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Crohn's disease (CD) is a chronic relapsing 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 predominantly in the intestine, although all parts of the gastrointestinal tract can be affected, including the esophagus, stomach, and oral cavity. Allocate BC with lesions 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 the stomach, or the duodenum, or the perianal region.
Nonspecific immune inflammation spreads over the entire thickness of the intestinal wall, has a regional character: zones of inflammatory infiltration with cellular elements (lymphocytes, plasma cells, to a lesser extent - neutrophils) alternate with relatively unaltered sections of the intestine. In the mucous membrane, in the infiltration zone, deep ulcers form, 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 and 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 affects more often people of working age (20-50 years) of both sexes. Relatives of the first line of patients with CD have a 10-fold higher risk of developing this disease than in the population.
Etiology. The causes of the disease are unknown. They suggest the etiological role of bacteria, viruses, food allergens, genetic factors (the familial nature of the disease was noted in 5% of cases). It is noted that BK is associated with histocompatibility antigen HLA-B27.
Pathogenesis. There are no exact ideas about the mechanisms of the disease development. Currently, the working hypothesis is the assumption of a violation of the body's immune response to the intestinal microflora in genetically predisposed persons. It is assumed that the organs of immunogenesis produce autoantibodies to the cells of the intestinal mucosa, as well as sensitized lymphocytes, which have a damaging effect. It is noted that the intestinal microflora plays an important role, since in BC there are significant violations of the intestinal microbiocenosis. A decrease in the number of bifidobacteria with a simultaneous increase in the number of enterobacteria and the appearance of enterobacteria with signs of pathogenicity are characteristic.
In the development of the inflammatory process, great importance is attached to proinflammatory cytokines, especially tumor necrosis factor-a (TNF-a), synthesized by different cell types (macrophages, T-lymphocytes, endothelial cells). In inflammation, TNF-a behaves as an active pro-inflammatory agent. The biological reactions associated with its hyperproduction are very extensive (in particular, the induction of free oxygen radical synthesis, an increase in vascular permeability, inhibition of inflammatory cell apoptosis, the induction of synthesis of IL-1 and IL-2, etc.). One of the most powerful inducers of TNF-a is bacterial lipopolysaccharides, which, when CD is abundant, are present in the lumen of the colon, therefore, disruption of the composition of microflora may be the cause of 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 extends to all layers of the intestinal wall. In the submucosal layer against the background of diffuse infiltration by lymphocytes and plasma cells, hyperplasia of the lymphoid follicles, which may ulcerate, is observed. Ulcers with CD have an elongated slit-like shape and penetrate deeply into the mucous and muscular layers, forming fistulas and abscesses. The presence of fistulas, strictures and intestinal stasis contributes to the development of dysbacteriosis. A common lesion of the small intestine causes severe absorption disorder syndrome (malabsorption). Reducing the absorption of iron, vitamin B12 and folic acid causes anemia, which is facilitated by repeated blood loss.
The occurrence of inflammation and ulceration in the intestines also leads to intoxication, profuse diarrhea, loss of body weight, electrolyte metabolism disorders.
Clinical picture. The clinical manifestations and nature of the course of the disease are determined by the severity of morphological changes, anatomical localization and extent of the pathological process, the presence of complications and extraintestinal lesions.
The manifestation of the actual intestinal lesions include abdominal pain, diarrhea, syndrome of insufficient absorption, damage to the anorectal region (fistula, fissures, abscesses), rectal bleeding (rarely). Non-intestinal symptoms include fever, anemia, weight loss, arthritis, erythema nodosum, aphthous stomatitis, eye damage (iritis, uveitis, episcleritis), 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 stage I of the diagnostic search, abdominal pain is noted, which occurs in almost all patients, more often they are dull or cramping (with a lesion of the colon). The maximum severity of pain is observed with the involvement of the small intestine. The causes of pain are diverse: a) involvement in the pathological process of the peritoneum; b) an increase in 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 impaired absorption; c) complications (partial intestinal obstruction, fistula, abscesses).
Patients also complain of diarrhea, which has a rather persistent nature. Stool frequency reaches 4-6 times / day, the mass of feces - more than 200 g / day, feces liquefied or watery. Diarrhea occurs after every meal, but maybe at night. The volume of the stool depends on the localization of the pathological process in the intestine: if a high part of the small intestine is affected, the volume of feces is greater than at the distal localization of the inflammatory process. Tenesmus occurs only with involvement of the anorectal region. Rectal bleeding, usually scant, occurs in half of the patients.
During the period of exacerbation, fever is observed, combined with general weakness and weight loss. The body temperature can rise to 39 ° C. In some cases, the temperature rises ahead of the local chi-cheek symptoms, this situation can last for a long time, which creates great diagnostic difficulties. Other The frequent extra intestinal manifestation of the disease is arthralgia in large joints.
Thus, during the collection of anamnesis, intestinal symptoms and systemic (extra-intestinal) manifestations are detected. These signs do not allow yet
formulate a specific diagnostic concept, but the direction of the diagnostic search can be determined. It is much more difficult when “common” signs (fever, weight loss, arthralgia, arthritis) dominate in the clinical picture.
At stage II of the diagnostic search, symptoms of the gastrointestinal tract are clarified in the form of pain on palpation of the abdomen (mainly around the navel), rumbling, painful hardening of the terminal ileum, pain, rumbling and "splashing noise" on palpation of the cecum. There is a decrease in body weight, especially with a long course of the disease. The decrease in body weight is primarily due to impaired absorption syndrome. The syndrome of impaired absorption has a complex pathogenesis and is caused by a number of factors: a) a decrease in the suction 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; g) violation of the absorption of bile acids, which leads to blocking the absorption of water and electrolytes. In addition, weight loss 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. At the same time, external anal lesions prevail over lesion of the mucous membrane of the rectum, in contrast to ulcerative colitis (UC), in which these ratios are reversed.
On examination, extra-intestinal manifestations may be detected in the form of arthritis of large joints (joint deflection), erythema nodosum, eye lesions.
In severe disease and severe impaired absorption, symptoms of hypovitaminosis and iron deficiency are noted: dry skin, hair loss, brittle nails, cheilitis, glossitis, gingival bleeding.
At the third stage of the diagnostic search, it is necessary to ensure the nature and extent of intestinal lesions, as well as assess the severity of metabolic disorders and extraintestinal lesions.
To make a final diagnosis, first of all, you need to perform an endoscopy (colonoscopy), which allows you to inspect the mucous membrane of the entire colon and terminal ileum. They reveal edema of the mucous membrane, the disappearance of the vascular pattern, small aphthous ulcers with the subsequent formation of deep slit-like cracks, which change the relief of the mucous membrane like “cobblestone”, the appearance of bowel strictures may occur. A biopsy of the intestinal mucosa allows the detection of characteristic morphological changes in the form of tuberculoid and sarcoid granulomas of the types that contain multinuclear giant Pirogov-Langhans cells. Similar changes in the mucous membrane are detected during gastroduodenoscopy (in cases of lesions of the upper gastrointestinal tract).
X-ray examination of the intestine (irrigoscopy, enteroscopy) in severe cases of the disease demonstrates segmentation of intestinal lesions 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 “cobblestone pavement”, pseudodiver diversions (representing deep ulcers,
^ drooping as a result of fibrous changes in the intestinal wall - “cord symptom”).
Laboratory blood tests can determine the degree and nature of anemia (iron deficiency, B12-deficient). For relapse of the disease, it is practical to increase the ESR, sometimes reaching significant values (50-60 mm / h). Biochemical examination of blood reflects disorders of protein, fat and electrolyte metabolism (hypoalbuminemia, hypo-hypidemia, hypoglycemia, hypocalcemia) caused by the severity of impaired absorption syndrome.
A test with D-xylose and vitamin B12 (Schilling test) is also used to identify a violation of absorption. In more detail on these tests, we stopped when describing chronic enteritis. Stool analysis involves microscopy, chemical and bacteriological examination. The lack 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 coprogram changes is determined by the severity of the disease and its phase (remission -
When other organs of the digestive system (liver, bile ducts, pancreas) are involved in the pathological process by laboratory and instrumental examination, appropriate changes can be detected.
Complications. Most of the complications of CD are a surgical problem: intestinal obstruction, bowel perforation with the development of abscesses and peritonitis, intestinal bleeding, the formation of entero-enteric, enteric-dermal, intestinal-vesicular and rectovaginal fistulas.
Diagnostics. The 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 there are situations when the general symptoms dominate for a long period: fever, weight loss, signs of vitamin deficiencies, non-specific laboratory parameters in the absence of local intestinal signs. This makes it difficult to timely diagnosis, forcing the doctor to assume a completely different disease. In any case, a large number of diseases that have similar features with CD are included in the diagnostic search range for CD. First of all, these are malignant tumors, chronic infections, systemic diseases (diffuse diseases of the connective tissue). Despite the excellence of the research methods, the diagnosis of CD is made 1–2 years after the first symptoms appear. If intestinal symptoms dominate, 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 (UC), chronic non-ulcerative colitis, chronic enteritis, colon cancer. In any case, in case of “intestinal” symptoms in a patient, CD should be included in the diagnostic search range.
The wording of the expanded clinical diagnosis is based on the following scheme: 1) the clinical form (taking into account the predominant lesion of one or other sections of the gastrointestinal tract); 2) the severity of
intestinal irradiation (taking into account endoscopy data); 3) the phase of the disease (re_ mission - exacerbation); 4) extraintestinal lesions; 5) complications.
Treatment. In the treatment of CD, the localization of the activity and duration of the disease, the age and the general condition of the patient should be taken into account.
Diet, approaching normal, should not contain poorly tolerated foods. If a small intestine is affected, with the presence of steatorrhea and fat intolerance, a diet high in protein and limiting fat, lactulose and coarse fibrous products is recommended. Etiological treatment of CD is impossible, since the etiology and pathogenesis of the disease are unknown. Nevertheless, sulfas-lasine, glucocorticoids, and metronidazole are among the first-line drugs.
When exacerbation of mild and moderate severity in the case of localization of the process in the ileum and large intestine, mesalazine is taken by 3-4 g / day orally with a gradual decrease in dose upon reaching remission (1 g / week) or sulphasalazine orally 3-6 g / day and then 2–4 g / day for 6–8 weeks with a gradual transition to a maintenance dose (half of the treatment), which lasts for at least 1 year. The drug is taken with food, which prevents irritation of the stomach. Perhaps the use of metronidazole orally at 10 mg / (kgsut), but for a long time this drug should not be prescribed because of the risk of peripheral polyneuropathy.
For acute exacerbations of severe and severe use of glucocorty-carteroid (GCS) drugs - orally prednisone 40–60 mg / day (up to 4 weeks) with a subsequent dose reduction (5 mg each week). Maintenance dose may be 5-10 mg for 6 months or more.
More than 50% of patients treated with GCS in the acute phase become steroid-dependent or steroid-resistant. Adding azathioprine to the GCS by 2.5 mg Dggsut or parenteral methotrexate (25 mg / week) increases the effectiveness of the treatment.
When diarrhea, antidiarrheal drugs (loperamide, reacec), enzyme preparations are prescribed. Hypoalbuminemia is corrected by the introduction of plasma, albumin solutions and amino acids, with electrolyte disturbances injected solutions of potassium, calcium.
Upon reaching remission, active drug therapy is stopped and switched to maintenance doses (sulfasalazine or mesalazine more than 3 g / day), the use of cytostatics is possible (azathioprine or metho-trexate in combination with small doses of GCS).
Replacement therapy, including vitamins B12, folic acid, and trace elements, is being conducted. Antidiarrheal drugs (loperamide, reacek) are prescribed if necessary. The duration of remission of BC is different, on average it is 2 years.
Forecast. Depends on the prevalence of lesions, the severity of the syndrome of impaired absorption and complications. Combined therapy can significantly alleviate the manifestations of the disease, but long-term 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 does not exist. Prevention comes down to the prevention of exacerbations, which is achieved by persistent treatment. Patients put on dispensary registration in time to identify the beginning exacerbation or complication. 332
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