Beware, cereals! How to distinguish celiac disease from allergies.

Consultation with a gastroenterologist – 1,750 rubles.

  • Causes
  • Symptoms
  • Diagnostics
  • Treatment
  • Prevention

Celiac disease (gluten enteropathy, intestinal infantilism, G-Herter-Heubner disease) is a pathological disorder of the intestines in which gluten intolerance is observed. This protein is found in cereals. As a rule, symptoms manifest themselves most clearly in childhood; over time, signs of the disorder become less pronounced. In women, the disorder is diagnosed more often.

Celiac disease is common throughout the world. According to the World Association of Gastroenterology, the incidence of celiac enteropathy in different populations ranges from 1:100 to 1:300. In Russia, the estimated incidence of celiac disease is 1:1000 Source: Bai J. WGO-OMGE / J. Bai, E. Zeballos, M. Fried // Practice Guideline Celiac Disease. - 2005. - Vol. 10. - P. 1-8. .

Undiagnosed celiac disease can lead to serious consequences, such as: malignant diseases of the gastrointestinal tract, in particular small intestinal lymphoma, unexplained infertility, osteoporosis, growth impairment, autoimmune diseases that occur 10 times more often in adult patients with celiac disease Source: Kamalova A.A. Evolution of approaches to the diagnosis and treatment of celiac disease / A.A. Kamalova, M.O. Pirogova // Bulletin of modern clinical medicine. - 2013. - T.6. — Vol. 3. - pp. 40-48. . The mortality rate among patients with untreated celiac enteropathy is 10-30%, while with adequate treatment - a strict gluten-free diet - it drops to 0.4% Source: Mikhalik D.S. Celiac disease: disease and lifestyle / D.S. Mikhalik [and others] // Zemsky doctor. - 2012. - No. 4. - P. 35-38. .

Etiology

The leading role is played by gliadin - the alcohol-soluble fraction of gluten

- squirrel. Gluten is a water-insoluble complex of proteins (prolamins, glutenins) with a low content of lipids, sugars and minerals. Prolamins that are toxic to patients with celiac disease are: wheat gliadin; rye secalin; barley hordenine; Ovein does not cause atrophy of the mucous membrane of the small intestine and an increase in autoantibodies, but contamination of oat products with other grains cannot be ruled out, so it is also not recommended for use in celiac disease.

How to check if you have gluten intolerance and find out the correct diagnosis

There is only one way out - go to see a doctor. It is now possible to test blood for the presence of antibodies to an insidious protein that causes irreversible damage to the villi of the small intestine. Do not forget that the disease can remind itself at any age - not only in the very first years, but also much later.

We have already told you what kind of disease this is - celiac disease, but have not yet given clinical recommendations. Meanwhile, they are especially important, since the key to health and reducing the frequency of exacerbations is proper nutrition.

Pathogenesis

There is no doubt that celiac disease does not occur without gluten, but there are still no clear opinions about its pathogenesis, so there are a number of hypotheses.

1) Sensitization with gliadin,

as a result, the intestinal epithelium becomes a target for the development of the immunological process. Once in the mucous membrane, the protein antigen (gluten) undergoes cleavage in the macrophage lysosomes into peptides. Peptides bind to HLA class II molecules located in the endoplasmic reticulum of the same cell. In this case, the peptides undergo deamination in the presence of the tissue transglutaminase enzyme – TG2, which ensures closer binding of gluten peptide residues to the DQ2 and DQ8 molecules. This complex is presented on the macrophage membrane and is recognized by lymphocytes that have passed through Peyer's patches. Activated T-lymphocytes turn into cytotoxic cells carrying CD8 markers (killer cells) and helpers (Th1 and Th2), which are CD4-positive. At the same time, the content of CD4 lymphocytes in the lamina propria of the mucous membrane increases almost 50 times, and CD8 T cells in the epithelium - almost 10 times. Th1 produces IL-2, tumor necrosis factor (TNF) and interferon-γ, which induce inflammation and activate a cytotoxic immune response; Th2 – a significant amount of IL-4, 5 and 10, inhibiting Th1 activity. In turn, TNF activates metalloproteases, in particular MMP-3 and MMP-1, disrupting the structure of the subepithelial region of the mucosa and destroying collagen. B lymphocytes potentiate the production of antibodies to gluten and tissue transglutaminase. In parallel, the production of autoantibodies to TG2 occurs, which in the form of IgA deposits are located in the subepithelial layer of the intestine, on fibroblasts, as well as in the liver, lymph nodes, muscles, and blood vessels. Blocking tissue transglutaminase by autoantibodies leads to destruction of the epithelium and mucosa, villous atrophy and proliferation of crypt epithelial cells, which increases the permeability of the mucosa, including gluten.

2) The role of viruses

in the pathogenesis of celiac disease (in some patients, an increase in antibody titers to adenovirus type 12 is detected in the blood, a decrease in which was noted when the patients’ condition improved on the background of the agliadine diet).

In celiac disease, there is an autosomal dominant type of inheritance with incomplete penetrance. In the patient's closest relatives, the incidence of the disease varies from 2 to 12% according to histological examination of the mucous membrane of the small intestine. In identical twins, concordance for celiac disease is approximately 70%, and in HLA-identical individuals it is up to 30%. Parents of patients with celiac disease themselves suffer from latent celiac disease in approximately 14% of cases.

Refractory disease

In rare cases, patients suffer from refractory disease. These patients do not benefit from a gluten-free diet. They are usually prescribed corticosteroids and immunosuppressive drugs.

If celiac disease is left untreated, your risk of developing certain types of cancer may increase. The study found that "celiac disease is associated with intestinal lymphoma and other forms of cancer, especially adenocarcinoma of the small intestine, pharynx, and esophagus." Complications of celiac disease can include small intestinal ulcers. People with celiac disease may have an increased risk of polyneuropathy.

Symptoms of celiac disease

Clinical manifestations and symptoms of celiac disease are as follows.

Celiac disease manifests itself after the introduction of gliadin-containing products (formulas, complementary foods) into children's diets.
After 2-3 months, the first signs of the disease appear. The onset of the disease may also be late - 5-6 months or more after the first introduction of gluten into the diet, sometimes after an infectious disease (intestinal infection, ARVI), and often for no apparent reason. The most common clinical manifestations of the disease
: 1) persistent decrease in weight and height indicators, 2) vomiting from rare to daily 3) diarrhea (malabsorption syndrome, stools are frequent, mushy, abundant with a grayish tint) 4) abdominal pain syndrome, 5) increase in abdominal circumference, 6) edema syndrome (decrease in blood protein levels), 7) development of food allergies (more often - intolerance to cow's milk proteins),8) delayed psychomotor development (loss of acquired skills), 9) polyhypovitaminosis (development of signs of rickets, osteoporosis), 10) development of lactase insufficiency.

Forecast

Clinical improvement is noted after just a few days of following a special gluten-free diet, with persistent improvement after 3-6 months. With good adherence to the diet, the prognosis is relatively favorable; observation by a gastroenterologist is required 1-2 times a year.

The prognosis worsens with a late start of treatment, the development of refractory celiac disease, the formation of complications, dynamic observation of a therapist and gastroenterologist, and consultations with other specialists (surgeon, endocrinologist, obstetrician-gynecologist, urologist, rheumatologist, dermatologist) are required. Mortality rates in patients not following a gluten-free diet are around 10-30%. Against the background of a diet, this figure becomes less than 1%.

It should be remembered that gluten intolerance lasts throughout life. Diet and treatment will only help remove disturbing symptoms. In the process of mastering a new lifestyle, societies of people suffering from the same disease and Internet sites specializing in the supply of gluten-free products can help you.

Classification of celiac disease in children

(St. Petersburg, May 2010)

Shapes:

  • Typical
  • Atypical (asymptomatic)

Periods:

  • Latent (from the introduction of gluten to the appearance of clinical manifestations - 1.5-2 months)
  • Active (clinical manifestation)
  • Remission (clinical, clinical-serological, morphological); initial remission (up to 3 months of diet), incomplete remission (3-12 months of diet)

Severity

(determined by the presence and number of deficiency conditions and complications:

  • Mild – deficiency conditions of the 1st degree (protein-energy deficiency of the 1st degree, anemia of the 1st degree, osteopenia, iodine deficiency goiter of the 1st degree, dysbiosis of the 1st degree), height 25-5 percentile
  • Moderate – deficiency conditions of the 2nd degree (protein-energy deficiency of the 2nd degree, anemia of the 2nd degree, osteoporosis, iodine deficiency goiter of the 2nd degree, dysbiosis of the 2nd-3rd degree), growth less than the 5th percentile
  • Severe – deficiency conditions of degree 3 or more, complications

An example of a diagnosis:

  • Celiac disease, typical form, period of incomplete remission, moderate severity. Diagnosed at age 10. Gluten-free diet with disorders for 1 year. Genetic diagnosis: HLA – DQА1*501*501HLA – DQВ1*303*301. Atopic dermatitis, common, moderate course (polyvalent food allergy).

How to treat gluten intolerance

Unfortunately, no cure for gluten sensitivity has been invented. The basis of treatment is a special diet - with the complete exclusion from food of provoking foods containing protein that causes harm to the intestines. Lactose and other possible allergens are often additionally excluded from the diet.

At the same time, you shouldn’t think that you can limit yourself for some time, and then gorge yourself on buns and pies. Your doctor's recommendations regarding nutrition should be followed throughout your life. Only this guarantees victory over a serious diagnosis.

Diagnostics

Stages of primary diagnostic examination (

when verifying the diagnosis before prescribing a gluten-free diet):

  • clinical and anamnestic stage,
  • serological
  • histological
  • genetic (if necessary).

Stages of diagnosis of the disease period

(against the background of a gluten-free diet during dispensary observation):

1) clinical and anamnestic,

2) serological (not earlier than 3 months from the prescription of the diet),

3) histological (not earlier than 1 year from the prescription of the diet, provided there is no increase in AGA and Anti-TSH).

Stages of diagnosis in genetic risk groups

(1st degree relatives):

1) genetic stage,

2) clinical and anamnestic,

3) serological,

4) histological.

Research methods

To mandatory laboratory research methods

for celiac disease include (in a hospital setting):

  • clinical blood test - repeat once every 10 days;
  • general urine analysis;
  • fat microscopy of stool (scatology);
  • bacteriological examination of stool;
  • histological examination of the biopsy;
  • serum immunoglobulins (Ig A, Ig G, Ig M);
  • total protein and protein fractions, albumin, cholesterol, total lipids, triglycerides, glucose, bilirubin, AST, ALT, calcium, phosphorus, serum iron, zinc, potassium, sodium, chlorides;
  • Gluten-sensitive enteropathy tests - GSE (Gluten-sensitive enteropathy):

    antigliadin antibodies (AGA, AGA) IgA – AGA, IgG – AGA;

    endomysial antibodies (EMA, EMA) IgA – EMA, IgG – EMA;

    tissue transglutaminase antibodies (tTG, tTG) IgA - tTG, IgG - tTG);

    anti-reticulin antibodies (ARA);

    Anti-actin antibodies (AAA).

Additional laboratory tests:

  • elastase-1 feces;
  • determination of bone age and bone density;
  • genetic analysis – HLA-DQ2 (DQA1*0501, DQB1*0201) HLA-DQ8 (DQA1*0301, DQB1*0302);
  • stool lipid profile;
  • excretion of plasma protein in feces;
  • determination of antibody titer to food antigens (for young children!);
  • stress test with D-xylose and gluten;
  • cortisol, TSH, T3, T4, STH.

Mandatory instrumental research methods:

  • anthropometry (weight, height, head circumference, chest, abdomen);
  • Ultrasound of the liver, biliary tract and pancreas;
  • EGD with targeted biopsy of the mucous membrane from the distal duodenum or the initial part of the jejunum (no later than 2-3 months from the start of a gluten-free diet).

Additional instrumental research methods:

  • detection of antibodies to glutenin and deamidated gliadin; instant test for tissue transglutaminase (TSG) using test strips;
  • CD Medics chip system – determination of several types of AT, Ig A, HLA DQ2/DQ8 status.

Mandatory consultations with specialists

: geneticist.

Additional specialist consultations

: allergist, endocrinologist, orthopedist, dentist.

Nuances of serological diagnosis of celiac disease

1) Antigliadin antibodies

(AGA, AGA) IgA - AGA, IgG - AGA. Currently not recommended for the diagnosis of celiac disease in adults and used only for the diagnosis of celiac disease in children under two years of age due to insufficient maturation of the components of the complement system responsible for the production of autoantibodies (12%).

2) Tissue transglutaminase antibodies

(tTG, tTG) IgA – tTG, IgG – tTG). They are not specific enough and, in addition to diagnostic markers of celiac disease, can be used as indicators of the activity of inflammatory processes and destruction in other inflammatory bowel diseases.

The main microscopic signs of celiac disease:

atrophy and decrease in the height of the villous epithelium, deepening of the crypts, an increase in the number of interepithelial lymphocytes over 30-40 per 100 epithelial cells, pronounced plasmacytic infiltration of the stroma of the mucous membrane. Most studies for celiac disease recommend taking 4 pieces of mucosa: 2 from the proximal part, 2 from the distal part.

Problems in the histological diagnosis of celiac disease:

unsuccessful sampling of material, incorrect orientation of the biopsy, lack of clinical information, Brunner's glands in the mucous membrane.
In three situations, the histological picture is almost impossible to distinguish from celiac disease:
autoimmune enteritis; exposure to medications, especially non-steroidal anti-inflammatory drugs; Helicobacter gastritis.

N.B !
The initial examination for diagnosis should be carried out during the active period of the disease before prescribing a gluten-free diet!
The final diagnosis is established on the basis of two mandatory signs :

a) characteristic clinical manifestations and anamnesis data

b) specific morphological data of the upper mucous membrane of the small intestine (“gold standard of diagnosis”)

and one of
research
methods :

a) serological examination,

b) HLA – typing.

Celiac disease treatment

And now about the treatment of celiac disease.

Key points in the treatment of patients with celiac disease:

1) Consultation with a skilled dietitian.

2) Education about the disease.

3) Lifelong adherence to a gluten-free diet.

4) Diagnosis and treatment of nutritional deficiencies.

5) Access to an advocacy group.

6) Continuous long-term followup by a multidisciplinary team.

Celiac disease: diet

Gluten-free products

Currently not recognized as gluten-free by

products with a gluten content level of 200 ppm (mg/kg) for products from which gluten is removed during production - based on wheat starch (the so-called “Scandinavian standard”).
The ADA and the National Food Authority (USA) gluten-free
products in which
gluten is absent
, i.e., not determined by modern methods, the sensitivity threshold of which is 1.5 mg/kg, and products containing <200 ppm are called
“low-gluten products.” gluten content"

Gluten containing products

Let's look at gluten-containing foods. This

: Rye, wheat, barley, oats and their processed products (flour and bread from corresponding cereals, bakery, pasta and confectionery products, cereals - wheat, semolina, bulgur, couscous, oatmeal, pearl barley, Hercules, oatmeal, pearl barley , barley, “Artek”, “Poltavskaya”, “7 grains”, “4 grains”, etc., bran, “Muesli”, baby cereals, bread, confectionery, pasta, pancakes, dumplings, manti, cutlets , breaded dishes, etc.)

Gluten Free Products

The following products do not contain gluten.

  • Cereals:

    rice, buckwheat, corn, millet (millet), Italian millet (chumiza), sago, sorghum, amaranth, quinoa, montina, teff.

  • Roots

    : potatoes, sweet potatoes, yams, tapioca, cassava.

  • Legumes:

    soybeans, peas, beans, lentils, chickpeas, mung beans.

  • Nuts, chestnuts, carob gum.
  • Vegetables and fruits.
  • Meat, fish, eggs.
  • Milk and natural fermented milk products (kefir, yogurt, fermented baked milk, yogurt, etc.).
  • Hard cheeses, butter and vegetable oil.

Products with hidden gluten

Products containing “hidden” gluten:

  • Sausages, frankfurters, semi-finished products from minced meat and fish.
  • Canned meat and fish, especially in tomato sauce.
  • Canned vegetables and fruits, especially tomato pastes and ketchups.
  • Ice cream, yoghurts, processed cheeses, margarines with gluten-containing stabilizers.
  • Some types of vinegars and salad sauces, mayonnaises.
  • Some types of soy sauces.
  • Concentrated dry soups, bouillon cubes.
  • Instant coffee, cocoa mixtures, teas for “quick preparation”.
  • Multi-component dry seasonings and spices.
  • Corn flakes when using barley molasses.
  • Imitation seafood: “crab” sticks, “crab” meat.
  • Caramel, soy and chocolate candies with filling, oriental sweets, industrial jam.
  • Kvass and alcoholic drinks - beer, whiskey, vodka, gin.
  • Some types of toothpaste, lipstick. Some medications (in excipients).
  • Nutritional supplements:

    dye annatto extracts E 160b, caramel colors E150a-E150d, oat gum E 411, maltol E 636, ethyl maltol 637, isomalt E953, maltitol and maltitol syrup E965, mono- and diglycerides of fatty acids E471.

Basic principles of therapeutic nutrition

  • It is vitally important to monitor the purity of products: they should not contain E-additives, preservatives, flavor enhancers, stabilizers, or dyes. Anything free from gluten and synthetic additives is safe.
  • Do not overload the body with food containing refined carbohydrates (potatoes, rice, corn, etc.). This can provoke a deterioration in the patient’s well-being and reduce the effectiveness of the diet. The diet should first of all be balanced. Only then will it be useful to you.

What can you eat if you are gluten intolerant and have diabetes as a comorbidity? An excellent solution is to add to the menu products containing natural plant ingredients: stevioside, amaranth, Jerusalem artichoke.

  • Foods with a predominance of starchy carbohydrates can lead to candidiasis, especially if immunity is at zero. In order not to fight a fungal-yeast infection, protect yourself from it: always have eggs, chicken, fish, lean meat and other animal products on your menu.

Drug treatment in the acute period of celiac disease

  • Correction of digestion processes with preparations of highly active microencapsulated pancreatic enzymes (Creon 1000 U for lipase/kg per day).
  • Infusion therapy - for severe diarrhea with dehydration and electrolyte disorders.
  • IV albumin – for severe nutritional disorders, which are accompanied by anorexia and metabolic disorders (hypoproteinemia, hypoglycemia)
  • Enterosorbents – against the background of severe diarrhea (smecta, enterosgel, filtrum, lactofiltrum, etc.)
  • The use of loperamide (Imodium) is not indicated
  • Correction of intestinal microflora disorders - the use of lactose-free probiotics (Primadophyllus, Linex)
  • Calcium malabsorption is corrected by administering calcium (per os or intravenously, depending on the severity) and prescribing vitamin D3 supplements.
  • Treatment of anemia - with severe iron deficiency and diarrhea syndrome - parenteral iron supplements, folic acid (per os).
  • In case of severe symptoms of hypovitaminosis, additional preparations of fat-soluble vitamins (A, E), C and group B are prescribed.
  • For hemorrhagic syndrome, Vicasol (vitamin K) is prescribed parenterally
  • The use of glucocorticoid drugs for celiac disease is indicated in cases of severe disease with significant impairment of physical development, for example, with grade III malnutrition with anorexia, and as replacement therapy for the correction of adrenal insufficiency. The drugs are prescribed in standard doses of prednisolone 1 mg/kg body weight, for a short period (2-3 weeks) followed by gradual withdrawal.

Challenges of following a gluten-free diet

  • Insufficient understanding by patients, parents and attending physicians of the need for strict and lifelong adherence to a gluten-free diet for celiac disease
  • Traditional in Russia, widespread use of wheat products and other gluten-containing grains
  • The inability to provide adequate nutrition for a child with celiac disease in a preschool, school, sanatorium, or summer camp is social deprivation of children.

    Lack of production of domestic gluten-free products, low availability and high cost of imported ones

  • The presence of “hidden gluten” in prepared foods, semi-finished products, canned food, seasonings and sauces
  • Lack of information from patients and treating doctors about the presence of gluten in products

Celiac disease in children. Kindergarten

Kindergarten and celiac disease:

When a child attends kindergarten, maintaining a gluten-free diet is impossible even with the efforts of cooks and teachers, since the child requires a separate menu, separate kitchen utensils for cooking, separate dishes and a table for eating. Organizing a gluten-free diet in kindergarten is only possible if there are specialized groups for children suffering from celiac disease.

The problem with gluten-free catering in the Krasnoyarsk Territory: Catering

(English cater - supply provisions; catering - public catering). In the Krasnoyarsk Territory, there is no well-functioning system for the existence of patients on a gluten-free diet: the choice of gluten-free products in city stores is very limited, there is no list of proven food products from local producers, and there is no special training system for preparing gluten-free dishes. In addition, no person with celiac disease can feel confident in cafes and restaurants in our city. All foreign guests with celiac disease who visit our city are in the same situation. For example, in Finland, where there are 20,000 people with celiac disease, in every cafe and restaurant, even in a very small town, when opening the menu you can see a mark next to the name of some dishes “GF” (Gluten Free) - this means that this dish can be ordered a person who follows a gluten-free diet.

Rating
( 1 rating, average 4 out of 5 )
Did you like the article? Share with friends:
For any suggestions regarding the site: [email protected]
For any suggestions regarding the site: [email protected]
Для любых предложений по сайту: [email protected]