, autoimmune thyroiditis are recommended to test antibodies in the blood serum.

Patients over 18 years of age with suspected symptoms of celiac enteropathy and people with antibody titers of 30 IU/ml or higher should be referred to a gastroenterologist for histological confirmation of the diagnosis. It is recommended that those living in Moscow be referred to the Central Research Institute of Gastroenterology.

If the diagnosis of celiac enteropathy is confirmed, the patient should be advised to exclude foods containing gluten from the diet for life and be monitored by a gastroenterologist.

In cases autoimmune processes, allergies of unknown etiology or identification of allergens to cereals and soy, it is recommended to study antibodies to gliadin in the blood serum.

Treatment of Celiac Enteropathy

With a gluten-free diet, wheat, rye, and barley are completely excluded from the diet. You can consume up to 60g of oats per day. Long-term dynamic observation for patients with GEP shows that in those who strictly adhere to a gluten-free diet, clinical remission is more stable than in those who violate it.

In the group of patients diagnosed with celiac enteropathy who do not strictly adhere to a gluten-free diet, that is, occasionally consuming some bread products, there is a pronounced tendency to worsen diarrhea with polyfecal matter, weakness, symptoms of hypopolyvitaminosis, and calcium deficiency persist for a long time.

With long-term adherence to a gluten-free diet, the concentration of antigliadin and antiendomysial antibodies in IgA decreases significantly, down to threshold values. In patients who stop following the diet, the content of antigliadin and antiendomysial antibodies increases sharply even before the appearance of clinical symptoms of relapse of the disease.

With strict adherence to a gluten-free diet, after 6–12 months, some patients diagnosed with celiac enteropathy recover normal structure mucous membrane of the small intestine. In the rest, the villi remain atrophied, but the height of the epithelium clearly increases in all cases. Thus, the main method of rehabilitation therapy for patients suffering from GEP is strict adherence to a gluten-free diet throughout life.

Treatment of celiac enteropathy is considered successful if:

sustained clinical remission;

reduction to threshold values of the concentration of antigliadin, antiendomysial antibodies, antibodies to tissue transglutaminase;

restoration of the morphological structure of the mucous membrane of the small intestine.

Treatment of celiac enteropathy by lifelong adherence to a gluten-free diet leads to recovery. Use of diet for those associated with celiac enteropathy autoimmune diseases significantly improves treatment results.

When following a gluten-free diet, there is a cessation of diarrhea, weight gain, and an increase in the level of hemoglobin and red blood cells in the blood. Mineralization gradually increases bone tissue and autoimmune disorders and allergies associated with celiac disease decrease or completely disappear. The incidence of cancer is also reduced, the risk of which in patients with GEP is 100–200 times higher than in the general population.

Clinical example of successful therapy for a diagnosis of celiac enteropathy

A.K.P., 60 years old. Anamnesis. Gastrointestinal diseases manifested themselves throughout life. There has been significant deterioration over the past 10 years. The patient was examined in local and foreign clinics. Three years ago in England hemorrhoids in serious condition were operated on, part of the sphincter was operated on. Current complaints: diarrhea alternating with constipation, indigestion, clayey stools, sometimes foamy, abdominal pain, bloating, weakness. On ART: immune depletion, anemia, osteoporosis, enterocolitis, autoimmune thyroiditis. Intestinal infection is not tested. In the allergy section, rye, wheat, barley, and rice are tested.

Eliminate grains and rice.

Take decoctions of oats and flax seeds.

BRT along meridians: lungs, bladder, allergies.

EPT – E-programs: 1; 124; 192; eleven.

Complex preparation: organopreparation ( ileum D6, mucous membrane of the small intestine D6, jejunum D6) + homeopathy ( Colocynthis D6, Colehicum D6).

Homeopathic medicine – Nux vomica comp.

After 2 weeks, the patient’s health improved significantly, but her immunity remained in a state of exhaustion. The above treatment of gluten enteropathy was supplemented: TF (classic transfer factor), 4 capsules per day, alternating with TF Advensd, 3 capsules per day for 20 days. Then, every 20 days, reduce by 1 capsule (both drugs).

A month later, the patient’s well-being improved significantly. Test for antibodies to gliadin 40 IU/ml (weak positive).

After 4 months: the patient diagnosed with celiac enteropathy feels good. Test for antibodies to gliadin 30 IU/ml (risk zone number).

The patient continues to take complex homeopathy and has eliminated cereals and rice from her diet. I feel good, no complaints.

Clinical example of treatment No. 2 for the disease celiac enteropathy

The patient's eldest daughter, 40 years old. Complaints of allergies, allergic dermatitis, abdominal pain, stool - frequent diarrhea. Allergy to cereals and rice was tested for ART. Test for antibodies to gliadin 40 IU/ml (weak positive).

The same treatment for celiac enteropathy was given as for the mother. I feel good. The observation period is 4 months. Test for antibodies to gliadin 30 IU/ml (risk zone).

Clinical example of treatment of enteropathy No. 3

Youngest daughter, 34 years old. Complaints of periodic abdominal pain, sometimes diarrhea. History of late onset of menstruation, anemia, growth retardation. Allergies to cereal products and rice were also tested at ART. Test for antibodies to gliadin 30 IU/ml (risk zone). Recommended: exclude cereals and rice from the diet; the drug Nux vomica comp was tested in a potency of 500: 3 peas 2 times a week.

Risk groups for celiac disease

The following risk groups are identified that should undergo immunological screening diagnostics:

patients with clinical symptoms of celiac enteropathy, giving reason to suspect malabsorption in the intestine: short children who are lagging behind in physical development; people suffering from unexplained allergies, anemia, hypocalcemia, osteoporosis, and delayed puberty; patients with amenorrhea and infertility, the cause of which could not be determined;

immediate relatives of patients diagnosed with celiac enteropathy (parents, children, grandchildren);

patients suffering from diseases associated with celiac enteropathy.

Factors that provoke an exacerbation of the disease or the manifestation of the first clinical symptoms of gluten enteropathy are most often pregnancy and childbirth, neuropsychic injuries, and less often - intercurrent (concomitant) diseases, acute intestinal infections.

Groups of people with celiac disease

People with suspected potential GEP can be divided into two groups:

the first group - people with normal mucous membrane and a normal total number of MEL, but a high proportion of gamma/delta lymphocytes among them;

the second group is the immediate relatives of patients with celiac enteropathy, whose small intestinal mucosa is normal. However, a detailed immunological and ultrastructural analysis reveals that most people in this group have an increased number of MEL, especially gamma/delta cells, an increased number of mitoses in crypt cells and the expression of HLA class II.

The problem of celiac enteropathy (GE) is currently becoming particularly relevant, given modern data on its prevalence. Many pediatricians are convinced that GE is rare disease children of the first years of life, which has typical clinical manifestations of malabsorption syndrome.

Modern epidemiological data indicate that the incidence of GE in the population reaches 1%. This makes GE one of the most common genetically determined diseases of the gastrointestinal tract. The clinical signs of HE are highly variable, making it difficult to timely diagnosis. Insufficient attention is paid to extraintestinal symptoms of GE. These include various deficiency states(iron deficiency anemia, osteoporosis, refractory to therapy), skin manifestations (cheilitis, dermatitis), impaired physical and sexual development. Children with this pathology are observed for a long time by many specialists, undergo repeated examinations and receive drug therapy without a significant effect, which negatively affects their quality of life and worsens the prognosis of the disease.

GE (celiac disease) is a chronic genetically determined autoimmune T-cell-mediated enteropathy, characterized by persistent intolerance to specific endosperm proteins of the grain of some cereal crops with the development of hyperregenerative atrophy of the mucous membrane of the small intestine and associated malabsorption syndrome.

“Toxic” for patients with HE are prolamins (alcohol-soluble proteins rich in glutamine and proline), namely: wheat gliadin, rye secalin and barley hordenin. The membership of oat avenin proteins in this group has recently been discussed, but in practice it should still be classified as “toxic”. IN medical literature For the sake of brevity, all cereal proteins that are dangerous for patients with GE are referred to as “gluten.” The triggering factor for the development of GE is the consumption of gluten and the presence of a genetic predisposition (HLA-DQ2 or DQ8 haplotypes diagnosed in patients).

Clinical picture of celiac enteropathy

Typical symptoms of GE - abdominal pain, vomiting, loss of appetite, copious foul stools, diarrhea, flatulence, delayed physical development - are more common at an early age, developing 1.5-2 months after the introduction of cereal products into the diet, possibly after infectious disease. Also characteristic are an increase in bowel movements, polyfecality, steatorrhea, an increase in abdominal circumference against the background of a decrease in body weight, signs of malnutrition (loss of body weight, thinning of the subcutaneous fat layer), decreased muscle tone, loss of previously acquired skills and abilities, hypoproteinemic edema.

In accordance with the latest ESPGHAN (European Society of Pediatric Gastroenterology, Hepatology and Nutrition) recommendations, children and adolescents who have the following conditions or symptoms should be screened for the presence of GE: chronic or recurrent diarrhea, nausea or vomiting, chronic pain syndrome, feeling of distension, chronic constipation, developmental delay, weight loss, growth retardation, delayed sexual development, amenorrhea, iron deficiency anemia refractory to therapy, spontaneous fractures (osteopenia/osteoporosis), recurrent aphthous stomatitis, dermatitis herpetiformis, increased liver enzyme activity, chronic fatigue syndrome. Diagnosis of GE in such cases is usually not difficult, and timely administration of a gluten-free diet quite quickly leads to relief of clinical symptoms and normalization of the rate of physical and neuropsychic development of the child.

Detection of one or more specified symptoms in a child requires a mandatory serological examination (determining the concentration of IgA antibodies to tissue transglutaminase) on an outpatient basis. Currently, this test is not available in all medical institutions. If an increased level of antibodies to tissue transglutaminase is detected, the child is sent for hospitalization to a hospital that has tools for targeted diagnosis of celiac disease for a more detailed examination and endoscopic examination of the duodenum and jejunum with a biopsy taken for histological analysis (required!). It must be remembered that examination of a child with suspected GE, both serological and morphological, must be carried out strictly against the background of a normal diet!

Diagnostics

The diagnosis of GE is made on the basis of:

characteristic clinical manifestations and anamnesis data;
positive results of serological examination;
histological diagnosis based on the assessment of elementary damage (increased number of interepithelial T-lymphocytes (IEL)), structural changes (shortening of villi and crypt hyperplasia).

Instrumental research methods

Patients undergo esowith a biopsy of the distal portions of the duodenum and the initial parts of the jejunum. Endoscopic signs of GE: there are no patho-gnomonic endoscopic signs of celiac disease. The following are described general signs: absence of folds in the small intestine (intestine in the form of a “pipe”) and transverse striations of the folds.

Laboratory research methods

Histological features of celiac enteropathy

In the active period of GE, diffuse changes in the mucous membrane of the small intestine are observed, which are referred to as “atrophic enteropathy,” with shortening of the villi up to complete disappearance, as well as an increase in the depth of the crypts and a decrease in the number of goblet cells. The presence of deep crypts and increased mitotic activity, indicating hyperplasia of the generative region, serve as the basis for the diagnosis of “Hyperregenerative atrophy”. Interepithelial lymphocytic infiltration and lymphoplasmacytic infiltration of the lamina propria of the small intestinal mucosa are characteristic, indicating the presence of an ongoing immunological process causing damage to villous enterocytes.

Serological tests for the diagnosis of celiac enteropathy

Children with suspected GE should undergo a serological test to confirm the diagnosis. It is possible to detect antigliadin (AGA), antiendomysial (AEMA) antibodies, as well as antibodies to tissue transglutaminase (anti-tTG) in the blood. The most informative is the determination of antibodies to the cells of the intestinal mucosa: IgA to tissue transglutaminase (anti-tTG) and IgA to endomysium (AEMA). Currently, these tests, as noted above, are not available in all clinics. The most common test is anti-agliadin antibodies (AGA), but this is not recommended due to its low specificity and sensitivity. It must be taken into account that the assessment of AGA content will be unreliable in patients with an initially low IgA value, therefore, serum IgA should be determined first.

Treatment of Celiac Enteropathy

Diet

The only method of treating GE and preventing its complications is a strict and lifelong gluten-free diet! Elimination diet therapy is based on the complete exclusion of gluten-containing foods from the diet. It is fundamentally important to avoid eating not only those products that contain “obvious” gluten (bread, bakery and pasta, wheat, semolina, barley, pearl barley, breaded semi-finished meat, fish and vegetable dishes, dumplings, dumplings, etc.), but also those that contain “hidden” gluten, used as food additives in the production process (sauces, confectionery, chips, kvass, etc.). Parents need to explain the importance of clearly monitoring the composition of products indicated on the packaging.

Currently on the Russian market there are gluten-free products made from “safe” grains, which have good taste and allow diversification of children’s diets. A properly formulated gluten-free diet is absolutely complete, ensures normal growth and development of the child, prevents relapses of the disease and prevents the risk of developing serious complications. A child following a gluten-free diet should and can lead a normal life and does not need constant hospitalization or registration due to disability.

Children with GE can eat meat, fish, vegetables, fruits, eggs, dairy products, rice, legumes, buckwheat, corn, millet, chocolate, marmalade, some candies, marshmallows, and some types of ice cream.

Specialized gluten-free products are recommended for feeding patients with celiac disease. Acceptable gluten levels are< 2 ppm (ppm — «pro pro mille» — одна миллионная часть; 1 ppm = 1/1000000 = 0,000001 = 1 × 10-6 = 0,001‰ = 0,0001%) (менее 0,2 мг/100 г сухого продукта) для продуктов питания, естественным образом не содержащих глютен, и 20-200 ppm — для продуктов, из которых глютен удаляют в процессе их выработки .

Almost all milk formulas for feeding children in the first year of life and all medicinal formulas do not contain gluten. In Russia, certified products for nutrition of patients with celiac enteropathy are presented by the companies Glutano (Germany) and Doctor Scher (Italy).

Recently appeared on the baby food market New Product— “Babiki” gluten-free cookies. According to expert opinions, cookies do not contain genetically modified microorganisms, nanomaterials, dyes, artificial stabilizers, preservatives and meet Russian and international requirements for complementary feeding products. Gluten-free Bebiki cookies - unique product: comprises corn flour, does not contain gluten, the most suitable option for all children who are starting to get acquainted with cereal dishes, recommended for GE. Cookies are an important cereal part of a baby’s diet, and cereal products provide easy-to-digest protein, vitamins and minerals, as well as high calorie content, which gives a long-lasting feeling of satiety, and dietary fiber for optimal intestinal function. Eating cookies independently by a child helps develop coordination of movements of the head, hands, eyes, and the consistency of the product contributes to the formation of chewing skills.

Drug therapy

Drug therapy for GE is auxiliary and may be vital. It is mainly aimed at correcting metabolic disorders, developed against the background of malabsorption syndrome.

Correction of digestion processes is carried out by prescribing highly active pancreatic enzymes (Creon, Micrasim, Ermital). The dose of the drug is determined by the age of the child, the nature of the diet and the severity of steatorrhea. Against the background of severe diarrhea, mucocytoprotective adsorbents (Smecta) can be used. If necessary, correction of violations is indicated intestinal microflora. With the development of hypoproteinemic edema, in order to restore the oncotic pressure of the blood - intravenous drip administration 10% albumin solution, however, when prescribing parenteral nutrition, preference should be given to sets of amino acids. Against the background of restoration of protein concentration in the blood, it is advisable to prescribe non-steroidal anabolic drugs, such as potassium orotate, glycine, etc., and in some cases, steroid drugs. Hypoglycemia with GE occurs in infants and young patients more often than in older children, and is directly related to impaired intestinal absorption. Hypoglycemia is corrected intravenous administration 5-10% glucose solution.

Fluid and electrolyte disorders require infusion therapy, based on a deficiency of water and electrolytes. The basic solutions for infusion therapy are isotonic sodium chloride solution and 5-10% glucose solution, the ratio of which is determined by the type of dehydration (isotonic or hypotonic). To correct the potassium level in the blood, use a 4-7.5% potassium chloride solution. The dose is determined by potassium deficiency. The drug is administered only intravenously, drip-wise, slowly, pre-diluted with isotonic sodium chloride solution to a concentration not exceeding 70 mmol/l.

Malabsorption of calcium and vitamin D is corrected by administering calcium and prescribing vitamin D 3 preparations.

The use of glucocorticoid drugs for GE is indicated in cases of severe disease with significant impairment of physical development, for example, with grade III malnutrition, and as a replacement therapy for correction of adrenal insufficiency. Possible negative consequences of long-term therapy with glucocorticoid drugs, especially in high doses, may be an increase in osteoporosis up to episodes of spontaneous fractures. In order to correct secondary transient hypothyroidism, children with hyperthyroidism can be prescribed L-thyroxine 25 V small doses(5 mg/kg per day) for a course of up to 1 month while monitoring the serum levels of thyroid-stimulating hormone, triiodothyronine and thyroxine.

Observation

Dispensary observation of children with GE is lifelong. Frequency of observation: after diagnosis during the first 2 years - once every 6 months, from the 3rd year of observation, subject to stable remission and regular sufficient weight gain - once a year. Examination during clinical observation: interview, examination, measurement of height and weight, coprogram, clinical analysis blood, biochemical research blood; according to indications - endoscopic and serological examination.

Endoscopic and serological examinations are mandatory upon first admission and during the active period of the disease. A repeat endoscopic examination is prescribed 6-12 months after starting a gluten-free diet or exiting the active period of the disease, or if the patient’s condition worsens.

Serological testing should be repeated annually. The patient's relatives are also recommended to undergo a serological examination, and if elevated titers of the corresponding antibodies are detected, to conduct a full range of examinations, including endoscopic and histological examination.

Preventive vaccinations are carried out during the period of remission according to a gentle scheme.

Conclusion

Diagnosis of GE requires comprehensive assessment clinical, serological and histological data.
All specialists dealing with the problem of GE must take into account the variability of the clinical, endoscopic and histological picture of the disease when assessing the patient’s condition. This is the key to high-quality and timely diagnosis.
The only method for treating GE and preventing its complications is a strict and lifelong gluten-free diet!

Literature

Zakharova I. B. Koning F. Such an insidious celiac disease... // Med. newspaper. 2012; 46:2-3.
Memeo L. Report "Celiac disease: histological aspects and differential diagnosis." Congress of Pediatric Gastroenterologists, Moscow. 2010.
Zaprudnov A. M. Intestinal diseases in children. M.: Anacharis. 2009. 119-129.
Belmer S. V., Mukhina Yu. G., Gasilina T. V. etc. Information letter “Draft standards for the diagnosis and treatment of celiac disease in children.” X Congress of Pediatric Gastroenterologists of Russia, Moscow. 2003.
Korovina N. A. Zakharova I. N., Berezhnaya I. V. Celiac disease: possibilities of diagnosis and treatment in children // Russian Medical Journal. 2004. No. 13. pp. 786-789.
Parfenov A. I. Mysteries of gluten enteropathy // Moscow Medical Journal. 1997; May, 24-26.
Revnova O. M., Lyle H. B. Clinical aspects of celiac disease in children // Pediatrics. 2000; 5: 107-109.
Cherkasova T. A., Snigireva D. G. and others. Celiac disease (textbook). 2000. 3-5, 10, 17-18.
Celiac disease. WGO-OMGE: Practice guidelines // World Gastroenterology News. 2005; 10(2), Suppl. 1-8: 1-8.

T. M. Osheva, candidate medical sciences
N. S. Zhuravleva, Candidate of Medical Sciences, Associate Professor
O. V. Osipenko,Candidate of Medical Sciences

GBOU VPO UGMA Ministry of Health of the Russian Federation, Ekaterinburg

Celiac disease is a pathology in which plant protein is not tolerated by the body, which has many negative consequences. Plant protein - gluten, contained in cereals, causes an inflammatory process in the mucous membrane of the small intestine. As a result, digestion suffers and the person develops severe malabsorption (impaired absorption of nutrients). Similar protein is found in four cereals - wheat, rye, barley, oats.

This pathology goes by different names - celiac disease, celiac enteropathy. Patients with this diagnosis are forced to follow a strict diet. If the diet is violated, they develop severe dyspepsia.

However, not every person has this sensitivity to gluten. Cereal intolerance is a rare phenomenon and is associated with a hereditary predisposition. One in three hundred people have signs of celiac disease. The disease can occur at any age and regardless of gender. The pathology is typical for the countries of North America, Ireland, and Austria.

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Causes of pathology

Celiac enteropathy is hereditary disease- genetic predisposition was found in 97% of patients. It is inherited in an autosomal dominant manner.

The disease is chronic and occurs with periods of exacerbations and remissions. The patient is in remission as long as he follows a special diet. If the diet is violated, an exacerbation of the disease develops with external symptoms and changes in the mucous membrane of the small intestine.

What happens in the body?

When vegetable protein enters the stomach, digestive enzymes break it down into constituent components. One of them (alpha-gliadin) has immunogenic activity. It is resistant to the action of digestive enzymes, therefore it is absorbed unchanged by the villi of the small intestine.

In genetically predisposed people, lymphocytes have special receptors that bind to this protein and provoke allergic inflammation in the intestinal mucosa.

As a result, the structure of the epithelium changes and immature cells appear on its surface. They are unable to perform the digestive function, and the absorption of nutrients stops. The surface area of the digestive villi of the intestine is significantly reduced.

As a result, all stages of small intestinal digestion are affected. Most of the food is excreted unchanged. The part that has been processed in the mouth and stomach is not able to be absorbed and practically no nutrients enter the body.

This leads to the development of corresponding symptoms.

Symptoms of the disease

Symptoms of celiac disease in adults and children depend on the degree and area of damage to the mucous membrane. An asymptomatic course is more often observed. The classic picture with pronounced manifestations is rarely observed. In the scientific literature, celiac disease is represented schematically in the form of an iceberg. Its broad basis consists of those people who have a genetic predisposition to enteropathy, but there are no clinical manifestations. In the middle are patients with latent course, scant manifestations. The top - the smallest number of patients - are people with typical, pronounced symptoms.

Celiac enteropathy begins to manifest itself with early childhood when a child receives complementary foods from cereals. Children begin to lose weight, have stunted growth, and are stunted mental development. The child is bothered by bloating and rumbling stomach, diarrhea.

If left untreated, conditions such as:

rickets;
mental disability;
delayed sexual development;
Iron-deficiency anemia.

Exacerbations of celiac disease in adults can be triggered by poor diet, pregnancy, intestinal infections, and abdominal surgery.

The main symptom of celiac disease in adults is iron deficiency anemia and the signs associated with it:

pale skin;
frequent dizziness;
low blood pressure;
fast fatiguability.

However, this is not the only sign of the disease. Celiac disease syndrome is accompanied by the development of many concomitant pathologies:

Dühring's dermatitis herpetiformis is the most common - these diseases are related;
on the part of the hematopoietic system, folate deficiency anemia and blood clotting disorders develop;
lesions of internal organs include liver steatosis, enlarged spleen and increased function, insufficient production of pancreatic enzymes;
characterized by often recurrent aphthous stomatitis;
Women develop secondary infertility, and subsequent pregnancies end in miscarriages.

Celiac disease in adults provokes the development of many autoimmune diseases:

diabetes;
autoimmune thyroiditis - damage to the thyroid gland;
Addison's disease - pathology of the adrenal cortex;
systemic diseases connective tissue- Sjogren's syndrome, systemic lupus erythematosus, scleroderma;
rheumatoid arthritis - joint damage;
primary biliary cirrhosis - inflammation of the bile ducts;
damage to the liver, kidneys, heart and lungs;
epilepsy.

The presence of celiac disease tens of times increases the risk of developing cancer, especially gastric adenocarcinoma.

Signs of celiac disease directly from the gastrointestinal tract include:

flatulence;
rumbling in the stomach;
diarrhea with a characteristic appearance of feces - shiny (due to undigested fat), foamy (undigested carbohydrates), mixed with mucus and pieces of food;
weight loss.

All these symptoms are characteristic only for the period of exacerbation. When following a gluten-free diet, the patient feels normal.

Depending on the intensity of malabsorption, three forms of the disease are distinguished:

The typical form is the least common;
Atypical and latent forms are more often observed.

The diagnosis is usually made in people with typical form- that is, quite rarely. The remaining patients are usually not examined.

Typical celiac disease

The first signs appear within four months after starting to consume cereal products. During the course of the disease, three syndromes are distinguished.

Polyfecalia. Feces profuse, foul-smelling, frequency of bowel movements 3-5 times a day. The surface of the stool is shiny and is difficult to wash off.
Increased abdominal volume. At the same time, it is not tense or swollen, as with the accumulation of liquid or gases, but remains soft.
If the disease occurs in a child, he is noticeably behind in growth compared to his peers. At the same time, there is a lack of body weight.

Some patients experience other dyspeptic symptoms - epigastric discomfort, belching, nausea. Characteristic signs of vitamin and mineral deficiency:

bone pain;
the appearance of multiple caries;
hair becomes brittle and dull, baldness may begin;
the skin is thin, dry, flaky;
the muscles gradually atrophy;
gums are prone to bleeding;
stomatitis and glossitis often appear.

Atypical and latent forms

The first manifestations are detected late - by the age of 30. Characterized by one of the main symptoms in combination with several additional ones.

The latent form is typical for the patient’s closest relatives. Has no clinical manifestations. Most often, such patients are not examined and live their entire lives with an unknown diagnosis. Such people greatest number.

Diagnostic methods

Diagnosis of celiac disease in children begins with identifying hereditary burden. Next, the relationship of symptoms with eating cereals is assessed. This is followed by a clinical examination assessing the following symptoms:

palpation of the abdomen and identification of specific areas of pain;
measure abdominal circumference and identify signs of ascites or flatulence.

After this, the diagnosis proceeds in three stages. The first is the examination of the patient's blood serum. Then fibrogastroscopy is performed with tissue material sampling. After this, a gluten-free diet is prescribed and the patient is monitored for six months.

Laboratory methods are aimed at identifying pathological changes in the body:

IN general analysis blood tests can reveal signs of anemia. They are represented by a decrease in the content of hemoglobin, red blood cells, and platelets. Based on leukocytosis, the presence of an inflammatory process can be assumed.
Blood chemistry. Allows you to detect the presence of specific proteins - immunoglobulins.
Stool examination occult blood. This symptom indicates the presence of anemia.

The diagnosis is confirmed by a serological test - specific antibodies are determined in the blood serum. They are formed in the body in response to the appearance of the cereal protein gluten and its constituent components. There are four types of specific antibodies in total. If all four are identified, the diagnosis is absolute. If one thing is revealed, the diagnosis is questionable, additional examination is needed.

A scatological examination is carried out to determine the state of digestive function. In this study, undigested fats, proteins and carbohydrates can be detected in stool.

The diagnosis of celiac disease in adults includes an endoscopic examination, during which a section of the mucous membrane is taken - a biopsy. During endoscopy, signs of inflammation of the small intestinal mucosa can be detected. The pieces obtained during the biopsy are sent for histological examination, where changes characteristic of celiac disease are revealed.

To make a diagnosis of celiac disease, three factors must be present:

detection of specific antigliadin antibodies in the patient’s blood serum;
detection of typical changes in the mucous membrane of the small intestine during histological examination;
improvement of the patient's well-being after 6 months of following a gluten-free diet.

It is necessary to differentiate celiac enteropathy from other diseases manifested by malabsorption syndrome:

tropical sprue, infectious enteritis, giardiasis;
lactose intolerance, immunodeficiency enteropathy;
Whipple's disease, lymphoma.

After confirmation of the diagnosis, patients are prescribed specific treatment. When a diagnosis of celiac disease is established, testing is also carried out on all the patient’s relatives. It is recommended to examine all patients with autoimmune diseases and cancer.

Therapeutic measures and diet

The main treatment for celiac disease is lifelong adherence to a gluten-free diet.

This diet involves the complete exclusion from the diet of foods containing grains in any quantity (wheat, rye, oats, barley).

Therefore, patients should exclude:

all cereal dishes;
all dishes containing cereal flour - bread, pastries, cookies;
pasta;
bran;
breaded dishes;
jelly.

With the development of secondary lactase deficiency, all dairy products must be excluded. A small amount of gluten may be contained in filled chocolates and some drinks.

The following foods are allowed to be eaten:

meat and fish;
buckwheat and rice groats;
fruits and vegetables;
eggs;
butter;
marmalade, chocolate candies;
tea and coffee;
cheese and cottage cheese only in the absence of lactase deficiency.

With any error in the diet, exacerbations of celiac disease will develop. In this case, treatment will be aimed at eliminating malabsorption syndrome. An exacerbation of the disease will develop if the gluten content in the food consumed is more than 1 mg per 100 g of product.

To eliminate the symptoms of malabsorption, the following groups of drugs are used:

pancreatic enzymes - Creon, Pangrol;
probiotics - Maxilak, Bifiform;
sorbents - Polysorb, Enterosgel.

If there is an infection in the intestines, take one of the following medications:

Enterofuril;
Intetrix;
Mesalazine.

If iron deficiency or folate deficiency anemia occurs, iron supplements (Ferrum-lek, Sorbifer) or folic acid along with cyanocobalamin are prescribed, respectively.

If drug treatment and diet do not have an effect, the issue of prescribing immunosuppressive therapy should be decided. It is carried out using glucocorticoid drugs.

Following a strict gluten-free diet, in which a huge number of foods must be limited, can be difficult for patients. To make this process easier, you can follow some recommendations:

It is advisable to prepare food yourself at home. This way you can be sure that it does not contain prohibited components.
When purchasing products, you should always read the ingredients carefully. It is advisable to choose products from well-known brands. Larger stores have special sections for celiac disease patients, where only gluten-free products are sold.
It should also be remembered that the shell of some medicines contains gluten. Therefore, before purchasing the drug, you should carefully read the instructions.

Enough simple rules will make life easier for patients with celiac disease.

Forecast

The disease is currently incurable. The only way to help the patient lead familiar image life is a strict adherence to a gluten-free diet. People with this disease are monitored by a gastroenterologist and undergo regular medical examinations. It is also necessary to promptly diagnose the occurrence of concomitant pathologies.

celiac disease(syn.: celiac disease, celiac enteropathy, gluten-sensitive celiac disease, idiopathic celiac disease) - a disease caused by intolerance to one of the main parts of the protein of cereal plants - gluten, and due to congenital or acquired deficiency of one of the enzymes of intestinal juice.

G. b. isolated as an independent disease from a large group of patol. conditions united under the term “celiac disease” and representing a manifestation of enzyme deficiency. Unlike other forms of celiac disease (see), observed mainly in children, G. b. often occurs in adults, sometimes combined with disaccharidase deficiency, manifested by milk intolerance (see Malabsorption syndrome).

The harmful effects of gluten were first established by W. Dicke, H. Weijers, J. Van de Kamer in 1950. Gluten consists of two fractions - glutenin and gliadin, of which only the latter contributes to the manifestation of gluten b. The cause of the damaging effect of this protein fraction and the mechanism of development of G. b. are not yet completely clear. The damaging factor in its pure form has not been identified.

Pathogenesis

The pathogenesis of the disease is complex. Discussed various reasons, contributing to the development of the disease, but their role remains hypothetical. The leading pathogenetic significance is the deficiency of a specific enzyme from the group of peptidase-aminopeptidase, contained in intestinal juice and breaking down gliadin into a water-soluble peptide fraction (fraction 3). This peptide fraction, while retaining the damaging effect of gliadin, causes G. b. It has been proven that patol, the effect of gliadin and the peptide fraction disappears when they are incubated with an extract of the mucous membrane of the small intestine of a pig. The neutralizing effect is attributed to the enzyme gliadinamidase contained in the mucous membrane of the small intestine of pigs. It is known that the mucous membrane of the small intestine of a healthy person also has the ability to break down the peptide fraction into its constituent amino acids; mucous membrane of the patient G. b. lacks this ability. With a deficiency of specific enzymes, products of incomplete breakdown of gluten are absorbed, which determines the toxic effect.

In the development of G. b. A major role is played by the state of hypersensitization that occurs in response to the introduction of gluten and some of its fractions into the body. Extreme degree allergic reactions such patients are so-called. gliadin shock. Confirmation of immunol, the theory of G.’s pathogenesis b. serves as a decrease in the titer of complement-fixing antibodies to rye and wheat proteins in response to a gluten food test (gliadinotolerance test) and the presence in the serum of patients of antibodies to the peptide fraction, which decrease when following a gluten-free diet. Hypersensitization is also evidenced by accumulation during G. b. a large number of plasma cells in the contents of the small intestine and a decrease in their number against the background of a gluten-free diet. The role of immunol, the factor is confirmed by the appearance in the stool of patients of specific antibodies - coproantibodies, immunologically competent cells, the formation of which is associated with the production of antibodies in the small intestine itself in response to the introduction of gluten. The detection of immunoglobulins in the secretion of the proximal jejunum is of great importance. Intestinal plasma cells have a very high concentration of IgA, much less IgM and very little IgG.

Pathological changes

Pathoanatomical changes in G. b. differ little from changes in other forms of celiac disease and consist in atrophy of the villi of the small intestine, accompanied by a decrease in the activity of specific peptidases in the membranes of the brush border. Pronounced infiltration of the intestinal mucosa with plasma cells. Patol, the process is more intense in the proximal part of the small intestine, which is obviously associated with the direct effect of the damaging agent - the digestion and absorption of gluten in this section of the intestines.

Clinical picture

Characterized by persistent diarrhea with polyfecal matter, steatorrhea (see), flatulence (see); as the disease progresses, metabolic disorders (exhaustion, hypoproteinemia, hypovitaminosis, anemia, mineral and water-salt metabolism), caused by impaired absorption in the intestine. In advanced cases, mental changes occur, and children experience developmental delays.

Diagnosis

Accurate and direct methods for diagnosing G. b. No. Indirect methods include the gliadin tolerance test - a test with a load of gliadin (350 mg of gliadin per 1 kg of weight): taking gliadin causes a significant increase in the level of glutamine in the blood in patients. However, this test cannot be considered sufficiently reliable.

Most convincing diagnostic sign G. b. - disappearance of all symptoms when following a gluten-free diet and relapse when eating foods containing gluten.

Treatment

The only effective treatment is to prescribe a gluten-free diet for long periods (months, years). Breads and bread products made from gluten-free wheat starch are recommended. The diet should be complete in composition, mechanically and chemically gentle.

With the development of malabsorption syndrome, increase the amount of animal protein in the diet; if indicated, administer parenterally protein preparations, vitamins.

Forecast

Complete cure is possible, apparently, only in cases of acquired gluten enzymopathies, when the use of a gluten-free diet helps restore the architecture of the small intestine and its enzymatic activity.

Bibliography: Beyul E. A. and Ekisenina N. I. Chronic enteritis and colitis (Issues of pathogenesis, clinic and treatment), p. 164, M., 1975; Handbook of Gastroenterology, ed. V. X. Vasilenko, p. 95, M., 1976; Tashev T. A. et al. Diseases of the stomach, intestines and peritoneum, trans. from Bulgarian, p. 461, Sofia, 1964; Frolkis A.V. Functional diagnosis of intestinal diseases, p. 28, M., 1973; D i s s a n a u a k e A. S. a. O. Identifying toxic fractions of wheat gluten and their effect on the jejunal mucosa in coeliac disease, Gut, v. 15, p. 931, 1974, bibliogr.; F a 1 s h u k Z. M. a. S t r o-b e r W. Gluten-sensitive enteropathy, ibid., p. 947, bibliogr.; K a m e r J. H. a. ,W e i ] e r s H. A, Malabsorption syndrome. Fed. Proc., v. 20, p. 335, 1961.

Celiac disease (gluten enteropathy) is a disease of the small intestine, manifested by atrophy of the mucous membrane in response to the introduction of gluten. The prevalence of celiac disease varies considerably among different geographic areas. The disease occurs with the highest frequency in European countries (1-3:1000), with a lower frequency in African countries. It is believed that at least 1% of the world's population suffers from this disease. Celiac enteropathy is more often reported among women.

Damage to the small intestine in celiac disease occurs under the influence of gluten, a protein found in cereals. Gluten consists of several components: prolamin, glutenin, albumin, globulin. It is prolamine that has a damaging effect on the intestinal mucosa. Its amount in different cereals is not the same. So, millet, rye, and wheat contain this protein in large quantities. Prolamine is found in smaller quantities in barley, oats, and corn. Prolamin is heterogeneous in its structure; wheat prolamin is called gliadin, barley prolamin is called hordein, and oat prolamin is called avein.

The key factor in the development of the disease is genetic predisposition. In people with this feature, when gluten comes into contact with the intestinal villi, specific antibodies are produced. This is how autoimmune inflammation of the intestinal tissue develops, leading to gradual atrophy of the organ mucosa.

Villous atrophy and dystrophic changes in enterocytes that develop with celiac disease lead to a decrease in the absorption surface of the small intestine. As a result, the absorption of proteins, fats, carbohydrates, vitamins, and minerals is impaired. These changes lead to the appearance of characteristic clinical symptoms. Celiac disease can occur in three forms: classical, atypical, latent.

Gluten enteropathy occurs mainly in childhood. Children are stunted, muscle weakness, apathy, increased abdominal size, steatorrhea, and cramping abdominal pain are noted. Kids are emotionally labile and get tired quickly. But in some patients, the disease does not appear in childhood, but already in adulthood.

In general, the following symptoms are characteristic of classical celiac disease:

Loss of body weight (from 5 to 30 kg);
Decreased appetite;
Weakness, fatigue;
Stomach ache;
Dyspeptic symptoms: flatulence, nausea, ;
Edema;
Glossitis, ;
Iron deficiency;
Hypocalcemia with osteoporosis;
Hypovitaminosis.

Most constant symptom Celiac disease is recurring diarrhea, its frequency can reach ten or more times per day. The stool is mushy, light, liquid, foamy.

Constant, severe abdominal pain is not typical for celiac disease. However, people with celiac disease may experience cramping abdominal pain before or after bowel movements. And with flatulence, dull diffuse pain occurs.

When examining a person with celiac disease, attention is drawn to an enlarged abdomen.

Symptoms of atypical celiac disease

In most cases, celiac disease has an atypical course. In the clinical picture of the disease, gastroenterological symptoms may be absent or mild. Extraintestinal symptoms come to the fore:

Anemia;
Ulcerative stomatitis;
, frequent fractures;
Dermatitis herpetiformis (characterized by the appearance of itchy papulovesicular rashes on the elbows and buttocks);
Hemorrhagic syndrome;
Associated autoimmune diseases (autoimmune thyroiditis, diabetes mellitus, Addison's disease);
Defeat nervous system(, ataxia, epilepsy, polyneuropathy);
Deterioration of potency, menstruation disorders,.

If celiac disease is left untreated, complications of the disease can occur. The most common complications include:

Malignancy;
Chronic non-granulomatous ulcerative jejunoileitis and colitis;
Neuropathy.

Patients with celiac disease develop it much more often than in the general population. In addition, cancer of the esophagus, stomach, and rectum is also more common. Unreasonable deterioration of the patient's condition, as well as laboratory parameters, despite adherence to a gluten-free diet, should suggest the probable development of a malignant process.

Chronic non-granulomatous ulcerative jejunoileitis and colitis is characterized by the appearance of ulcerative defects on the mucous membrane of the jejunum, ileum, and colon. Ulcers may bleed or perforate.

Neuropathy manifests itself as numbness, tingling, weakness in the lower limbs. Damage to nerve fibers upper limbs observed less frequently. When the cranial nerves are damaged, diplopia, dysphonia, and dysarthria are observed.

Diagnostics

The symptoms of celiac disease are so varied and non-specific that certain tests should be carried out to confirm the suspected diagnosis. Since a key factor in the occurrence of celiac enteropathy is genetic predisposition, it is necessary to determine the family history of gluten intolerance.

The main diagnostic method is serological. In patients with celiac enteropathy, specific antibodies are detected in the blood:

Antigliadin (AGA IgG, IgM);
Endomysial (EMA IgA);
Antibodies to tissue transglutaminase (tTG).

No less important diagnostic method is a morphological study of the small intestinal mucosa. Endoscopy and histological examination of intestinal tissue reveal signs of atrophic damage to the mucous membrane with shortening of the villi and lengthening of the intestinal crypts.

Additional research methods:

- anemia is determined;
- hypoproteinemia, hypocalcemia, hypokalemia, hypomagnesemia are determined;
Scatological examination - a large amount of fat and soap is determined.

Treatment

Celiac disease is a disease that can be corrected through diet. When following a diet, the mucous membrane of the small intestine is restored and soon the person is no longer bothered by the unpleasant symptoms of the disease.

Principles of diet for celiac disease:

Excluding gluten-containing foods from the diet (bread, pasta and confectionery);
Mechanical and thermal sparing of the digestive tract (meals are steamed or boiled, consumed pureed or without chopping);
Elimination of foods that enhance fermentation (milk, legumes);
Limiting foods that stimulate the secretion of the pancreas and stomach (rich meat broths, fat meat).

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In case of exacerbation of the disease, in addition to a gluten-free diet, drug treatment is carried out in order to eliminate metabolic disorders. The following groups of drugs are used: