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Crohn's disease

Crohn's disease (CD) is a chronic recurrent disease of unknown etiology, characterized by granulomatous inflammation with segmental lesions of different parts of the digestive tract. The pathological process in CD is localized mainly in the intestine, although all parts of the gastrointestinal tract, including the esophagus, stomach and mouth, can be affected. Allocate CD with lesion of the ileum (terminal ileitis) - 30-35%; ileocecal department - about 40%; colon, including the anorectal zone, - 20%; small intestine - 10%. In 5% of cases, the disease can debut with damage to the esophagus or stomach, or duodenum, or perianal region.

Nonspecific immune inflammation extends to the entire thickness of the intestinal wall, has a regional character: zones of inflammatory infiltration by cellular elements (lymphocytes, plasma cells, to a lesser extent neutrophils) alternate with relatively unchanged areas of the intestine. Deep ulcers form in the mucous membrane, in the infiltration zone, abscesses and fistulas develop, followed by scarring and narrowing of the intestinal lumen. The extent of damage to the digestive tract in CD is very different: from 3-5 cm to 1 m or more.

The prevalence of CD in different regions of the world varies widely - 20-150 cases per 100,000 population. It is noted that BC is more likely to affect people of working age (20-50 years) of both sexes. Relatives of the first line of patients with CD have a 10 times higher risk of developing this disease than in the population.

Etiology. The causes of the disease are unknown. Assume the etiological role of bacteria, viruses, food allergens, genetic factors (the family nature of the disease is noted in 5% of cases). It is noted that CD is associated with the histocompatibility antigen HLA-B27.

Pathogenesis. There are no exact ideas about the mechanisms of the development of the disease. Currently, a working hypothesis is the assumption of a violation of the body's immune response to the intestinal microflora in genetically predisposed individuals. It is believed that the organs of immunogenesis produce autoantibodies to the cells of the intestinal mucosa, as well as sensitized lymphocytes that have a damaging effect. It was noted that intestinal microflora plays an important role, since in CD significant violations of the intestinal microbiocenosis are detected. A characteristic decrease in the number of bifidobacteria with a simultaneous increase in the number of enterobacteria and the appearance of enterobacteria with signs of pathogenicity.

In the development of the inflammatory process, great importance is attached to pro-inflammatory cytokines, in particular tumor necrosis factor-a (TNF-a), synthesized by different types of cells (macrophages, T-lymphocytes, endothelial cells). In inflammation, TNF-a behaves as an active pro-inflammatory agent. The biological reactions associated with its overproduction are very extensive (in particular, the induction of the synthesis of free oxygen radicals, increased vascular permeability, inhibition of apoptosis of inflammatory cells, the induction of the synthesis of IL-1 and IL-2, etc.). One of the most powerful inducers of TNF-a is bacterial lipopolysaccharides, which are present in excess in the lumen of the colon with CD, therefore, a violation of the microflora composition can cause an increase in the level of this cytokine. In addition, TNF-a is involved in the formation of inflammatory granulomas.

The inflammatory process in CD begins in the submucosal layer and spreads to all layers of the intestinal wall. In the submucosal layer against the background of diffuse infiltration by lymphocytes and plasma cells, hyperplasia of lymphoid follicles is noted, which can ulcerate. Ulcers in CD are elongated, slit-like and penetrate deeply into the mucous and muscle layers, forming fistulas and abscesses. The presence of fistulas, strictures and intestinal stasis contributes to the development of dysbiosis. A common lesion of the small intestine causes severe malabsorption syndrome (malabsorption). Reduced absorption of iron, vitamin B12 and folic acid causes anemia, which is also facilitated by repeated blood loss.

The occurrence of an inflammatory process and ulceration in the intestine also leads to intoxication, profuse diarrhea, weight loss, and disturbances in electrolyte metabolism.

The clinical picture. Clinical manifestations and the nature of the course of the disease are determined by the severity of morphological changes, the anatomical localization and extent of the pathological process, the presence of complications and extraintestinal lesions.

The manifestation of intestinal lesions proper includes abdominal pain, diarrhea, syndrome of insufficient absorption, lesions of the anorectal region (fistulas, fissures, abscesses), rectal bleeding (rarely). Extra-intestinal symptoms include fever, anemia, weight loss, arthritis, erythema nodosum, aphthous stomatitis, eye lesions (iritis, uveitis, episiscleritis), and secondary amenorrhea in women. However, despite the significant variability of clinical manifestations in CD, abdominal pain, diarrhea, and weight loss dominate in 90% of cases.

At the first stage of the diagnostic search, abdominal pain is noted that occurs in almost all patients, more often they are dull or cramping in nature (with damage to the colon). The maximum severity of pain is observed when the small intestine is involved in the process. The causes of pain are diverse: a) involvement of the peritoneum in the pathological process; b) increased pressure in the lumen of the intestine as a result of increased gas formation and an increase in the volume of intestinal contents due to malabsorption; c) complications (partial intestinal obstruction, fistulas, abscesses).

Patients also complain of diarrhea, which is quite persistent in nature. The frequency of stool reaches 4-6 times / day, the mass of feces - more than 200 g / day, feces liquefied or watery. Diarrhea occurs after each meal, but may be at night. The volume of stool depends on the localization of the pathological process in the intestine: with the defeat of the high sections of the small intestine, the volume of feces is greater than with the distal localization of the inflammatory process. Tenesmus is noted only when the anorectal region is involved in the process. Rectal bleeding, usually mild, occurs in half of the patients.

During an exacerbation, a fever is noted, combined with general weakness and a decrease in body weight. Body temperature can rise to 39 ° C. In some cases, a temperature increase “outstrips” the local intestinal symptoms, this situation can continue for a long time, which creates great diagnostic difficulties. Another Common extraintestinal manifestation of the disease is arthralgia in large joints.

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Thus, when collecting an anamnesis, intestinal symptoms and systemic (extraintestinal) manifestations are revealed. These signs do not yet allow

formulate a specific diagnostic concept, but the direction of the diagnostic search can be determined. It is much more difficult when the "general" signs dominate in the clinical picture (fever, weight loss, arthralgia, arthritis).

At the second stage of the diagnostic search, the symptoms of the gastrointestinal tract are specified in the form of pain during palpation of the abdomen (mainly around the navel), rumbling, painful compaction of the terminal ileum, pain, rumbling and “splashing noise” during palpation of the cecum. A decrease in body weight is noted, especially with a long course of the disease. Weight loss is primarily due to malabsorption syndrome. The syndrome of impaired absorption has a complex pathogenesis and is due to several factors: a) a decrease in the absorption surface of the intestine due to the inflammatory process of the mucous membrane; b) deficiency of intestinal enzymes (disaccharidase, lactase); c) a decrease in the activity of pancreatic enzymes; d) impaired absorption of bile acids, which leads to blocking the absorption of water and electrolytes. In addition, a decrease in body weight is associated with a decrease in food intake due to anorexia (especially during an exacerbation of the disease).

In 25% of cases, perianal lesions can be detected: swelling of the skin around the anal sphincter, fissures and ulceration of the sphincter, fistulas and perianal abscesses. In this case, external anal lesions prevail over lesions of the rectal mucosa, in contrast to ulcerative colitis (ULC), in which these ratios are reversed.

On examination, extraintestinal manifestations in the form of arthritis of large joints (joint configuration), erythema nodosum, and eye damage can be detected.
In severe illness and severe malabsorption, symptoms of hypovitaminosis and iron deficiency are noted: dry skin, hair loss, brittle nails, cheilitis, glossitis, bleeding gums.

At the III stage of the diagnostic search, it is necessary to verify the nature and extent of intestinal lesions, as well as to assess the severity of metabolic disorders and extraintestinal lesions.

To make a final diagnosis, first of all, it is necessary to perform endoscopy (colonoscopy), which allows you to examine the mucous membrane of the entire colon and terminal ileum. Puffiness of the mucous membrane, the disappearance of the vascular pattern, small aphthous ulcers with the subsequent formation of deep slit-like cracks that change the relief of the mucous membrane as a “cobblestone bridge” are revealed, intestinal strictures may occur. A biopsy of the intestinal mucosa allows detecting characteristic morphological changes in the form of granulomas of the tuberculoid and sarcoid types, containing multinuclear giant Pirogov-Langhans cells. Similar changes in the mucous membrane are detected with gastroduodenoscopy (in cases of damage to the upper gastrointestinal tract).

An X-ray examination of the intestine (irrigoscopy, enteroscopy) in severe cases of the disease demonstrates the segmental nature of the bowel lesion with the presence of unchanged sections of the intestine between the affected segments. In the area of ​​the lesion, a wavy or uneven contour of the intestine, longitudinal ulcers forming the relief of the “cobblestone pavement”, pseudodiverticula (which are deep ulcers,

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^ drooping as a result of fibrotic changes in the intestinal wall - “symptom of the cord”).

A laboratory blood test allows you to determine the degree and nature of anemia (iron deficiency, B12 deficiency). For a relapse of the disease, an elevated ESR, sometimes reaching significant values ​​(50-60 mm / h), is characteristic. A biochemical blood test reflects violations of protein, fat and electrolyte metabolism (hypoalbuminemia, hypo-ipidemia, hypoglycemia, hypocalcemia), due to the severity of the syndrome of impaired absorption.

To detect malabsorption, a test with D-xylose and vitamin B12 (Schilling test) is also used. In more detail on these tests we stopped at the description of chronic enteritis. Analysis of feces involves microscopy, chemical and bacteriological studies. Insufficiency of digestion and absorption in the small intestine is manifested by a large number of muscle fibers, a significant amount of fatty acids and soaps; a small amount of connective tissue, neutral fat and iodophilic flora is determined. The degree of change in the coprogram is determined by the severity of the disease and its phase (remission -

exacerbation).

When other organs of the digestive system (liver, biliary tract, pancreas) are involved in the pathological process by laboratory and instrumental research, corresponding changes can be detected.

Complications Most of the complications of CD are a surgical problem: intestinal obstruction, perforation of the intestine with the development of abscesses and peritonitis, intestinal bleeding, the formation of entero-enteric, intestinal-cutaneous, intestinal and rectovaginal fistulas.

Diagnostics. Recognition of the disease in a developed form in the presence of pain and typical intestinal symptoms, increased ESR is not difficult and is based on a combination of endoscopic, radiological and morphological data indicating focal, asymmetric, transmural and granulomatous inflammation. However, quite often situations arise when for a long period general symptoms dominate: fever, weight loss, signs of hypovitaminosis, nonspecific laboratory parameters in the absence of local intestinal symptoms. This significantly complicates timely diagnosis, forcing the doctor to assume a completely different disease. In any case, a large number of diseases that have similar features to CD are included in the circle of the diagnostic search for CD. First of all, these are malignant formations, chronic infections, systemic diseases (diffuse diseases of the connective tissue). Despite the perfection of research methods, the diagnosis of CD is made 1-2 years after the onset of the first symptoms. If "intestinal" symptoms dominate, then the diagnosis can be made much earlier. In the presence of "intestinal" symptoms, differential diagnosis is carried out with intestinal infections (dysentery, salmonellosis), ulcerative colitis (ULC), chronic non-ulcer colitis, chronic enteritis, colon cancer. In any case, with "intestinal" symptoms in a patient, CD should be included in the circle of the diagnostic search.

A detailed clinical diagnosis is formulated according to the following scheme: 1) clinical form (taking into account the predominant lesion of certain sections of the gastrointestinal tract); 2) the severity of

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intestinal rash (taking into account the data of endoscopy); 3) phase of the disease (re_ mission - exacerbation); 4) extraintestinal lesions; 5) complications.

Treatment. When treating CD, the localization of the process activity and duration of the disease, age and general condition of the patient should be taken into account.

Diet, approaching normal, should not contain poorly tolerated foods. For lesions of the small intestine with the presence of steatorrhea and fat intolerance, a diet with a high protein content and restriction of fat, lactulose and coarse fiber products is recommended. The etiological therapy of CD is impossible, since the etiology and pathogenesis of the disease are unknown. Nevertheless, sulfas-lasin, glucocorticoids and metronidazole are classified as first-line drugs.

With exacerbation of mild to moderate severity in the case of localization of the process in the ileum and colon, it is shown that mesalazine is taken 3-4 g / day orally with a gradual dose reduction when remission is achieved (1 g / week) or sulfasalazine orally 3-6 g / day, and then 2-4 g / day for 6-8 weeks with a gradual transition to a maintenance dose (half therapeutic), which lasts at least 1 year. The drug is taken with food, which prevents stomach irritation. It is possible to use metronidazole orally at 10 mg / (kgsut), however, this drug should not be prescribed for a long time because of the danger of developing peripheral polyneuropathy.

For exacerbations of moderate severity and severe use glucocortiosteroid (GCS) drugs - inside prednisolone at 40-60 mg / day (up to 4 weeks), followed by a dose reduction (5 mg every week). The maintenance dose can be 5-10 mg for 6 months or more.

More than 50% of patients receiving corticosteroids in the exacerbation phase become steroid-dependent or steroid-resistant. Adding to the GCS azathioprine inside of 2.5 mgDcgsut) or parenteral methotrexate (25 mg / week) increases the effectiveness of treatment.

With diarrhea, antidiarrheal drugs (loperamide, reasek), enzyme preparations are prescribed. Hypoalbuminemia is corrected by the introduction of plasma, solutions of albumin and amino acids, with electrolyte disturbances, solutions of potassium and calcium are introduced.

Upon reaching remission, active drug therapy is stopped and transferred to maintenance doses (sulfasalazine or mesalazine more than 3 g / day), it is possible to use cytostatics (azathioprine or meto-traxate in combination with small doses of corticosteroids).

Substitution therapy is carried out, including vitamins B12, folic acid, trace elements. Antidiarrheal drugs (loperamide, reasek) are prescribed if necessary. The duration of remission of CD is different, on average, it is 2 years.

Forecast. It depends on the prevalence of the lesion, the severity of the syndrome of impaired absorption and complications. Combination therapy can significantly alleviate the manifestations of the disease, but prolonged remission usually does not occur. Surgical interventions in the pathology of the anorectal region improve the condition of patients. With adequate treatment, patients can "coexist" with their disease and lead a full life. With the development of complications, the prognosis is poor. Prevention Specific methods of prevention do not exist. Prevention is reduced to the prevention of exacerbations, which is achieved by persistent treatment. Patients are put on a dispensary account in order to promptly identify a beginning exacerbation or complication. 332
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Crohn's disease

  1. CROHN'S DISEASE
    — неспецифический инфекционный воспалительный и гранулематозно-язвенный процесс, поражающий различные отделы пищеварительного тракта от пищевода до прямой кишки. По локализации процесса различают: грануле-матозный — эзофагит, гастрит, энтерит, илеоколит, колит; регионарный илеит, терминальный илеит. Чаще поражается тонкая и толстая кишка. Классификация Единой общепринятой
  2. Крона болезнь
    Болезнь Крона, также известная как ИЛБИТ, - это воспаление подвздошной кишки, последнего участка тонкой кишки. Начало этой болезни может быть очень острым и похожим на аппендицит, но чаще всего она начинается медленно и скрыто. Основные симптомы начального этапа болезни Крона - постоянный или перемежающийся понос, который сопровождается болями в животе. Развиваясь, эта болезнь принимает
  3. Болезнь Крона.
    В 1932 г. В.В.Сrohn дал полное описание клиники и морфологии заболевания, при котором имеет место изолированное поражение терминального отдела подвздошной кишки — терминальный илеит, и с этого времени заболевание носит название болезни Крона. В дальнейшем было показано, что при этом заболевании поражаются все отделы желудочно-кишечного тракта, начиная с полости рта и заканчивая перианальной
  4. 5.10. БОЛЕЗНЬ КРОНА
    Цель фармакотерапии: достижение в максимально короткие сроки ремиссии, устранение имеющихся осложнений, их предупреждение и профилактика рецидивов. Тактика применения лекарственных средств при болезни Крона (их сочетание, дозировки, характер воздействия - местный или системный, длительность лечения) зависит от фазы настоящего заболевания (обострение - его тяжесть, неполная ремиссия, ремиссия),
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  6. Болезни кишечника. Инфекционнные энтероколиты (дизентерия, брюшной тиф, холера). Nonspecific ulcerative colitis. Болезнь Крона. Ишемическая болезнь кишечника. Аппендицит. Рак толстой кишки.
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  7. БОЛЕЗНЬ КРОНА (шифр К 50)
    Болезнь Крона - хроническое гранулематозное поражение желудочно-кишечного тракта, в 90% случаев с избирательным вовлечением в процесс терминального отдела подвздошной кишки (терминальный илеит), в 50% случаев с сочетанным поражением толстой и тонкой кишки (илеоколит). Клиника: боли внизу живота, чаще в правой подвздошной области, усиливающиеся после еды; поносы; анорексия, слабость, снижение
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