New in the study of Crohn's disease. Etiology of Crohn's disease

People of any age get sick, but most often young people (from 15 to 35 years old). Among residents of Northern Europe, the disease is somewhat more common than in the south, and whites get sick more often than representatives of the Negroid or Asian races.

It is still not clear what exactly provokes the development of the disease. Wrong diet and stress can lead to exacerbation of the disease, but are not the root cause. In some cases, the appearance of the first symptoms is associated with taking non-steroidal anti-inflammatory drugs: ibuprofen, diclofenac and others.

Most doctors believe that for Crohn's disease to develop, several factors must coincide:

Genetic. More than 200 different genes have been identified that are more common in people with Crohn's disease than in other populations. 3 out of 20 patients have close relatives suffering from this disease. If one twin is diagnosed with Crohn's disease, the second has a 70% chance of developing it. The fact that this disorder is more common in certain ethnic groups(in particular, it occurs 3-4 times more often in Jews than in people of other nationalities), also indirectly confirms the role of genetics in the development of inflammation.
State immune system. According to available data, in Crohn's disease, a malfunction of the immune system leads to the formation of a specific protein (tumor necrosis factor alpha, TNF-alpha). This protein destroys all bacteria living in the intestines and damages the cells of the digestive organs.
Past illnesses, particularly childhood infections, can impair the immune system, increasing the likelihood of developing Crohn's disease.
Smoking is considered the main risk factor. Smokers are twice as likely to get the disease as non-smokers. According to doctors' observations, in patients with Crohn's disease who continue to smoke, the manifestations of inflammation are much more serious and they more often require surgery.
Lifestyle. Crohn's disease is more common in developed countries and less common in poor countries. An increase in incidence has been observed since 1950, which coincides with the increase in prosperity in Europe and North America. These facts have formed the basis of some theories about the connection between Crohn's disease and lifestyle, but none of them have been convincingly confirmed.

The pathogenesis of Crohn's disease (the mechanism of development) is now being actively studied, and various assumptions are put forward, the essence of which boils down to the following. Exposure to one of the factors (microorganisms, toxins, food components) causes an immune reaction, which, in turn, leads to damage to the cells of the digestive tract and the development of inflammation, which causes an additional immune response that aggravates pathological processes.

Differences between Ulcerative Colitis and Crohn's Disease

Because of their similarities, Crohn's disease and ulcerative colitis have been grouped together as inflammatory bowel diseases (IBD), which also includes collagenous and lymphocytic colitis.

There are 3 key differences between Crohn's disease and ulcerative colitis:

1.Localization of the process. Ulcerative colitis affects exclusively the large intestine, while Crohn's disease affects any part of the digestive tract (mouth, esophagus, stomach, small or large intestine, anus). In this case, ulcerative colitis affects only the inner layer of the intestinal wall (the mucous membrane), and Crohn's disease affects everything.

Prevalence of inflammation. In people with Crohn's disease, affected areas alternate with healthy ones; with ulcerative colitis, certain part intestine, which does not contain inclusions of healthy tissue.

Symptoms. As a rule, the main manifestations are the same, although blood in the stool is more typical of ulcerative colitis. Localization difference inflammatory process also leads to differences in symptoms, for example, when the mouth is affected, patients with Crohn's disease have sores on the tongue or between the gums and upper lip, and in case of inflammation of the anus - cracks, ulcers, fistulas, narrowings or infectious lesions.

Classification of Crohn's disease (forms of Crohn's disease, ICD-10 code)

There are several approaches to the classification of Crohn's disease, most based on the localization of the inflammatory process. But there are also more detailed approaches that take into account the patient’s age, the location of the inflammation, the form of Crohn’s disease (inflammatory, stenotic, fistulous) and the severity of the disease.

By International Classification The disease code of the 10th revision (ICD-10) for Crohn's disease is K50. Depending on the location and characteristics of the course, 4 subgroups are distinguished: Crohn's disease of the small intestine, Crohn's disease of the large intestine, other types of Crohn's disease and unspecified Crohn's disease.

Symptoms and signs of Crohn's disease

Signs of Crohn's disease depend on the location and stage of the inflammatory process. The severity of the disease in different people not the same. For some, the symptoms are not pronounced or develop gradually, appearing one after another and increasing over time, for others, the disease is very difficult from the very beginning. Crohn's disease - chronic illness, which is characterized by alternating exacerbations and quiet periods(remissions).

Symptoms may include:

diarrhea (diarrhea) is the most common symptom;
weakness;
slight increase in temperature;
pain and cramps in the abdominal area;
blood in stool (red or dark);
mouth ulcers;
lack of appetite and weight loss;
pain and itching in the anus.

At severe course diseases develop inflammation of the skin, eyes, joints, as well as hepatitis and cholangitis.

Crohn's disease in children may delay growth and puberty.

Diagnosis of Crohn's disease, tests

A gastroenterologist deals with the diagnosis and treatment of diseases of the digestive tract. During your first visit, be prepared to answer the following questions:

When did the first symptoms appear?

Are the symptoms always present or do they disappear and reappear?

have you noticed patterns associated with exacerbations (after stress, taking pills, a heavy dinner, etc.)

how much the problems are serious with health?

What medications are you taking or were you taking when the first symptoms appeared (you need to prepare a list)?

Based on the information collected and general clinical trial(palpation of the abdomen, examination oral cavity) the doctor forms a further plan comprehensive examination, which in most cases includes:

blood test - to detect anemia and indirect signs of infection;

general stool analysis - shows the digestibility of food, the presence of obvious or hidden blood, presence of inflammatory cells;

colonoscopy or flexible sigmoidoscopy to examine the inner surface of the intestine using a flexible tube with a video camera (endoscope and sigmoidoscope, respectively). In addition to a video camera, these devices are equipped with tools for taking biopsies, removing foreign bodies, cauterizing blood vessels;

Capsule endoscopy is a subtype of endoscopy in which the patient swallows a capsule camera that takes pictures while moving along the digestive tract. The images are transferred to a computer and then examined by a doctor to look for signs of Crohn's disease.

double balloon enteroscopy - a visualization method developed in 2001 thin section intestines (which is not accessible during colonoscopy). A long and thin endoscope is advanced through the intestine by alternately deflating the balloons fixed on it. As with an endoscope, the doctor can biopsy altered areas of the intestine or cauterize bleeding vessels. Such a study is carried out in cases where pathological areas in the small intestine are visible on images obtained using capsule endoscopy, but these data are not sufficiently informative.

visual diagnostics (MRI, CT, X-ray) (including with the introduction of a contrast agent).

Treatment of Crohn's disease

To date, Crohn's disease cannot be completely cured. But the reception modern medicines reduces inflammation and controls the course of the disease. Such therapy does not relieve a person of the disease, but significantly improves his quality of life. Best result Treatment is considered to be the transfer of the active phase into a state of long-term remission. In severe cases of Crohn's disease, surgery may be indicated.

Therapy includes the following groups drugs:

a) Anti-inflammatory medications are the first step to controlling Crohn's disease. Two main groups of drugs are used:

5-aminosalicylates (sulfasalazine and mesalazine) are prescribed for damage to the colon, but they have side effects(nausea, vomiting, diarrhea, increased heart rate and headache), so in modern medicine rarely used.

glucocorticosteroids (prednisolone) also have many side effects (hyperactivity, sleep disturbances, night sweats, intense facial hair growth), in some cases quite severe - diabetes, high arterial pressure, glaucoma, cataracts, osteoporosis, susceptibility to infectious diseases.
Some drugs newest generation have few negative effects, but they only “work” in certain cases and are prescribed when other medications do not help.

b) Immunosuppressants reduce inflammation by suppressing immune reactions, playing an important role in the development of the disease. They are taken alone or in combination with anti-inflammatory drugs. Immunosuppressants are a broad group of drugs that act on different components of the immune system. Selection of a specific drug and dose selection - difficult task due to differences in the effectiveness of use in different patients.

V) Antibacterial drugs prescribed additionally for infection. The most commonly used drugs for Crohn's disease are metronidazole and ciprofloxacin.

In order to eliminate the symptoms of the disease and improve the patient’s quality of life, symptomatic treatment. For diarrhea, antidiarrheals are prescribed, and for pain, painkillers. In case of anemia due to bleeding, iron supplements and vitamin B12 (necessary components for the formation of red blood cells) are added to the treatment regimen. Taking certain medications increases the risk of developing osteoporosis, which your doctor will prescribe calcium and vitamin D to prevent. better absorption food, nutrients are introduced into the body through a tube (special mixtures for tube feeding are used) or in the form of solutions directly into a vein ( parenteral nutrition).

If the reception medicines, lifestyle changes, diet or other treatment do not help, your doctor may recommend surgery. Its essence is to remove the affected area and connect the healthy ends of the digestive tract.

Surgery is also performed when abscesses (ulcers) occur in the intestinal wall. After the operation, the patient’s condition improves, but, unfortunately, in most cases, after some time the disease returns with the formation of a new focus next to the removed one (at the site of reunification). In order to delay relapse as much as possible, the patient is given a course of drug therapy after surgery.

Treatment of Crohn's disease with traditional methods

Treatment of Crohn's disease is a complex task, and achieving lasting positive result it can be difficult. Patients sometimes turn to alternative methods treatment. But before you start using any such “additional” method, you should discuss it with your doctor. What is most often used:

taking probiotics (cultures of “useful” microbes) and prebiotics (substances that create conditions favorable for the growth of “good” microorganisms);

acupuncture, hypnosis, breathing exercises and other relaxation and meditation techniques (to relieve pain syndrome, stress and anxiety);

fish oil (as a source of vitamins A and D, as well as polyunsaturated fatty acids);

turmeric, green tea(they are believed to have an anti-inflammatory effect).

Healthy lifestyle (quitting smoking, avoiding stressful situations and moderate physical exercise), and good nutrition improve the patient's condition.

Diet for Crohn's disease

To date, there is no evidence that any nutritional disorders can trigger the development of Crohn's disease. But it is known that the diet alleviates the patient’s condition and reduces the severity of complaints, which is especially important during exacerbations. There are general nutritional recommendations. But each patient may have his own list of foods that should be avoided. To compile such a list, it is recommended to keep a food diary and write down all the food you eat and its effect on your well-being. Analysis of records allows you to prepare an individual diet.

reduce the amount of dairy products;

choose products from low content fat;

reduce your intake of foods rich in fiber ( fresh vegetables, fruits, whole grain cereals);

give up alcohol, strong tea, coffee, spices;

Go to fractional meals(5-6 times in small portions);

drink enough water.

Complications of Crohn's disease

Uncontrolled Crohn's disease can lead to a number of complications:

scarring or narrowing of the intestinal lumen, which can lead to blockage (obstruction);

intestinal fistula (hole connecting the intestinal lumen with the skin, other organs (vagina, bladder) or abdominal cavity);

insufficient intake of nutrients, vitamins, and minerals into the blood;

colon cancer;

complications associated with taking medications (diabetes, glaucoma, cataracts, high blood pressure, osteoporosis, fractures, lymphoma, skin cancer).

Prognosis and prevention of Crohn's disease

Crohn's disease - serious illness, which requires regular medical control and taking medications. However, this pathology usually does not significantly affect life expectancy. In the first year after diagnosis, relapses occur in half of patients, while chronic course disease (if appropriate treatment is carried out), exacerbation is observed in only 10%. Most patients will have surgery sooner or later. According to statistics, in the first five years after diagnosis, 37% of patients undergo at least one operation, 12% undergo two or more; and 51% receive only drug therapy. In the first 10 years, 39% undergo 1 operation, 23% - 2 or more, 39% do without operations. In 34% of patients, the first 15 years after diagnosis are spent with 1 operation, with two or more – in 36%, without – in 30%.

Patients with upper small bowel disease have a slightly higher risk of mortality than any other site.

Since the exact causes of the disease are currently unknown, preventive measures have not been developed.

Crohn's disease and pregnancy

Women with Crohn's disease need to plan their pregnancies carefully to carry a child to term while the disease is in remission. It is necessary to review the list of medications you are taking with your doctor.

Crohn's disease (granulomatous ileitis) is a chronic inflammatory disease of an autoimmune nature, characterized by stenosis of intestinal segments, fistula formation and extraintestinal manifestations (arthritis, erythema nodosum, eye damage, etc.). Granulomatous inflammation of the terminal ileum was first described by V. Crohn in 1932. It was later established that terminal ileitis is only one of the forms of Crohn's disease.

Classification Clinically, acute chronic form. Anatomical characteristics: a) the lesion is limited to the small intestine; b) the ileocecal area is affected; c) the lesion is limited to the colon; d) segments of the small and large intestines are affected; e) combined damage to the intestine with other organs (stomach, esophagus). Complications: narrowing of the intestine, toxic megacolon, fistulas, amyloidosis, nephrolithiasis, cholelithiasis, B12-deficiency anemia. Approximate formulation of the diagnosis: 1.

Crohn's disease with damage to a segment of the ileum, a chronic, relapsing form, complicated by narrowing of the small intestine with partial small intestinal obstruction, B12-deficiency anemia. 2. Crohn's disease with damage to the ileocecal region and sigmoid colon, acute form, complicated by toxic dilatation of the colon.

Etiology

The etiology of Crohn's disease is still unknown. Currently, the role of viruses, bacteria and their metabolic products in the etiopathogenesis of the granulomatous inflammatory process is being discussed again.

Pathogenesis

The pathological process occurs in the submucosal layer of the intestine, where inflammatory infiltrates, having the appearance of granulomas. Granulomas consist of clusters of lymphocytes, in the center of which single giant cells of the Langhans type can be found. Unlike tuberculous granulomas, Crohn's disease never develops foci of caseous necrosis. Infiltration extends to both the mucous membrane and the serous layer intestinal wall. As a result, the intestinal wall becomes dense, the mucous membrane acquires an uneven texture, and multiple erosions and ulcers form on its surface, like cracks penetrating the entire intestinal wall. Sometimes ulcers perforate, which leads to the formation of intestinal fistulas. Scar changes walls can lead to narrowing of the intestinal lumen, development intestinal obstruction.

Epidemiology

The prevalence of the disease in European countries is 25-27 per 100,000 people. In approximately 90% of patients pathological process localized in typical place, for the rest - in other parts of the small intestine or in the large intestine.

Clinic

In patients with acute form diseases and with localization of the process in the terminal ileum correct diagnosis usually installed during laparotomy for suspected acute appendicitis. During the operation, a dense hyperemic area of the intestine and enlarged lymph nodes of the mesenteric root are detected, which makes it possible to diagnose Crohn's disease and the presence of complications (perforation, abscess, stenosis). In other cases, the correct diagnosis is established, as a rule, several years after the first clinical manifestations.

The clinical picture is often characterized by vague abdominal pain, loose stools, weight loss, and malaise. Symptoms of intestinal obstruction are usually mild.

Patients experience abdominal pain, aggravated by active peristalsis, loud rumbling and transfusion in the abdomen. Sometimes peristalsis of the small intestine is visible when shaking the anterior abdominal wall or palpating the intestine.

Characterized by increased body temperature, leukocytosis, increase in ESR. These symptoms are signs of the active phase of the disease.

During this period, patients may develop inflammatory infiltrates or intestinal conglomerates in the abdomen, most often in the right iliac region. As Crohn's disease progresses, patients develop systemic complications: erythema nodosum, pyoderma gangrenosum, perianal ulcerations, iridocyclitis, keratitis and conjunctivitis.

Acute arthritis and ankylosing spondylitis are common. Clear symptoms of impaired absorption are revealed: weight loss, trophic disorders (changes in nails, hair, mucous membranes).

Most patients have low levels of iron and protein in the blood serum, anemia, and osteoporosis. Characteristic radiological signs are areas of narrowing of the intestine with clear boundaries of the lesion, the so-called cord or suitcase handle symptoms.

They alternate with normal loops that have an expanded lumen. The relief of the mucous membrane in the narrowing zone is sharply changed and has a cellular pattern formed as a result of the flow of barium suspension into deep narrow ulcers.

The length of pathologically altered areas of the intestine varies from several centimeters to tens of centimeters. During endoscopic examination, the main attention is paid to the ileocecal zone and the terminal section of the ileum up to 50 cm in length.

In typical cases, the intestinal mucosa is sharply swollen, thickened, with rough folds, ulcerated, easily vulnerable, with numerous hemorrhages.

Differential diagnosis

Histological examination of biopsy specimens in most cases does not allow obtaining pathognomonic signs of Crohn's disease, since sarcoid-like granulomas with Langhans cells are located in the submucosal layer, areas of which are not included in the biopsy specimen. Therefore, characteristic histological features diseases can only be detected by examining a section of intestine resected during surgery. If symptoms of Crohn's disease are detected in a patient and changes suspicious for a granulomatous process are detected, it is necessary to exclude a number of diseases with segmental damage to the small intestine. These include tuberculous ileotiphlitis, small intestinal lymphoma, lymphogranulomatosis, diverticulosis, polyposis, nodular lymphoid hyperplasia. In addition, differentiation is often necessary with diseases that have a similar clinical picture (yersiniosis, ulcerative colitis, amoebic dysentery, bacillary dysentery, acute appeidicitis, ischemic abdominal syndrome, chronic enteritis).

Changes in the relief of the small intestine, reminiscent of those in granulomatous enteritis, may appear in patients with chronic circulatory failure in the upper system. mesenteric artery. Some other symptoms also give similarities: diarrhea, abdominal pain, weight loss. Main distinctive features syndrome chronic failure mesenteric circulation is vascular noise above the navel, a clear connection between pain and food intake. In difficult cases, differential diagnostic issues are resolved during selective angiography(mesentericography).

Diagnostics

Diagnosis of Crohn's disease is based on X-ray and endoscopic examination with a biopsy that reveals inflammatory lesion one or more areas gastrointestinal tract, usually spreading to all layers of the intestinal wall. Leukocytes in the stool indicate inflammation of the intestinal wall. In case of diarrhea (at the onset of the disease or during relapse), feces are examined for pathogens of intestinal infections, protozoa, helminth eggs and clostridia. In the diagnosis of Crohn's disease important role belongs X-ray examinations with contrast (irrigoscopy with double contrast, study of barium passage, intubation enterography - study of the small intestine with barium, which is administered through a nasogastric tube into duodenum). Scintigraphy with labeled leukocytes allows one to distinguish inflammatory lesions from non-inflammatory ones; it is used in cases where clinical picture does not correspond to X-ray data. Endoscopy of the upper or lower sections gastrointestinal tract (with a biopsy if necessary) allows you to confirm the diagnosis and clarify the location of the lesion. With colonoscopy in patients who have undergone surgery, it is possible to assess the condition of the anastomoses, the likelihood of relapse and the effect of treatment carried out after surgery. A biopsy can confirm the diagnosis of Crohn's disease, in particular, distinguish it from ulcerative colitis, exclude acute colitis, identify dysplasia or cancer.

Treatment

Activity index of Best et al. can also be used to monitor the effectiveness of treatment. With little disease activity good effect provides basic therapy with sulfasalazine.

In patients with more severe exacerbations, remission is achieved by administering hormones and using partial or complete parenteral nutrition. In some cases, patients require surgical treatment.

Patients with disease activity less than 150 points according to Best et al. Diet No. 4c is prescribed.

Products to which tolerance is reduced are excluded. With a high degree of activity (over 150 points), partial parenteral nutrition is prescribed.

Patients receive diet No. 4 with the addition of slag-free products (Viosorb, Survimed, Enpit). They contain short- and medium-chain fats, easily digestible proteins, and easily dissolve in water.

The dosage of drugs depends on the need for energy value. You should start taking it with small doses due to poor tolerance» associated with the possibility of osmotic diarrhea.

Usually, 1 tablespoon of the drug dissolved in 200 ml of water is first prescribed. If well tolerated, the patient can take this dose 3-4 times during the day.

Because of bad taste Slag-free nutrition can be administered by drip through gastric tube, administered intranasally. In addition, parenteral nutrition is used: solutions of amino acids (aminazole, alvesin, etc.

) 500 ml daily, 10% glucose solution 1-1.5 l, fat emulsions (intralipid, lipofundin) 500 ml daily. The transition to enteral nutrition (diet No. 4c) is carried out after the body temperature has decreased to normal levels, abdominal pain and diarrhea have stopped.

The basis drug therapy consist of sulfasalazine (salazopyrine) and corticosteroids. Sulfasalazine is prescribed for low activity of the inflammatory process (less than 150 points) 1 g 3 times a day for 2 weeks.

As it subsides inflammatory phenomena the dose of the drug is reduced to 1? tablets per day. If there is no effect, the dose of sulfasalazine can be increased to 6 g per day if there are no side effects (headache, nausea, skin rash).

With pronounced activity (over 150 points), as well as in the absence of effect from treatment with sulfasalazine, the use of prednisolone is indicated. The initial dose of the drug is 30-40 mg/day.

After 3-4 weeks, the dose of the drug is reduced by 5 mg per week. The occurrence of a relapse is prevented by administering hydrocortisone 125 units intravenously in 150 ml of isotonic sodium chloride solution daily in the first 3-5 days of the next reduction in the dose of prednisolone.

Treatment with sulfasalazine and prednisolone should be long-term and continue after the patient is discharged from the hospital under the supervision of a clinic physician. Patients can take the minimum doses of drugs, 1.5-1 g for sulfasalazine and 5-10 mg for prednisolone, for several months, especially if withdrawal syndrome cannot be avoided.

At long-term therapy corticosteroids in order to achieve stable clinical effect by using minimum doses(2.5-5 mg for prednisolone), the use of immunosuppressants - azathioprine or imuran - is justified. The drug is prescribed at a dose of 50 mg per day.

Patients with signs of immunosuppression should be prescribed levamisole. The dose of the drug is 2.5 mg/kg for 2 days with a break between courses of 6 days, a total of 3-4 courses.

In case of secondary infection (appearance high fever during therapy with sulfasalazine or prednisolone) and purulent complications semi-synthetic penicillins (methicillin, ampicillin, pentrexil) are used in a dose of 0.5-1 g intramuscularly every 4-6 hours. The course of treatment should usually not exceed 2 weeks due to the risk of developing severe dysbiosis.

At the same time apply symptomatic remedies to eliminate diarrhea, pain, anemia, etc.

Thus, if the patient continues to have diarrhea despite treatment with salazopyridazine or prednisolone, it is recommended to additionally prescribe cholestyramine or bilignin, which have the property of adsorbing bile acids. The latter may be poorly absorbed from the affected ileum and, once in the colon, cause the secretion of water and electrolytes, resulting in persistent diarrhea.

The drugs are prescribed 1-2 teaspoons 3 times a day 40 minutes before meals, washed down with water. The course of treatment is 7-14 days.

Imodium (loperamide), Reacek (Lomotil), and codeine phosphate also have an antidiarrheal effect. These medications increase intraintestinal pressure and therefore pose a certain danger, since in patients with ulcerative-destructive changes in the intestine they can cause intestinal perforation.

In this regard, in acute period diseases, these drugs are contraindicated. They can only be used on final stage inpatient treatment and in outpatient settings during remission.

In patients with localization of the process in ileum In connection with the possible development of B12-deficiency anemia, courses of replacement therapy are systematically carried out at the rate of 600 mcg of vitamin B12 intramuscularly every 6-8 weeks. Patients require essentially continuous maintenance therapy with both pathogenetic (salazopyridazine and prednisolone) and symptomatic drugs.

Experience shows that after complete withdrawal of drug therapy, relapses are usually inevitable within 6-12 months. Prevention of exacerbations is also achieved by selecting symptomatic medications.

Thus, cholestyramine can be used for a long time to eliminate chronic diarrhea. In these cases, the watery diarrhea induced by bile acids usually resolves quickly.

At the same time, regular intake of cholestyramine leads to steatorrhea, since the bile acids bound by it do not participate in the formation of micelles necessary for efficient digestion fat Therefore, along with cholestyramine, patients are recommended short-chain triglycerides contained in special nutritional mixtures (vivasorb, nutrinant, survimed), as well as in enpits.

They reduce steatorrhea. Cholestyramine therapy should also be combined with parenteral administration fat-soluble vitamins A, D, E and K.

Patients are prescribed a solution of retinol acetate in oil, 50,000 IU intramuscularly; 0.5% solution of ergocalciferol in alcohol, 10-15 drops orally; 5% solution of tocopherol acetate in oil 1 ml intramuscularly; 1% solution of Vikasol 1 ml intramuscularly daily for 2-3 weeks at least 2 times a year. Due to poor absorption nutrients and, in particular, fats, other dietary problems are possible in the treatment of patients with Crohn's disease.

It is known that with poor absorption fatty acid in conditions of shortage bile acids connect in the intestinal lumen not with oxalates, as is normal, but with calcium. As a result, most of the oxalates produced in the intestines are absorbed in the colon, which can contribute to the formation of kidney stones.

Therefore, in order to prevent urolithiasis, it is advisable to reduce the oxalate content in the diet and prescribe calcium gluconate internally. Spinach, tea, cocoa, chocolate, onions, gooseberries and plums contain especially high levels of oxalates, which the patient should be warned about.

Calcium gluconate is prescribed 0.5 g 1-2 times a day continuously. There are absolute and relative readings for surgical treatment of Crohn's disease.

TO absolute indications include perforation and peritonitis, toxic bowel dilatation, severe bleeding and complete obstruction. In these cases surgery should be carried out for urgent indications.

When septic complications associated with covered perforations, abscesses, fistulas, resistant to therapy, surgical treatment should be carried out as planned. Relative indications for surgical treatment arise when there is no effect from complex drug therapy and the patient has partial intestinal obstruction, as well as in patients with lesions of the skin, eyes and joints that are not amenable to conservative therapy.

There are no indications for surgical treatment only in patients with uncomplicated Crohn's disease, which is inferior to drug therapy. Although surgery and does not, as a rule, bring recovery and relapses occur in at least 40% of operated patients, but sooner or later indications for resection of the affected part of the intestine usually appear.

Before transferring the patient under observation and treatment to a surgeon, it is necessary to conduct a thorough X-ray and endoscopic examination of the entire gastrointestinal tract, since the simultaneous localization of the inflammatory process in several organs or intestinal loops can never be ruled out. After resection of the affected area of the intestine, the patient should be under the supervision of a gastroenterologist and, if necessary, he will be re-prescribed drug treatment.

Attention! The described treatment does not guarantee a positive result. For more reliable information, ALWAYS consult a specialist.

Crohn's disease is classified (together with nonspecific ulcerative colitis) to the group of chronic inflammatory diseases of the gastrointestinal tract of unknown etiology. Synonyms for this name are “regional”, “stenotic”, “segmental” enteritis (colitis), “terminal ileitis”.

The incidence of Crohn's disease has increased 4-6 times over the past 50 years and is 4-6 per 100,000 population, and the prevalence is about 70-75 per 100,000 population. The peak incidence occurs at the age of 15-35 years, and both men and women get sick equally often. Average age deceased - 38 years old.

Etiology and pathogenesis. The cause of Crohn's disease is not completely clear. It is believed that this is a polyetiological disease with a monopathogenetic mechanism of development. As probable etiological factors indicate the following:

a) infectious (mycobacterium tuberculosis, pseudomonas, measles virus);

b) allergic (food allergy to milk protein, hydrated fats, flavorings, disaccharides);

c) smoking (increases the likelihood of disease by 4 times);

d) genetic (a defect in chromosome 16 apparently explains cases of the disease in first-degree relatives, characterized by identical localization and variant of the clinical course of the disease).

Crohn's disease can be classified as a disease whose pathogenesis involves an autoimmune mechanism:

association with certain HLA antigens (in Russia, a positive association with the A3 and B14 antigens, as well as a negative association with the Aw 19 antigen has been established);

lymphoplasmatic infiltration in the lesion (pathognomonic morphological feature Crohn's disease is considered an epithelioid granuloma that affects all layers of the intestinal wall);

the presence of anti-tissue antibodies (anti-colon autoantibodies were found in 60-75% of patients, ANCA - antineutrophil cytoplasmic antibodies are found much less often);

systemicity of the pathological process (in addition to the digestive tube, extraintestinal lesions are found - polyarthritis, ankylosing spondylitis, ulcerative necrotizing dermatitis, thyroiditis, iridocyclitis, sclerosing cholangitis, etc.);

effectiveness in treatment with corticosteroids and immunosuppressants.

The pathogenesis of Crohn's disease is based on gross damage to immune mechanisms. Genetic predisposition (connection with HLA antigens) allows various damaging factors to occur (bacterial antigens, toxins, autoantigens and other currently unknown agents). Secondary effector mechanisms arising from such a symbiosis of genetic and external factors, lead to the development of nonspecific transmural immune inflammation in the mucous membrane of the intestinal wall. Impaired immune response is expressed primarily in selective activation T cell immunity and changes in the function of macrophages, which leads to the release of inflammatory mediators (interleukins) and the formation immune complexes at the site of the lesion. Damage to the epithelium caused by these factors is accompanied by the formation of new antigens, already of epithelial origin. Migration of mononuclear cells and neutrophils to the site of inflammation again leads to an increase in the release of interleukins and growth factors (inflammatory mediators). Thus, the vicious circle of pathogenesis closes.

In this case, the balance between pro-inflammatory and anti-inflammatory cytokines shifts towards the predominance of the former (primarily IL-1, IL-6, TNF, IFN). Proinflammatory cytokines are involved in the formation of epithelioid granulomas, consisting of T cells, monocytes and monophages. The interaction between them is regulated by cytokines (TNF, IFN, IL-1). Presence of TNF - required condition granuloma formation. This cytokine activates CD4+ lymphocytes and monocytes, stimulates the synthesis by endothelial cells of the powerful chemokine MCP-1, which has chemotactic activity and promotes the migration of monocytes to the site of granulomatous inflammation.

When the intestine is damaged, its absorption, secretory, reservoir and evacuation functions are disrupted. An integral reflection of these processes is insufficiency of digestion. This in turn leads to an imbalance of electrolytes, protein, fat, carbohydrate, vitamin and salt metabolism, and weight loss. Excess bacterial growth in the intestine and superinfection, further changing metabolism, inhibiting reparative processes and gland function internal secretion, bone marrow, lymphoid tissue, lead to involvement in the pathological process of the liver, kidneys, heart, nervous system, the emergence of lr i ralgia, trophic ulcers, necrotizing pyoderma and, as a consequence, the emergence of circulation of immune complexes, progressive cachexia, and sepsis.

Pathological picture. Crohn's disease can affect any part of the digestive tube - from the mouth to the rectum. Granulomatous inflammation affects the esophagus, stomach and duodenum in 3-5% of patients, only small intestine- in 25-30%, only the colon - in 30%, combined damage to both the small and large intestine is found in 40-45%, and the rectum is involved in the pathological process in approximately 20% of patients.

With this disease, damage to the anal area and perineum may develop, manifesting itself in the form of cracks and fistulas with the formation of a kind of paraproctitis.

A distinctive feature of the disease is a focal or multifocal, “jumping” nature with alternation of affected and unchanged segments with fairly clear boundaries between them. The length of one affected area can vary from 3-4 cm to 1 m or more.

Morphological changes in the intestinal wall depend on the stage of the disease. On early stage detect segmental edema and thickening of the intestinal wall, small deposits of fibrin on the serous membrane, and regional lymphadenitis.

At the stage of chronic inflammation, the wall of the organ sharply thickens, its lumen decreases significantly, the serous membrane becomes granular, and the intestine looks like a “garden hose.” Visible on the mucous membrane aphthous ulcers(pale, with a pink rim, 1-5 mm in diameter). Particularly characteristic are slit-like ulcers running in parallel rows in the longitudinal direction (“rake marks”). They intersect with the same transverse ulcers, which, against the background of swelling of the mucous membrane, resembles a “cobblestone street”. The ulcers are deep and can penetrate up to serous membrane, penetrate into abdominal wall and neighboring organs. In this case, dense adhesions develop, interintestinal, enterovesical, enterovaginal and external fistulas are formed.

On late stage chronic inflammation transforms into fibrosis of the intestinal wall with the formation of single or multiple scar strictures.

The activity of the process is confirmed by characteristic granulomatous infiltrates (non-caseating granulomas), they are detected in the submucosal layer, but they can cover the entire thickness of the intestinal wall and are found even in neighboring lymph nodes. According to biopsy data, they are found in 30-50% of patients; when studying material removed during surgery - in 50-60% of patients. The granuloma consists of clusters of epithelioid histiocytes with or without Langhans giant cells, surrounded by lymphocytes. They also find local lymphoid hyperplasia, deep fissures, segmental fibrosis, crypt abscesses (cryptitis) occur in the colon.

Classification of Crohn's disease

By location of the lesion:

a) isolated (esophagitis, gastritis, duodenitis, jeunitis, ileitis, colitis, proctitis);

b) combined (ileocolitis, etc.).

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Crohn's disease is classified (together with ulcerative colitis) as a group of chronic inflammatory diseases of the gastrointestinal tract of unknown etiology. Synonyms for this name are “regional”, “stenotic”, “segmental” enteritis (colitis), “terminal ileitis”.

Etiology and pathogenesis. The cause of Crohn's disease is not completely clear. It is believed that this is a polyetiological disease with a monopathogenetic mechanism of development. The following are indicated as probable etiological factors:

a) infectious (mycobacterium tuberculosis, pseudomonas, measles virus);

b) allergic (food allergy to milk protein, hydrated fats, flavoring additives, disaccharides);

c) smoking (increases the likelihood of disease by 4 times);

d) genetic (a defect in chromosome 16 apparently explains cases of the disease in first-degree relatives, characterized by identical localization and variant of the clinical course of the disease).

Crohn's disease can be classified as a disease whose pathogenesis involves an autoimmune mechanism:

association with certain HLA antigens (in Russia, a positive association with the A3 and B14 antigens, as well as a negative association with the Aw 19 antigen has been established);

lymphoplasmatic infiltration in the lesion (the pathognomonic morphological sign of Crohn's disease is considered to be epithelioid granuloma, affecting all layers of the intestinal wall);

the presence of anti-tissue antibodies (anti-colon autoantibodies were found in 60-75% of patients, ANCA - antineutrophil cytoplasmic antibodies are found much less often);

effectiveness in treatment with corticosteroids and immunosuppressants.

The pathogenesis of Crohn's disease is based on gross damage to immune mechanisms. Genetic predisposition (connection with HLA antigens) allows various damaging factors to occur (bacterial antigens, toxins, autoantigens and other currently unknown agents). Secondary effector mechanisms that arise from such a symbiosis of genetic and external factors lead to the development of nonspecific transmural immune inflammation in the mucous membrane of the intestinal wall. The disruption of the immune response is expressed primarily in the selective activation of T-cell immunity and changes in the function of macrophages, which leads to the release of inflammatory mediators (interleukins) and the formation of immune complexes in the lesion. Damage to the epithelium caused by these factors is accompanied by the formation of new antigens, already of epithelial origin. Migration of mononuclear cells and neutrophils to the site of inflammation again leads to an increase in the release of interleukins and growth factors (inflammatory mediators). Thus, the vicious circle of pathogenesis closes.

In this case, the balance between pro-inflammatory and anti-inflammatory cytokines shifts towards the predominance of the former (primarily IL-1, IL-6, TNF, IFN). Proinflammatory cytokines are involved in the formation of epithelioid granulomas, consisting of T cells, monocytes and monophages. The interaction between them is regulated by cytokines (TNF, IFN, IL-1). The presence of TNF is a prerequisite for the formation of granuloma. This cytokine activates CD4+ lymphocytes and monocytes, stimulates the synthesis by endothelial cells of the powerful chemokine MCP-1, which has chemotactic activity and promotes the migration of monocytes to the site of granulomatous inflammation.

When the intestine is damaged, its absorption, secretory, reservoir and evacuation functions are disrupted. An integral reflection of these processes is insufficiency of digestion. This in turn leads to an imbalance of electrolytes, protein, fat, carbohydrate, vitamin and salt metabolism, and weight loss. Excessive bacterial growth in the intestine and superinfection, further changing the metabolism, inhibit reparative processes, the function of the endocrine glands, bone marrow, lymphoid tissue, lead to the involvement of the liver, kidneys, heart, nervous system in the pathological process, the appearance of pulmonary diseases, trophic ulcers, necrotizing pyoderma and, as a consequence, the emergence of circulation of immune complexes, progressive cachexia, and sepsis.

Pathological picture. Crohn's disease can affect any part of the digestive tube - from the mouth to the rectum. Granulomatous inflammation affects the esophagus, stomach and duodenum in 3-5% of patients, only the small intestine - in 25-30%, only the large intestine - in 30%, combined damage to both the small and large intestine is found in 40-45%, and the rectum is involved in the pathological process in approximately 20% of patients.

With this disease, damage to the anal area and perineum may develop, manifesting itself in the form of cracks and fistulas with the formation of a kind of paraproctitis.

Morphological changes in the intestinal wall depend on the stage of the disease. At an early stage, segmental edema and thickening of the intestinal wall, small deposits of fibrin on the serous membrane, and regional lymphadenitis are detected.

At the stage of chronic inflammation, the wall of the organ sharply thickens, its lumen decreases significantly, the serous membrane becomes granular, and the intestine looks like a “garden hose”. Aphthous ulcers are visible on the mucous membrane (pale, with a pink rim, 1-5 mm in diameter). Particularly characteristic are slit-like ulcers running in parallel rows in the longitudinal direction (“rake marks”). They intersect with the same transverse ulcers, which, against the background of swelling of the mucous membrane, resembles a “cobblestone street”. The ulcers are deep, can penetrate to the serous membrane, and penetrate into the abdominal wall and neighboring organs. In this case, dense adhesions develop, interintestinal, enterovesical, enterovaginal and external fistulas are formed.

At a late stage, chronic inflammation transforms into fibrosis of the intestinal wall with the formation of single or multiple scar strictures.

The activity of the process is confirmed by characteristic granulomatous infiltrates (non-caseating granulomas), they are detected in the submucosal layer, but they can cover the entire thickness of the intestinal wall and are found even in neighboring lymph nodes. According to biopsy data, they are found in 30-50% of patients; when studying material removed during surgery - in 50-60% of patients. The granuloma consists of clusters of epithelioid histiocytes with or without Langhans giant cells, surrounded by lymphocytes. Local lymphoid hyperplasia, deep fissures, segmental fibrosis are also found, and crypt abscesses (cryptitis) occur in the colon.

Classification of Crohn's disease

By location of the lesion:

a) isolated (esophagitis, gastritis, duodenitis, jeunitis, ileitis, colitis, proctitis);

b) combined (ileocolitis, etc.).