Inflammatory pseudopolyps. Diseases. Treatment of pseudopolyposis colon

The term "inflammatory bowel disease" is a collective term and is usually used to refer to ulcerative colitis and Crohn's disease, since they have much in common in etiopathogenesis and clinical picture. The etiology of both diseases is still unknown, and their natural history and response to treatment are unpredictable. This term is particularly useful in differentiating between these two diseases and other inflammatory bowel diseases with a well-known etiology, such as infectious, ischemic, or radiation.

Definition.

Ulcerative colitis is a chronic recurrent disease of the colon of unknown etiology, characterized by hemorrhagic-purulent inflammation of the colon with the development of local and systemic complications.

Epidemiology.

Accurate data on the prevalence of ulcerative colitis is difficult to obtain, since mild cases often go unreported, especially in the initial period of the disease. These patients are usually observed in non-specialized outpatient facilities and are difficult to account for. Ulcerative colitis is most common in urbanized countries, particularly in Europe and North America. In these regions, the incidence of ulcerative colitis (primary incidence) ranges from 4 to 20 cases per 100,000 population, averaging 8-10 cases per 100,000 population per year. The prevalence of ulcerative colitis (number of patients) is 40-117 patients per 100,000 inhabitants. The largest number of cases occurs between the ages of 20-40 years. The second peak of incidence is observed in the older age group - after 55 years. The highest mortality rates are observed during the 1st year of the disease due to cases of extremely severe fulminant course of the disease and 10 years after its onset due to the development of colorectal cancer in a number of patients.

The role of environmental factors, in particular smoking, remains unclear. Numerous epidemiological studies have shown that ulcerative colitis is more common in non-smokers. This even made it possible to propose nicotine as a therapeutic agent. People who have had an appendectomy have a lower risk of developing ulcerative colitis, as do people who do excessive exercise. The role of dietary factors in ulcerative colitis is much less than in Crohn's disease. Compared to healthy individuals, the diet of patients suffering from ulcerative colitis contains less dietary fiber and more carbohydrates. Patients with ulcerative colitis have a history of childhood infectious diseases more often than the general population.

Etiology.

The exact etiology of ulcerative colitis is currently unknown. Three main concepts are discussed:

1. The disease is caused by direct exposure to some exogenous environmental factors that have not yet been established. Infection is considered the main cause.

2. Ulcerative colitis is an autoimmune disease. In the presence of a genetic predisposition of the body, the influence of one or more triggering factors triggers a cascade of mechanisms directed against its own antigens. A similar pattern is characteristic of other autoimmune diseases.

3. This is a disease caused by an imbalance of the immune system of the gastrointestinal tract. Against this background, exposure to a variety of unfavorable factors leads to an excessive inflammatory response, which occurs due to hereditary or acquired disorders in the regulatory mechanisms of the immune system.

Pathogenesis.

Numerous mechanisms of tissue and cellular damage are involved in the development of inflammation in ulcerative colitis.

Bacterial and tissue antigens cause stimulation of T and B lymphocytes. With an exacerbation of ulcerative colitis, a deficiency of immunoglobulins is detected, which promotes the penetration of microbes, compensatory stimulation of B cells with the formation of immunoglobulins M and G. Deficiency of T suppressors leads to an increase in the autoimmune reaction. Enhanced synthesis of immunoglobulins M and G is accompanied by the formation of immune complexes and activation of the complement system, which has a cytotoxic effect, stimulates the chemotaxis of neutrophils and phagocytes with the subsequent release of inflammatory mediators, which cause the destruction of epithelial cells. Among the inflammatory mediators, the cytokines IL-1ß, IF-y, IL-2, IL-4, IL-15 should be mentioned first of all, which affect the growth, movement, differentiation and effector functions of numerous cell types involved in the pathological process in ulcerative colitis . In addition to pathological immune reactions, active oxygen and proteases have a damaging effect on tissues; a change in apoptosis, i.e., the mechanism of cell death, is noted.

An important role in the pathogenesis of ulcerative colitis is played by disruption of the barrier function of the intestinal mucosa and its ability to recover. It is believed that through defects in the mucous membrane, a variety of food and bacterial agents can penetrate into the deeper tissues of the intestine, which then trigger a cascade of inflammatory and immune reactions.

The patient’s personality traits and psychogenic influences are of great importance in the pathogenesis of ulcerative colitis and the provocation of relapse of the disease. An individual reaction to stress with an abnormal neurohumoral response may be a trigger for the development of the disease. In the neuropsychic status of a patient with ulcerative colitis, features are noted that are expressed in emotional instability.

Pathological anatomy.

In the acute stage of ulcerative colitis, exudative swelling and congestion of the mucous membrane with thickening and smoothing of the folds are noted. As the process develops or becomes chronic, destruction of the mucous membrane increases and ulcerations form, penetrating only to the submucosal layer or, less commonly, to the muscular layer. Chronic ulcerative colitis is characterized by the presence of pseudopolyps (inflammatory polyps). They are islands of the mucous membrane, preserved after its destruction, or a conglomerate formed as a result of excessive regeneration of the glandular epithelium.

Inflammatory polyps (pseudopolyps) of the colon resulting from ulcerative colitis

In severe chronic disease, the intestine is shortened, its lumen is narrowed, and haustra are absent. The muscular layer is usually not involved in the inflammatory process. Strictures are not typical for ulcerative colitis. With ulcerative colitis, any part of the colon can be affected, but the rectum is always involved in the pathological process, which is diffuse and continuous. The intensity of inflammation in different segments may be different; the changes gradually transform into the normal mucous membrane, without a clear boundary.

Histological examination in the acute phase of ulcerative colitis in the mucous membrane reveals dilation of capillaries and hemorrhages, the formation of ulcers as a result of necrosis of the epithelium and the formation of crypt abscesses. There is a decrease in the number of goblet cells, infiltration of the lamina propria with lymphocytes, plasma cells, neutrophils and eosinophils. In the submucosal layer, changes are insignificantly expressed, with the exception of cases of ulcer penetration into the submucosa.

Clinic.

The modern clinical classification of ulcerative colitis takes into account the prevalence of the process, the severity of clinical and endoscopic manifestations, and the nature of the course of the disease.

According to the length of the process, they are distinguished:

Distal colitis (in the form of proctitis or proctosigmoiditis);

Left-sided colitis (damage to the colon up to the right flexure);

Total colitis (damage to the entire colon with involvement in the pathological process in some cases of the terminal segment of the ileum);

Based on the severity of clinical manifestations, the disease is classified into mild, moderate and severe. According to the nature of the disease:

Lightning form;

Acute form (first attack);

Chronic relapsing form (with repeated exacerbations, no more than once every 6-8 months);

Continuous form (protracted exacerbation for more than 6 months, subject to adequate treatment).

There is a correlation between the extent of the lesion and the severity of symptoms, which in turn determines the volume and nature of treatment.

The diagnosis of ulcerative colitis is formulated taking into account the nature of the course (recurrence) of the disease, the prevalence of the process (distal, left-sided, total colitis), the severity of the disease (mild, moderate, severe), the phase of the disease (exacerbation, remission) with an indication of local and systemic complications. For example: ulcerative colitis, total lesion, chronic relapsing course, moderate severity.

By the time the diagnosis is made, approximately 20% of patients have total colitis, 30-40% have left-sided lesions, and 40-50% have proctitis or proctosigmoiditis.

The clinical picture of ulcerative colitis is characterized by local symptoms (intestinal bleeding, diarrhea, constipation, abdominal pain, tenesmus) and general manifestations of toxemia (fever, weight loss, nausea, vomiting, weakness, etc.). The intensity of symptoms in ulcerative colitis correlates with the extent of the pathological process in the intestine and the severity of inflammatory changes.

Severe total damage to the colon is characterized by profuse diarrhea mixed with a significant amount of blood in the stool, sometimes blood clots, cramping pain in the abdomen before defecation, anemia, symptoms of intoxication (fever, weight loss, severe general weakness). With this variant of ulcerative colitis, life-threatening complications can develop - toxic megacolon, colon perforation and massive intestinal bleeding. A particularly unfavorable course is observed in patients with the fulminant form of ulcerative colitis.

With an exacerbation of moderate severity, frequent stools up to 5-6 times a day with a constant admixture of blood, cramping abdominal pain, low-grade body temperature, and fatigue are noted. A number of patients experience extraintestinal symptoms - arthritis, erythema nodosum, uveitis, etc. Moderate attacks of ulcerative colitis in most cases respond successfully to conservative therapy with modern anti-inflammatory drugs, primarily corticosteroids.

Severe and moderate exacerbations of ulcerative colitis are characteristic of total and, in some cases, left-sided lesions of the colon. Mild attacks of the disease with total damage are manifested by a slight increase in stool and a slight admixture of blood in the stool.

In the clinical picture of patients with proctitis and proctosigmoiditis, it is very often not diarrhea that manifests itself, but constipation and a false urge to defecate with the release of fresh blood, mucus and pus, and tenesmus. If the transit of intestinal contents through the inflamed distal sections of the colon is accelerated, then stasis is observed in the proximal segments. Constipation in distal colitis is associated with this pathophysiological mechanism. Patients may not notice the admixture of blood in the stool for a long time, their general condition suffers little, and their ability to work is preserved. This latent period from the onset of ulcerative colitis to diagnosis can be very long - sometimes several years.

Currently, criteria developed by Truelove and Witts are usually used to assess the severity of an attack of ulcerative colitis.

Complications.

With ulcerative colitis, various complications are observed, which can be divided into local and systemic.
Local complications include colonic perforation, acute toxic dilatation of the colon (or toxic megacolon), massive intestinal bleeding, and colon cancer.

Acute toxic dilatation of the colon is one of the most dangerous complications of ulcerative colitis. It develops as a result of a severe ulcerative-necrotic process and associated toxicosis. Toxic dilatation is characterized by expansion of a segment or the entire affected bowel during a severe attack of ulcerative colitis. Patients with toxic dilatation of the colon in the initial stages require intensive conservative therapy. If it is ineffective, surgery is performed.

Perforation of the colon is the most common cause of death in the fulminant form of ulcerative colitis, especially with the development of acute toxic dilatation. Due to an extensive ulcerative-necrotic process, the wall of the colon becomes thinner, loses its barrier functions and becomes permeable to a variety of toxic products located in the intestinal lumen. In addition to stretching the intestinal wall, bacterial flora, especially E. coli with pathogenic properties, plays a decisive role in the occurrence of perforation. In the chronic stage of the disease, this complication is rare and occurs mainly in the form of a pericolytic abscess. Treatment of perforation is only surgical.

Massive intestinal bleeding is relatively rare and, as a complication, is a less complex problem than acute toxic dilatation of the colon and perforation. In most patients with bleeding, adequate anti-inflammatory and hemostatic therapy allows surgery to be avoided. With ongoing massive intestinal bleeding in patients with ulcerative colitis, surgical intervention is indicated.

The risk of developing colon cancer with ulcerative colitis increases sharply with a disease duration of more than 10 years, if colitis began before the age of 18 and, especially, 10 years.

Colorectal cancer of the colon due to ulcerative colitis

Systemic complications of ulcerative colitis are otherwise called extraintestinal manifestations. Patients may experience damage to the liver, oral mucosa, skin, and joints. The exact genesis of extraintestinal manifestations is not fully understood. Their formation involves foreign, including toxic, agents entering the body from the intestinal lumen, and immune mechanisms. Erythema nodosum occurs not only as a reaction to sulfasalazine (associated with sulfapyridine), but is observed in 2-4% of patients with ulcerative colitis or Crohn's disease, regardless of drug use. Pyoderma gangrenosum is a fairly rare complication, observed in 1-2% of patients. Episcleritis occurs in 5-8% of patients with exacerbation of ulcerative colitis, acute arthropathy - in 10-15%. Arthropathy manifests itself as asymmetrical damage to large joints. Ankylosing spondylitis is detected in 1-2% of patients. Liver lesions are observed in 33.3% of patients with ulcerative colitis and Crohn's disease, manifesting in the majority either a transient increase in the level of transaminases in the blood or hepatomegaly. The most characteristic serious hepatobiliary disease in ulcerative colitis is primary sclerosing cholangitis, which is a chronic stenotic inflammation of the intra- and extrahepatic bile ducts. It occurs in approximately 3% of patients with ulcerative colitis.

Diagnostics.

The diagnosis of ulcerative colitis is established based on an assessment of the clinical picture of the disease, sigmoidoscopy data, endoscopic and x-ray examinations.

According to the endoscopic picture, four degrees of inflammation activity in the intestine are distinguished: minimal, moderate, severe and pronounced.

I degree (minimal) is characterized by swelling of the mucous membrane, hyperemia, absence of a vascular pattern, mild contact bleeding, and pinpoint hemorrhages.

II degree (moderate) is determined by edema, hyperemia, granularity, contact bleeding, the presence of erosions, confluent hemorrhages, fibrinous plaque on the walls.

III degree (severe) is characterized by the appearance of multiple merging erosions and ulcers against the background of the changes in the mucous membrane described above. There is pus and blood in the intestinal lumen.

IV degree (sharply expressed), in addition to the listed changes, is determined by the formation of pseudopolyps and bleeding granulations.

In the remission stage, the mucous membrane is thickened, the vascular pattern is restored, but not completely and is somewhat rebuilt. The mucous membrane may remain granular and thickened folds.

In a number of countries, to assess the endoscopic activity of ulcerative colitis, they use the endoscopic index proposed by Rakhmilevich, which takes into account the same signs assessed in points.

Endoscopic Rakhmileich index (1989)

1. Light-scattering granulations on the surface of the mucous membrane (granularity): no - 0, yes - 2.

2. Vascular pattern: normal - 0, deformed or blurred - 1, absent - 2.

3. Bleeding of the mucous membrane: absent - 0, slight contact - 2, severe (spontaneous) - 4.

4. Damage to the surface of the mucous membrane (erosions, ulcers, fibrin, pus): absent - 0, moderately expressed - 2, significantly expressed - 4.

Often, with high activity, the surface of the intestinal mucosa is completely covered with fibrinous-purulent plaque, after removal of which a granular, diffusely bleeding surface is revealed with multiple ulcers of varying depths and shapes without signs of epithelization. Ulcerative colitis is characterized by round and stellate ulcers, imprint ulcers, which usually do not penetrate deeper than the lamina propria of the mucous membrane, rarely into the submucosal layer. In the presence of multiple microulcers or erosions, the mucous membrane looks like it is eaten away by moths.

For ulcerative colitis in the active stage of the process, when studied with a barium enema, the following radiological signs are characteristic: absence of haustra, smooth contours, ulcerations, swelling, serration, double contour, pseudopolyposis, restructuring of the longitudinal type of folds of the mucous membrane, the presence of free mucus. With long-term ulcerative colitis, thickening of the mucous and submucous membranes may develop due to edema. As a result, the distance between the posterior wall of the rectum and the anterior surface of the sacrum increases.

After emptying the colon of barium, the absence of haustra, mainly longitudinal and rough transverse folds, ulcers and inflammatory polyps are revealed.

X-ray examination is of great importance not only for diagnosing the disease itself, but also its severe complications, in particular acute toxic dilatation of the colon. To do this, a plain radiography of the abdominal cavity is performed. With I degree of dilatation, the increase in intestinal diameter at its widest point is 8-10 cm, with II - 10-14 cm and with III - over 14 cm.
In the process of treating an attack of ulcerative colitis, there is a positive dynamics of all the main radiological manifestations of the disease - a decrease in the length, caliber and tone of the intestine. This is due to the fact that during irrigoscopy these changes manifest themselves as spasms, and not as organic narrowing, characteristic of granulomatous colitis and intestinal tuberculosis.

Differential diagnosis

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The clinical picture of ulcerative colitis requires a differential diagnosis with diseases of the colon of infectious and non-infectious etiology. The first attack of ulcerative colitis can occur under the guise of acute dysentery. Correct diagnosis is helped by data from sigmoidoscopy and bacteriological examination. Salmonellosis often simulates the picture of ulcerative colitis, as it occurs with diarrhea and fever, but in contrast, bloody diarrhea appears only in the 2nd week of the disease. Other forms of colitis of infectious origin that require differentiation from ulcerative ones include gonorrheal proctitis, pseudomembranous enterocolitis, and viral diseases.

The most difficult differential diagnosis is between ulcerative colitis, Crohn's disease and ischemic colitis.

Treatment.

Therapeutic tactics for ulcerative colitis are determined by the localization of the pathological process in the colon, its extent, the severity of the attack, and the presence of local and/or systemic complications. Conservative therapy is aimed at stopping the attack as quickly as possible, preventing relapse of the disease and progression of the process. Distal forms of ulcerative colitis - proctitis or proctosigmoiditis - are characterized by a milder course, therefore they are most often treated on an outpatient basis. Patients with left-sided and total lesions are usually treated in a hospital, since the course of the disease in them is characterized by greater severity of clinical symptoms and greater organic changes.

The food of patients should be high in calories and include foods rich in proteins, vitamins, limiting animal fats and excluding coarse plant fiber. We recommend low-fat fish, meat (beef, chicken, turkey, rabbit), boiled or steamed, pureed cereals, potatoes, eggs, dried bread, walnuts. Raw vegetables and fruits are excluded from the diet, as they contribute to the development of diarrhea. Patients often have lactase deficiency, so dairy products are added only if they are well tolerated. These recommendations correspond to diets 4, 4B, 4B of the Institute of Nutrition of the Russian Academy of Medical Sciences.

All medications used in treatment regimens for ulcerative colitis can be divided into two large groups. The first combines basic anti-inflammatory drugs and includes aminosalicylates, i.e. drugs containing 5-aminosalicylic acid (5-ASA, mesalazine), corticosteroids and immunosuppressants. All other drugs play either an auxiliary role in the treatment of ulcerative colitis or are at the stage of clinical study.

The first drug containing 5-ASA was sulfasalazine (salazosulfapyridine), which was introduced into clinical practice in 1942. Sulfasalazine consists of two components linked by a nitrogen bond - sulfapyridine sulfanilamide and 5-ASA. It has been proven that only 5-ASA has an anti-inflammatory effect. Sulfapyridine was forced into the composition of the sulfasalazine molecule, since “pure” 5-ASA is well absorbed in the small intestine, and in the mucous membrane it turns into an inactive metabolite - N-acetyl-5-ASA. In sulfasalazine, sulfapyridine acts solely as a “carrier” that allows delivery of 5-ASA to the affected areas of the colon. Under the influence of colonic microflora, the nitrogen bond is destroyed. Sulfapyridine is absorbed in the colon, undergoes detoxification in the liver through acetylation and is excreted in the urine, and 5-ASA, in contact with the mucous membrane, has an anti-inflammatory effect.

The mechanisms by which 5-ASA exerts its anti-inflammatory effect are not fully understood. Nevertheless, numerous effects are known due to which mesalazine inhibits the development of inflammation. Thus, by inhibiting cyclooxygenase, mesalazine inhibits the formation of prostaglandins. The lipoxygenase pathway of arachidonic acid metabolism is also suppressed, and the release of leukotriene B4 and leukotriene sulfopeptide is inhibited.

At high concentrations, mesalazine can inhibit certain functions of neutrophil granulocytes in humans (eg, migration, degranulation, phagocytosis, and the formation of toxic oxygen free radicals). In addition, mesalazine inhibits the synthesis of platelet-activating factor. Due to its antioxidant properties, mesalazine is able to scavenge free oxygen radicals.

Mesalazine effectively inhibits the formation of cytokines - interleukin-1 and interleukin-6 (IL-1, IL-6) - in the intestinal mucosa, and also suppresses the formation of IL-2 receptors. Thus, mesalazine interferes directly with immune processes.

The "bullet" component sulfapyridine has been shown to be primarily responsible for the overall incidence of sulfasalazine side effects. Literature data on the frequency of side effects caused by sulfasalazine range from 5 to 55%, averaging 21%. In addition to nausea, headache, male infertility, anorexia, dyspeptic disorders, hematological reactions (leukopenia and hemolytic anemia) and hypersensitivity reactions with multiple organ lesions occur.

In order to maintain the anti-inflammatory activity inherent in sulfasalazine and avoid the side effects associated with the sulfapyridine component, preparations containing “pure” 5-ASA have been developed in recent years. An example of a new generation of aminosalicylates is the drug salofalk, developed by the German pharmaceutical company Doctor Falk Pharma. The drug is available in three dosage forms: tablets, suppositories and microenemas. In tablets, mesalazine is protected from contact with gastric contents using a special acid-resistant polymer shell, which dissolves at pH levels above 6.5. These are the pH values ​​that are usually recorded in the lumen of the ileum. After dissolution of the membrane, a high concentration of the active anti-inflammatory component (mesalazine) is created in the ileum. The choice of a specific dosage form of salofalk is determined by the extent of the zone of inflammation in the colon. For proctitis, it is advisable to use suppositories, for left-sided lesions - microenemas, and for total colitis - tablets.
Pentasa, which recently appeared in Russia, while being just as effective, has a number of features. It differs from other mesalazine preparations in its microgranular structure and the nature of its coating. Pentasa tablets consist of microgranules in an ethylcellulose coating, the dissolution of which does not depend on the pH level in the gastrointestinal tract. This ensures a slow, gradual and uniform release of 5-ASA throughout the intestinal tube, starting from the duodenum. The uniformity of release contributes to a constant concentration of the drug in different parts of the intestine, which does not depend not only on pH, but also on the transit rate, so Pentasa can be successfully used for inflammatory bowel diseases with diarrhea with virtually no losses. These features make it possible to use the drug not only for ulcerative colitis and Crohn's disease with damage to the colon and ileum, but also, most importantly, in patients with high-intestinal localization of Crohn's disease.

The daily dose of aminosalicylates is determined by the severity of the attack of ulcerative colitis and the nature of the clinical response to the drug. To stop an acute and moderate attack, 4-6 g of sulfasalazine or 3-3.5 g of mesalazine per day are prescribed, divided into 3-4 doses. In the absence of a good clinical response, the daily dose of mesalazine can be increased to 4.0-4.5 g, however, it is usually not possible to increase the daily dose of sulfasalazine due to the development of severe side effects.

Sulfasalazine blocks the conjugation of folic acid in the brush border of the jejunum, inhibits the transport of this vitamin, and inhibits the activity of the enzymatic systems associated with it in the liver. Therefore, the treatment complex for patients with ulcerative colitis receiving treatment with sulfasalazine must include folic acid in a dose of 0.002 g 3 times a day.

It usually takes 3 to 6 weeks to stop an attack of ulcerative colitis. After this, anti-relapse treatment is carried out with sulfasalazine (3 g/day) or mesalazine (2 g/day).

Of the modern drugs for the treatment of proctosigmoiditis and left-sided colitis, the suspension of salofalk is most often used. Disposable containers contain 4 g of mesalazine in 60 ml of suspension or 2 g of mesalazine in 30 ml of suspension. The drug is administered into the rectum 1-2 times a day. The daily dose is 2-4 g, depending on the severity of the process in the intestine. If the extent of the inflammatory process in the rectum is no more than 12 cm from the edge of the anus, it is advisable to use salofalk suppositories. The usual daily dose in these cases is 1.5-2 g.

When using aminosalicylates, it is possible to achieve remission in 75-80% of cases of ulcerative colitis.

The most effective anti-inflammatory drugs in the treatment of ulcerative colitis remain steroid hormones, which in severe forms of the disease are superior in activity to aminosalicylates. Corticosteroids accumulate in inflammatory tissue and block the release of arachidonic acid, preventing the formation of prostaglandins and leukotrienes, which cause the inflammatory process. By blocking chemotaxis, steroid hormones indirectly exhibit an immunomodulatory effect. The effect on tissue fibrinolysis leads to a decrease in bleeding.

Indications for steroid therapy are:

Acute severe and moderate forms of the disease and the presence of extraintestinal complications;

Left-sided and total forms of ulcerative colitis with severe and moderate course in the presence of III degree of activity of inflammatory changes in the intestine (according to endoscopic examination);

Lack of effect from other treatment methods for chronic forms of ulcerative colitis.

In acute severe form of ulcerative colitis or severe attack of chronic forms of the disease, treatment should begin with intravenous administration of prednisolone at least 120 mg/day, evenly distributed over 4-6 injections with simultaneous correction of water and electrolyte disturbances, administration of blood and blood substitutes and (if possible) hemosorption in order to quickly eliminate endotoxemia. The hydrocortisone suspension should be administered intramuscularly, but the duration of such administration is limited to 5-7 days due to the likely development of abscesses at the injection sites and possible fluid retention. After 5-7 days, you should switch to oral prednisolone. During this time, gastroscopy is performed to exclude peptic ulcers of the stomach and duodenum. In case of a moderate form and the absence of clinical signs and anamnestic indications of gastroduodenal ulcers, treatment should immediately begin with oral prednisolone. Typically, prednisolone is prescribed at a dose of 1.5-2 mg/kg body weight per day. A dose of 100 mg should be considered the maximum.

If hormonal drugs are well tolerated, it is recommended to take the prescribed dose until a lasting positive result is obtained - within 10-14 days. After this, a reduction is carried out according to the so-called stepwise scheme - by 10 mg every 10 days. Starting from 30-40 mg, a single dose of prednisolone in the morning is recommended, which practically does not cause serious complications. At the same time, mesalazine or sulfasalazine is included in the treatment regimen, which should be taken until the hormones are completely withdrawn. Starting from 30 mg, prednisolone is withdrawn more slowly - 5 mg per week. Thus, the full course of hormonal therapy lasts from 8 to 12 weeks. depending on the form of ulcerative colitis.

In distal forms of the lesion and I-II degrees of process activity according to sigmoidoscopy data, hydrocortisone should be prescribed rectally by drip or in microenemas. Moreover, if patients have difficulty maintaining large volumes, then the administration of hydrocortisone (65-125 mg) should be started in 50 ml of isotonic sodium chloride solution and, as the inflammation subsides and the frequency of false urges decreases, gradually increase the volume to 200-250 ml per therapeutic enema. The drug is usually administered after bowel movements in the morning or before bed.

For ulcerative proctitis and sphincteritis, suppositories with prednisolone (5 mg), administered 3-4 times a day, have a fairly good effect. In more severe distal forms, accompanied by increased body temperature, general weakness, anemia and III-IV degrees of activity according to rectoscopy, in cases of no effect from sulfasalazine or mesalazine, treatment with oral prednisolone at a dose of 30-50 mg/day is indicated.

In middle-aged and elderly patients, the dose of prednisolone should not exceed 60 mg, since they are characterized by the presence of concomitant diseases: atherosclerosis, hypertension, diabetes mellitus, etc. In cases where ulcerative colitis occurs against the background of atherosclerotic lesions of the mesenteric arteries, therapeutic the complex should be administered with vascular drugs: trental, prodectin, etc.

Hormone therapy is associated with the development of side effects: retention of fluid, chlorides and sodium in tissues (edema is possible), arterial hypertension, hypokalemia, calcium loss, osteoporosis, various autonomic disorders, carbohydrate metabolism disorders, adrenal insufficiency, stomach ulcers, gastrointestinal bleeding . In these cases, it is recommended to prescribe adequate symptomatic therapy: antihypertensive drugs, diuretics, calcium supplements, antacids. If carbohydrate metabolism is impaired, a diet with limited carbohydrates is necessary; according to indications, fractional administration of insulin (according to glycemia) or oral antidiabetic drugs. To prevent the development of thrombosis in patients with severe forms of ulcerative colitis receiving hormonal treatment, constant monitoring of the blood coagulation system should be carried out and at the same time antiplatelet agents should be prescribed: chimes, prodectin, etc.

ACTH-zinc phosphate is effective only in the acute form of ulcerative colitis, since its effect is mediated by the preserved function of the own adrenal glands. The drug is administered intramuscularly at a dose of 20-40 mg, depending on the severity of the attack.

In recent years, in the treatment of inflammatory bowel diseases, especially Crohn's disease, drugs containing the glucocorticosteroid budesonide as an active component have been actively used. Unlike traditional glucocorticosteroids, budesonide has a very high degree of affinity for receptors and high (about 90%) first-pass metabolism in the liver. Due to this, it has a very powerful local anti-inflammatory effect with a minimum number of systemic side effects. As an alternative to prednisolone and hydrocortisone, the drug budenofalk can be recommended. When developing the structure of budenofalk, the physiological characteristics of the gastrointestinal tract were taken into account. Each capsule of budenofalk contains about 350 microspheres consisting of budesonide, coated with a polymer shell that is resistant to the action of gastric juice. Release of budesonide from microspheres occurs in the ileum and colon at pH values ​​above 6.4. Budenofalk is used to treat mild and moderate exacerbations of ulcerative colitis. The recommended daily dose is 1 capsule of budenofalk containing 3 mg of budesonide, 4-6 times a day.

The most serious problem in the treatment of ulcerative colitis is hormonal dependence and resistance. This group of patients has the worst results of conservative therapy and the highest surgical activity. According to the State Scientific Center for Cancer Research, hormonal dependence develops in 20-35% of patients with severe ulcerative colitis. Often, signs of dependence and resistance are observed simultaneously, forcing one to resort to unsafe and aggressive methods of influence.

Hormonal dependence is a reaction to glucocorticoid therapy, in which the positive therapeutic effect is replaced by reactivation of the inflammatory process due to dose reduction or withdrawal of corticosteroids. This is a special variant of refractory colitis. We believe that there are at least 4 different etiopathogenetic variants of hormonal dependence: true hormonal dependence, combined with steroid resistance, false, caused by inadequate treatment, chronic adrenal insufficiency itself, and a mixed or combined form.

Currently, the causes and mechanisms of the formation of hormonal dependence are completely unknown. Nevertheless, we believe that among the etiological factors, defects in hormonal therapy itself, persistent inflammatory activity, and a transient or persistent decrease in the function of the pituitary-adrenal system will undoubtedly find their place. Probably, in some cases, hormonal dependence and resistance are hereditary, in others they represent an acquired defect in hormonal receptors and an imbalance between proliferation and cell death, i.e., deregulation of apoptosis. The hypothesis of a low density of hormonal receptors in patients with inflammatory diseases of the colon, especially with refractory disease, has recently received convincing confirmation.

It is immunosuppressants that play a responsible role in the treatment of patients with inflammatory diseases of the colon with hormonal dependence and resistance. However, this role for various drugs is assessed ambiguously. First-line and long-term drugs include 6-mercaptopurine and azathioprine. They are excellent sparring partners for glucocorticoids. Purine analogues make it possible to reduce and cancel hormones in 60-70% of patients with hormonal dependence, subject to certain rules, namely: they must be prescribed simultaneously with hormones so that their effect has time to manifest itself. The daily dose of azathioprine should be no more than 150 mg. The effect can be expected only by the end of the 3rd month of continuous use. Purine analogues produce relatively few side effects, and they should be used in patients with hormonal dependence for as long as possible - 2-3 years or more.

The 2nd line drug for long-term therapy is methotrexate, which is used in cases of intolerance to azathioprine or the need to accelerate the effect. It is administered orally or intramuscularly at a dose of 30 mg/week. The result can be obtained in 2-4 weeks. Side effects are few. Unfortunately, like azathioprine, it does not provide a lasting effect. Exacerbations occur upon withdrawal. Outbreaks that are milder than before sometimes occur during therapy after 6 months. from the start of the reception.

Cyclosporine can be used orally, intravenously at a dose of 4-6 mg/kg body weight with a good and rapid effect, occurring within 5-7 days. The action is short-lived. It is more often used to interrupt an attack with a subsequent transition to immunosuppressants suitable for prolonged use.

Violation of the barrier functions of the colon in ulcerative colitis may cause the development of toxemia syndrome. To correct it, it is necessary to prescribe an appropriate complex, restore eubiosis, antibacterial therapy, hemosorption, and ultraviolet irradiation of autologous blood.
Due to pronounced metabolic disorders and the catabolic effect of steroid hormones, parenteral administration of protein preparations is advisable: serum albumin, plasma protein, essential amino acids.

To improve the processes of microcirculation and transcapillary exchange, the administration of rheopolyglgine and hemodez (in normal dosages) is indicated.

In case of anemia (hemoglobin 90 g/l and below), which is a sign of a severe attack of ulcerative colitis, it is recommended to carry out blood transfusion of 250 ml of same-type blood with an interval of 3-4 days. When the level of iron in the blood serum decreases, it is necessary to include iron supplements in the treatment complex.
Taking into account the immunological disorders in ulcerative colitis, immunomodulators, levamisole, thymalin, etc. are used in the treatment of the disease. However, their role is not completely clear, the therapeutic effect of their use is short-term, so the activity of these drugs as basic agents is doubtful.

It is advisable to recommend the use of immunomodulators in combination with basic anti-inflammatory treatment.
Vitamins of groups B, C, A, D, K are prescribed, which also help restore eubiosis in the intestines.

The treatment complex includes psychotropic drugs in usual dosages, focusing on individual tolerance.
Exacerbation of ulcerative colitis in some cases is accompanied by irritable bowel syndrome, most often manifested by constipation. In this case, it is justified to prescribe wheat bran or proprietary preparations containing ballast substances (mucofalk, etc.), which help normalize stool and at the same time act as enterosorbents.

Inpatient treatment ends when clinical-endoscopic remission is achieved, after which the patient is subject to dispensary observation in a clinic with a general practitioner, gastroenterologist or proctologist.

Anti-relapse treatment.

The question of the nature and duration of anti-relapse treatment for ulcerative colitis remains unresolved. According to one point of view, anti-relapse treatment is recommended for life. However, taking into account the high cost of drugs and the risk of side effects with their long-term use, the gastroenterology department of the State Scientific Center adheres to the following tactics: after stopping an attack of ulcerative colitis, a maintenance dose of aminosalicylates (3.0 g of sulfasalazine or 2.0 g of mesalazine per day) is recommended for a period 6 months If during this period there are no clinical signs of exacerbation of the disease, and during a control endoscopic examination after 6 months. remission is stated, anti-relapse treatment can be discontinued. If during the course of anti-relapse therapy the patient’s condition was unstable, sometimes it was necessary to increase the dose of aminosalicylates to eliminate the symptoms of exacerbation, and control endoscopy revealed signs of active inflammation, anti-relapse treatment should be extended for another 6 months. Patients with a chronic continuous course of ulcerative colitis require long-term continuous treatment, usually with high doses of aminosalicylates, but this therapy is not anti-relapse in the full sense of the word. It is more of a restraining anti-inflammatory treatment. In this category of patients, cytostatics (azathioprine or 6-mercaptopurine) and intermittent corticosteroid regimens are also widely used.

Surgery.

Surgical interventions for ulcerative colitis are necessary in 10-20% of patients. The surgical method can be radical, but for this it is necessary to completely remove the colon as a substrate for a possible relapse of the disease. However, this severe traumatic operation leads in the vast majority of patients to the loss of anal bowel movement and the formation of a permanent ileostomy on the anterior abdominal wall. In fact, operated patients become disabled, and this circumstance significantly limits the use of surgical treatment. Indications for surgery are currently divided into three main groups:
1. ineffectiveness of conservative therapy;

2. complications of ulcerative colitis (intestinal bleeding, toxic dilatation of the colon, perforation of the colon);
3. the occurrence of colorectal cancer against the background of ulcerative colitis.

The State Scientific Center has experience in the surgical treatment of more than 500 patients with ulcerative colitis. In recent years, comprehensive tactics for treating patients have been developed and implemented, including intensive therapy in the preoperative period, timely determination of indications for surgery, and effective rehabilitation in the postoperative period. New technologies of surgical intervention are used, including bloodless, gentle surgery (laparoscopically assisted operations, Ultracision, Ligasure). The goals of surgical rehabilitation are served by a differentiated approach using various options for ileorectollasty to restore anal bowel movements. All these approaches made it possible to reduce the incidence of postoperative complications from 55 to 12%, and mortality from 26 to almost 0%. Primary and delayed reconstructive interventions became possible in 53% of operated patients.

Indications for surgery.

Ineffectiveness of conservative therapy. In some patients, the progression of inflammatory changes cannot be prevented by medications, including hormonal ones (hormone-resistant form). The ongoing attack of ulcerative colitis, severe intoxication and blood loss lead to exhaustion of the patient, profound metabolic disorders, anemia, and carry the risk of developing septic complications. In these cases, a decision is made about the need for surgery. Preoperative preparation includes intensive conservative treatment, correction of anemia, hypoproteinemia and electrolyte disturbances. The time criterion (duration) for waiting for the effect of conservative therapy is 2-3 weeks. after the start of complex intensive therapy with an adequate dosage of glucocorticoids (prednisolone 2 mg/kg/day).

In a certain group of patients (20-25% of severe forms), so-called hormone-dependent ulcerative colitis is noted. Maintaining remission of the inflammatory process in the colon occurs only against the background of constant supportive hormonal therapy (15-30 mg of oral prednisolone per day. Long-term treatment with hormones for 6 months or more leads to the development of severe side effects: steroid diabetes, osteoporosis with pathological fractures, arterial hypertension, etc. This circumstance also dictates the need for surgery, which allows not only to cancel corticosteroids, but also to eliminate the source of inflammation.

Intestinal bleeding. Blood loss through the rectum in ulcerative colitis is rarely serious. However, sometimes blood loss cannot be corrected conservatively and becomes life-threatening. In such cases, the decision about surgery should be made without waiting for the effect of anti-inflammatory therapy, including steroids, hemostatic agents, transfusions of blood products, and the fight against hypovolemia. In this case, it is important to objectively assess the amount of blood excreted by patients with feces, since a visual assessment not only by the patient himself, but also by the doctor is usually inadequate. The most accurate method for determining blood loss is a radioisotope study, which allows, after preliminary labeling of the patient’s red blood cells with a chromium or technetium isotope, to determine the number of red blood cells in the stool on a daily basis. If blood loss is 100 ml per day or more, urgent surgery is indicated. Such an objective assessment of blood loss is not always possible and not everywhere. Indirect criteria for the severity of blood loss are diarrhea more than 10 times a day with an intense admixture of blood with a stool volume of more than 1000 ml per day, maintaining the initial red blood counts against the background of blood transfusion.

Toxic dilatation of the colon occurs as a result of cessation of peristaltic contractions of the colon wall, which leads to the accumulation of intestinal contents, including large amounts of gases, in the lumen. The colon under these conditions expands significantly, up to a critical level - 9-15 cm in diameter. Dangerous symptoms of the development of dilatation are a sudden decrease in stool against the background of initial diarrhea, bloating, as well as increased pain and an increase in symptoms of intoxication. A simple and valuable diagnostic technique is a dynamic x-ray examination of the abdominal cavity, in which an increase in pneumatosis of the colon and expansion of its lumen are noted. If dilatation of up to 6-9 cm is detected (I degree of dilatation), an attempt is made at endoscopic decompression (evacuation of intestinal contents through a colonoscope). Preservation of dilatation, as well as its increase (9-11 cm - II degree, 11-15 cm - III degree) are an indication for emergency surgical intervention.
Perforation of the colon usually occurs against the background of increasing toxic dilatation with unjustified refusal of timely surgery. The cause of perforation is also deep ulcerative defects with necrotic changes in all layers of the intestinal wall. It is important to keep in mind that with intensive hormonal therapy, the administration of antibiotics, antispasmodics and analgesics, patients with perforation due to ulcerative colitis do not have the classic picture of an acute abdomen, so it can be very difficult to make a correct diagnosis. Again, X-ray examination helps when the appearance of free gas in the abdominal cavity is noted. The success of the operation directly depends on the timeliness of diagnosis and the duration of development of peritonitis.
Cancer due to ulcerative colitis. In the population of patients with ulcerative colitis, colon cancer is significantly more common, especially when the disease has been more than 10 years old. Unfavorable features are malignant poorly differentiated forms, multiple and rapid metastasis, and extensive tumor damage to the colon. With ulcerative colitis, the so-called total form of colon cancer occurs, when intramural tumor growth is found in all sections during histological examination, while visually the intestine may remain characteristic of a chronic inflammatory process. The main methods of secondary prevention of cancer in ulcerative colitis are annual medical examination of patients, especially with total forms and a disease duration of more than 10 years, and multiple biopsies of the mucous membrane, even in the absence of visual changes. The detection of mucosal dysplasia in biopsy specimens should be regarded as precancer and be a reason for more in-depth and frequent examination.

Choice of surgical intervention.

For ulcerative colitis, radical surgery is total removal of the colon with the formation of a permanent single-barrel Brooke ileostomy. However, surgeons are looking for ways to rehabilitate this severe category of patients and are developing various reconstructive interventions to restore anal bowel movements. In addition, one-stage traumatic colproctectomy is associated with an increased incidence of complications and mortality in patients in an extremely severe initial condition.

Simultaneous colectomy with abdominal-anal resection of the rectum is used for massive intestinal bleeding, when the source of blood loss is the rectum.

A moderate course of ulcerative colitis against the background of a satisfactory condition of the patient can also be a reason for surgery if the disease is hormone-dependent. In this case, it is possible to perform a one-stage operation with a reconstructive stage - colectomy with the formation of an ileorectal anastomosis or colectomy with an abdominal-anal resection of the rectum, the formation of an ileal reservoir and the imposition of an ileoanal anastomosis with a preventive ileostomy.

When colon cancer develops against the background of ulcerative colitis, colectomy combined with abdominal-anal resection of the rectum is used. If the tumor is localized in the rectum, colectomy and abdominoperineal extirpation of the rectum are performed. Cancer operations are usually completed with the formation of a permanent single-barrel Brooke ileostomy.

Postoperative complications.

The severe initial condition of most patients before surgery affects the course of the postoperative period, the development of postoperative complications and mortality. Complications are often associated with poor tissue regeneration in weakened patients (eventration, failure of intestinal stoma sutures); serous peritonitis, exudative pleurisy as manifestations of polyserositis, abdominal abscesses, ileostomy dysfunction, and pneumonia are also observed. The surgeon’s active tactics are especially important in case of complications due to a decrease in the patient’s resistance.

During operations for intestinal bleeding, toxic dilatation and perforation of the colon, postoperative complications reach 60-80%, and mortality ranges from 12 to 50%. In cases of timely surgical intervention in a specialized hospital, complications and mortality do not exceed the level of other abdominal operations, amounting to 8-12% of postoperative complications and 0.5-1.5% of postoperative mortality.

Prognosis after surgical treatment.

If the operation is performed in a timely manner and patients are monitored dynamically, the prognosis for life is favorable. Annual monitoring is required in case of rectal preservation with multiple biopsies and monitoring for malignancy. Most patients are long-term disabled (need to register for disability).

Inflammatory colon polyps

Version: MedElement Disease Directory

Pseudopolyposis colon (K51.4)

Gastroenterology

general information

Short description

Pseudopolyps- areas of regenerating or preserved mucous membrane, surrounded by erosions and ulcers. Against the background of erosions and ulcers, normal epithelial islands look raised and resemble polyps Polyp is a pathological formation protruding above the surface of an organ and connected to it by a leg or its base
.
Some pseudopolyps contain granulation tissue Granulation tissue is connective tissue formed during the healing of tissue defects, chronic inflammation, organization of dead areas and encapsulation of foreign bodies; consists of a large number of newly formed vessels (such as capillaries), young and differentiated cells, reticular and collagen fibers; in an open wound it has a granular appearance.
. Some are represented by connective tissue and covered with glandular epithelium. These polyps have one thing in common - they are islands of the mucous membrane and contain inflammatory changes. Pseudopolyps are better visible on the thinned mucous membrane in nonspecific ulcerative colitis Nonspecific ulcerative colitis is a disease of unknown etiology, characterized by chronic colitis with the development of ulcers, hemorrhages, pseudopolyps, erosions and other lesions of the intestinal wall
than on lumpy Crohn's disease Crohn's disease is a disease in which parts of the digestive tract become inflamed, thickened, and ulcerated.
.

Classification

There is no uniform classification. Usually they describe parameters such as:
- localization of the process;
- prevalence (single, multiple, continuous lesions);
- sizes - from microscopic to gigantic (most often 5-10 mm).

Standardly also distinguished:
- ordinary pseudopolyps;
- cap-shaped (cap) pseudopolyps;
- deep cystic polyposis colitis.

Etiology and pathogenesis

The etiology corresponds to that of.
Direct damage due to peristalsis or trauma induced by prolapse plays a role in the pathogenesis of some types of pseudopolyps. Prolapse is a downward displacement of any organ or tissue from its normal position; The cause of such displacement is usually weakening of the tissues surrounding and supporting it.
mucous membrane. Stretching, torsion, and pressure on areas of the mucosa can lead to ischemia Ischemia is a decrease in blood supply to an area of ​​the body, organ or tissue due to weakening or cessation of arterial blood flow.
and subsequent regeneration.

Epidemiology

Age: mainly from 40 to 65 years

Sign of prevalence: Rare

According to various sources, pseudopolyps are found in 22-64% of cases with nonspecific ulcerative colitis.

Risk factors and groups

Older patients with nonspecific ulcerative colitis.

Clinical picture

Clinical diagnostic criteria

Diarrhea, rectal discharge, tenesmus, gradual onset, fever, bloating, lower left abdominal pain, abdominal pain, weight loss, leg swelling, constipation, hematochezia

Symptoms, course

Typical localization: colon, rectum, or the entire left colon, where pseudopolyps are sometimes found in large numbers.

The clinic is determined mainly by the localization of the process and does not differ from the clinical signs of nonspecific ulcerative colitis - see. " " - K51.9.

Diagnostics

1. Endoscopic examinations with biopsy- gold standard of diagnosis.
Endoscopy (colonoscopy with ileoscopy Ileoscopy - examination of the terminal part of the small intestine using a colonoscope
) is an objective tool for assessing disease activity, whereas subjective symptoms are not a reliable indicator of either the presence of pseudopolyps or its prevalence.
In addition, endoscopy may be useful in predicting the need to intensify drug therapy or surgical intervention. There are many assessments of severity and prognosis based on endoscopic findings.

When immunomodulators are used, endoscopic examination allows the conclusions necessary to assess the response to therapy to be made. In recent pharmaceutical studies, documentation of endoscopic mucosal healing has become one of the most important components of the outcome measure of drug efficacy. The sensitivity of the procedure is more than 85%.

A biopsy allows for morphological differential diagnosis and decides on the need for surgical intervention and influences the choice of its technique. Samples should be taken from both affected and adjacent normal-appearing areas of the mucosa. Biopsies from different sites should be labeled separately.

The frequency of endoscopic examinations, both before and after surgery, is also determined based on endoscopy and biopsy data. The methods are relatively contraindicated during periods of exacerbation; with severe fulminant form of nonspecific ulcerative colitis or with the development of its complications. In these cases, the issue is resolved individually, taking into account many data.

2. Barium contrast radiography may show a specific “reticular” or “villous” picture with a significant lesion and is not very informative with single small pseudopolyps.
Filling the colon with barium sulfate taken orally is ineffective in diagnosing tumors of this localization due to its uneven distribution throughout the colon, the impossibility of studying the relief of the mucous membrane and the use of double contrast. In addition, oral administration of contrast media may aggravate partial obstruction, which is often observed in colon cancer.
The double-fill method is more informative than a conventional barium enema, since in more than half of the cases the process is located in an area accessible to endoscopic examination. X-ray examination should be performed only if endoscopy is not possible.

3. CT scan(CT) is quite specific and sensitive, but does not have the differential diagnostic capabilities that endoscopic examination has. CT is indicated when endoscopy is not possible (for example, due to the severity of the disease).

There is such a completely non-invasive diagnostic technique as virtual colonoscopy. It is a type of colonoscopy in 2D/3D format, which is reconstructed from the results of a computed tomogram (CT) or nuclear magnetic resonance imaging (NMRI).
At the moment, the diagnostic capabilities of virtual colonoscopy are being discussed. Virtual colonoscopy does not allow for therapeutic procedures such as biopsy and removal of polyps/tumors, or for detecting lesions up to 5 mm in size.

4. Capsule endoscopy(CE) allows direct and minimally invasive visualization of the intestinal mucosa. During 8 hours of operation, the capsule takes about 60 thousand high-quality images. The images are encoded and automatically sent to a recording device in a special vest worn by the patient. After the study is completed, the capsule leaves the body naturally, and video information from the image recording device is transferred to a computer.

This method can help identify superficial lesions not detected by traditional endoscopy or radiography.
Capsule endoscopy may be useful in initial diagnosis, to detect relapses, to establish the extent of disease, to assess response to therapy, and, in part, to differentiate disease.

The main limitations of this technique are the inability to provide biopsy or therapeutic intervention and the risk of capsule retention in the intestine. Capsule retention occurs in small intestinal strictures and is a major problem occurring in 1% to 13% of patients. Capsular retention may require surgery in patients who would not otherwise require it. Patients with clinical, endoscopic, and radiological signs of narrowing of the intestine (especially the small intestine) should not undergo this research method. Capsular retention above the stricture can theoretically be treated with anti-inflammatory drugs, although there are no published studies on this issue.

5. Endoscopic ultrasound examination(EUS) is a fairly informative way to differentiate pseudopolyps from some other diseases of the colon that spread beyond the mucosa.

Laboratory diagnostics

Laboratory diagnosis corresponds to that for nonspecific ulcerative colitis (see " " - K51.9).
There are some studies showing the prognostic value of a comprehensive determination of procollagen III peptide (PIIIP), C-reactive protein (CRP) and complement C4 for the development of pseudopolyposis.

Differential diagnosis

Differentiation is required first according to morphological characteristics:

1. Polyps (single, group):

1.1 Glandular and glandular-villous polyps(adenomas and adenopapillomas)
They are tumors that develop from cells of the intestinal epithelium (the inner lining of the intestine).

Highlight three main groups of neoplasms(depending on the ratio of certain intestinal epithelial cells)6
- glandular adenomas;
- glandular villous adenomas;
- villous adenomas.
Glandular adenomas are the most common; they are detected in 60-80% of patients with benign tumors of the colon. The anatomical shape of such adenomas can be different, with a pronounced base (pedunculated) or spread out (creeping). The risk of malignancy (malignant degeneration) depends on the size and cellular structure of the polyp. About 5% of glandular polyps are malignant.

1.2 Hyperplastic polyps
Neoplasms are small in size, which are often localized in the distal parts of the colon. As a rule, they are found in patients of older age groups. Hyperplastic polyps do not become malignant and rarely occur as an independent disease. Some researchers consider them to be the original form of adenomas and papillomas. May occur in nonspecific ulcerative colitis.

1.3 Cystic granulating polyps(juvenile or hamartomas)
Polyps of the juvenile type are developmental defects; they are also called congenital, retention polyps, juvenile adenomas. The size of such polyps can reach 2 cm. Juvenile polyps are manifested mainly by the appearance of blood in the stool; they do not become malignant.

1.4 Fibrous polyps
By their nature they are polypoid growths of connective tissue. They develop due to chronic inflammatory diseases and vascular disorders, mainly in the anal canal. They occur frequently.

1.5 Nonepithelial polypoid neoplasms
Includes: lymphoid polyps, lipomas, carcinoid tumors, metastatic lesions, pneumatosis cystos intestinalis. When examining biopsy material obtained through an endoscope, no morphological changes in the mucosa are noted. Confirmation of the diagnosis is possible only after removal of the tumor.

2. Villous tumors of the colon
Villous tumors account for 14-20% of other colon tumors.
A villous tumor is a neoplasm of a round or slightly elongated shape, pinkish-red in color with a peculiar papillary or velvety surface. The main element of such a tumor is the villus (an elongated vascular-connective tissue formation covered with columnar epithelium). The characteristic appearance of the neoplasm is given by lobules formed by fused villi.

There are two forms of tumor by type:

- Nodal- a single tumor node with a pronounced wide base. In some cases, due to the loose submucosal layer of the intestinal wall and its movements, a tumor stalk, represented by a fold of the mucous membrane, can form. Most common.

- Creeping (“carpet”)- villous or small-lobular growths do not form a single node: they spread over the surface of the mucosa and can circularly line the lumen of the intestine, affecting it at a considerable distance.

Based on the nature of the surface, villous tumors are divided into:

- fringed- with pronounced villi on the surface;
- lobed- with clearly not defined papillae, a lobed surface resembling a “cauliflower” in appearance.

Villous adenomas can have different sizes - from a few millimeters in diameter to circular lesions of the intestine 60 cm or more in length. Villous tumors of the colon are in many cases diagnosed late due to minor changes in the patient’s well-being and the absence of clear clinical manifestations. As a result, upon hospitalization, patients already have tumors of significant size, often with symptoms of malignant transformation of the tumor. These tumors are a precancerous disease that must be radically cured.

3. Diffuse polyposis

3.1 True (familial) diffuse polyposis

There are many hereditary polyposis syndromes:
- familial adenomatous polyposis (high probability of developing cancer, surgical treatment is necessary immediately after this diagnosis is established);
- Gadner's syndrome;
- Turcotte syndrome;
- Cronkite-Canada syndrome - non-hereditary hamartomatous polyposis; typical signs: diffuse polyposis, alopecia, nail dystrophy, skin hyperpigmentation, weight loss, diarrhea, abdominal pain; accompanied by malabsorption syndrome.

Hereditary hamartomatous polyposis includes: Peutz-Jeghers syndrome (polyps of the gastrointestinal tract, pronounced pigmentation along the edge of the lips), neurofibromatosis, juvenile diffuse polyposis. In patients with juvenile polyposis, symptoms of the disease appear already in childhood (unlike diffuse familial polyposis), bleeding and acute intestinal obstruction are often present, necessitating intestinal resections.

3.2 Secondary pseudopolyposis

Inflammatory polyps are formed as a result of an inflammatory reaction to various damage to the colon (for example, infectious), and accompany not only ulcerative colitis.

4. Vascular malformations:
4.1. Vascular lesions.
4.2. Ischemic colitis.

With angiodysplasia, small arteriovenous shunts are formed. A common manifestation of this colon pathology is blood in the stool. Angiodysplasia causes bleeding from the lower intestines in 6% of cases. The source of bleeding is often localized in the right half of the colon.
Hemangiomas are observed less frequently than angiodysplasias and are predominantly localized in the rectum. Hemangiomas can be observed in Kaposi's sarcoma.
Secondary varicose dilation of mesenteric vessels with portal hypertension and telangiectasia can manifest as pathology of the colon.

5. Tumors:

5.1 Leiomyoma of the gastrointestinal tract
It is extremely rare. Diagnosis of this disease is difficult and sometimes impossible. This is explained by the fact that the disease is often asymptomatic and does not have a characteristic clinical picture. When describing leiomyomas, the authors note that they were discovered by chance during operations performed for other diseases. Leiomyomas are clearly circumscribed; the cells show a small number of mitoses or are absent altogether. In half of the observations, lipomas are localized in the cecum and ascending colon, located in the submucosal layer and occasionally in the subserosal layer. The tumor may have a wide base or a stalk of varying lengths.

5.2 Lipomas
Lipomas never become malignant. Lipoma easily changes size and shape when palpated or compressed during X-ray examination, since it is a fairly soft tumor. The intestinal wall at the location of the lipoma is elastic. The folds of the mucous membrane above the lipoma are thinned (above the tumor they may not be visible at all); in the parts adjacent to the tumor, the relief of the mucous membrane is usually not changed.

5.3 Carcinoids
They are considered low-grade tumors. Consist of neuroendocrine cells. Externally, they are small nodules of the mucosa or submucosa, most often not exceeding 2 cm in size. They are capable of local destructive growth with sizes less than 2 cm. They usually do not metastasize, metastases are possible with sizes greater than 2 cm. The clinic is characterized by carcinoid syndrome (hot flashes, diarrhea, bronchospasm ). In laboratory parameters, an increase in 5-hydroxyindoleacetic acid in the urine is possible.

6. Rectal cancer.

Complications

Regenerating epithelium is rare, but can acquire atypical features (dysplasia) and give rise to colon cancer.

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Treatment

Diet. The effectiveness of any diet for UC has not been established. Nutrition should be balanced and complete to correct existing deficiencies in energy, protein and microelements.

Drug treatment is prescribed taking into account the severity of exacerbation and localization of the process. Treatment goals:

Relieving exacerbation of the disease;

Maintaining remission;

Prevention of complications, including colorectal cancer.

Treatment of severe exacerbation

1. Glucocorticoids have been widely used in the treatment of UC attacks for more than 50 years. At the same time, the ineffectiveness of this group of drugs in maintaining clinical remission has been proven.
If the disease activity is high, it is advisable to begin treatment with parenteral administration. prednisone at a dose of 240-300 mg/day. When a clinical effect is achieved, they switch to oral administration of the drug (40-50 mg/day). After achieving a clinical effect, they begin to reduce the doses of prednisolone (the optimal rate of dose reduction is 5 mg per week). In this case, the degree of clinical and endoscopic regression of the disease, as well as the likelihood of developing side effects of hormonal therapy, should be assessed.
Of the glucocorticoid drugs with reduced systemic effect, only budesonide. It is prescribed at a dose of 9 mg/day in case of relatively low exacerbation activity and if there are concerns about the rapid development of side effects of glucocorticoid therapy (osteoporosis, hyperglycemia).

2. Immunosuppressors/anticytokines. In the absence of a pronounced clinical effect within 6-8 days from the start of parenteral administration of prednisolone, intravenous or oral administration should be considered cyclosporine at a dose of 4-5 mg/kg or infliximab at a dose of 5-10 mg/kg body weight. In approximately half of the cases of steroid-resistant forms of the disease, cyclosporine can stop the exacerbation. This drug has a pronounced hepato- and nephrotoxic effect, therefore, careful drug monitoring is necessary during treatment. Infliximab is a biological drug that binds tumor necrosis factor. Controlled studies confirm its high effectiveness in the treatment of severe steroid-resistant forms of the disease. During treatment, it was possible to achieve not only the induction of clinical remission, but also regression of inflammatory changes in the colon mucosa. Infliximab can also be used for maintenance treatment of the disease.

4. Surgical treatment is used when conservative measures are ineffective in a severe attack of UC.
Indications for surgery:

Absolute: perforation of the colon, massive intestinal bleeding, colon cancer, toxic megacolon when conservative therapy is ineffective within 12-24 hours;

Relative: pronounced clinical manifestations in UC resistant to conservative therapy; dysplasia of the colon mucosa with a long history of the disease (20 years or more); growth retardation in childhood and adolescence; extraintestinal manifestations.

If there are only relative indications for surgery, it is necessary to inform patients about the possible positive and negative aspects of surgical treatment.

The operation itself consists of a subtotal colectomy with the application of an ileostomy or the formation of an ileoanal pouch. Both methods have their advantages and disadvantages.

Treatment of exacerbations with moderate activity
In the treatment of mild and moderate exacerbations of UC, 5-ASA drugs are widely used - mesalazine (osacol, pentasa), sulfasalazine, olsalazine (dipentum), balsalazine (colazal). During an exacerbation, 2.5-3 g of the drug per day is usually prescribed; after the induction of clinical remission, the dose of the drug is reduced. For moderate attacks of the disease, it is advisable to combine 5-ASA preparations with the administration of oral glucocorticoids.

Treatment of exacerbations of distal forms of UC
Topical 5-ASA preparations in the form of enemas or suppositories can be used as monotherapy for mild to moderate exacerbations of ulcerative proctitis. It should be borne in mind that suppositories ensure that the drug reaches only the rectum and only the very initial parts of the sigmoid colon.
In the presence of proctosigmoiditis, it is advisable to use topical foam-based medications or dosage forms in the form of enemas (the latter ensure the deepest penetration of the drug).
Treatment of left-sided forms of UC in many cases requires the combined use of topical and oral forms of 5-ASA drugs. This prevents the spread of the inflammatory process to the proximal colon. For exacerbations of left-sided colitis, topical 5-ASA preparations are prescribed twice a day.
Rovaza- 5-ASA in enema form. Each ROVAZ enema contains 4 grams of 5-ASA. The enema is usually given during sleep so that patients can maintain the enema throughout the night. The enema contains sulfite and should not be used in patients with a sulfite allergy. If the patient is not allergic to sulfite, Rosaz enemas are safe and helpful.
Kanaza- 5-ASA in the form of a candle. Each suppository contains 500 mg of 5-ASA.
With more pronounced activity of the inflammatory process in the left parts of the colon or in the absence of a clinical effect on therapy with 5-ASA drugs, the issue of prescribing glucocorticoids is considered: enemas or hydrocortisone foam (Cortinema or Cortifoam), a topical form of budesonide. After the enema, the patient should remain on his left side for at least 20 minutes. In cases of severe tenesmus, enemas are performed in the patient's knee-elbow position.

Maintenance therapy

Effective drugs for anti-relapse therapy of UC are mesalazine and sulfasalazine. Prescribed in a dose significantly lower than in the treatment of the active phase of the disease: 1-2 g/day.

Currently, immunosuppressants (azathioprine, mercaptopurine) are widely used when 5-ASA drugs are ineffective in the anti-relapse treatment of patients with UC. The effective dose of azathioprine, which is most widely used in the CIS, is at least 2 mg/kg of patient weight per day. In the first week of treatment, the trial dose of the drug is usually 50 mg/day.
During the use of immunosuppressants, drug monitoring is necessary. During the first month of treatment, it is advisable to monitor liver markers and blood cellular composition weekly. In the future, control tests can be performed monthly. Since the clinical effect of immunosuppressive therapy appears only 3-4 months after the start of treatment, other maintenance therapy should be carried out in parallel during this time.

If azathioprine is ineffective, methotrexate can be included in the maintenance therapy program (it has less effectiveness as a maintenance drug for UC). Methotrexate is prescribed once a week at a dose of 25 mg intramuscularly. Subsequently, the dose of the drug is reduced to 7.5-15 mg. The drug monitoring regimen corresponds to that for azathioprine.

If other maintenance therapy regimens are ineffective, the possibility of using infliximab has been proven (based on the results of controlled studies). The drug is administered intravenously every 8 weeks. During the process, the patient’s general condition, liver markers, and blood cellular composition are monitored.

In distal forms of ulcerative colitis, after achieving clinical remission, topical 5-ASA preparations can be administered initially once a day, then every other day or even 1-2 times a week.

Complementary therapy
1. Antibiotics. The use of broad-spectrum antibacterial drugs is advisable in the presence of a pronounced inflammatory reaction, the threat of toxic dilatation, and numerous microabscesses of the colon mucosa. The use of metronidazole and ciprofloxacin is especially effective. During therapy with immunosuppressants, due to the risk of developing Pneumocystis pneumonia, trimethoprim-sulfamethoxazole may be prescribed according to indications.

2. The use of loperamide and anticholinergics (Lomotil) in severe forms of UC, despite a temporary slight improvement in the patient’s subjective condition (reduction of tenesmus, diarrhea), can provoke the development of severe complications of the disease (constipation, toxic dilatation, colon perforation). They are used very limitedly, according to strict indications.

3. Probiotics are traditionally used in the CIS for mild forms of the disease as part of complex therapy, although the effectiveness of these drugs in this case has not been clearly proven.

Forecast

Due to the complexity of the disease and the recurrent nature of the process, the prognosis for nonspecific ulcerative colitis is difficult.
In some cases, there is a remission that lasts for years, in others there are frequently recurring attacks. In both cases, patients can be of the same age, gender and with the same degree of damage to the colon.

Forms of UC often transform into one another. Limited damage to the rectum and sigmoid colon, detected in the patient during the first examination, with the development of the disease can gradually involve the overlying parts of the colon and, finally, the entire intestine. The speed of spread of the process increases with increasing intensity of the disease.

The prognosis for nonspecific ulcerative colitis is determined by the severity and extent of the lesion, as well as the age of the patients. The most severe attacks and failure of treatment are observed in patients under 20 and over 60 years of age. In children, the disease is especially severe and delays the child’s physical development.

In 25% of patients, it is not possible to achieve stable remission, severe complications develop and they require surgical treatment 5-10 years after the onset of the disease. About 5% of patients die within 1 year of the disease.

Colon adenocarcinoma develops in 3-5% of patients with ulcerative colitis, and the risk increases with the duration of the disease. The risk of adenocarcinoma is higher in cases of pancolitis Pancolitis - inflammation of the colon throughout its entire length
and in cases where the onset of the disease occurs before the age of 15 years. Benign strictures Stricture is a sharp narrowing of the lumen of a tubular organ due to pathological changes in its walls
, as a complication, rarely lead to intestinal obstruction.

Hospitalization

Indications for hospitalization:

Exacerbation that cannot be stopped in an outpatient setting;
- suspicion of the development of complications of the disease, including if surgical treatment is necessary;
- clarification of the diagnosis of the underlying disease, identification of its extraintestinal manifestations.

The choice of a specific treatment program for a patient with ulcerative colitis depends on the activity of the disease, the localization of the inflammatory process, the possible presence of extraintestinal manifestations, and the individual characteristics of the patient (age, gender, drug intolerance, concomitant diseases).

(possible presence of colon carcinoma in close relatives);

Combination of UC with primary sclerosing cholangitis;

Presence of retrograde ileitis

1.2 Conduct in risk groups pregular colonoscopies with multiple biopsies taken(at least 3 pieces) from the wall of the colon every 10 cm along the entire length of the colon, as well as from all suspicious areas.

The most important morphological criterion for identifying groups of UC patients with an increased risk of developing colorectal cancer is the presence of severe dysplasia of the colon mucosa. In European countries and the USA, when high-grade dysplasia is detected (especially when combined with colon polyps), the issue of preventive colectomy is usually decided upon.

A strategy for regular examinations in chronic ulcerative colitis to detect colorectal cancer.

* Dysplastic lesion or growth (DALM), which doesn't look as an adenoma, that is, a pathological proliferation of the mucous membrane, a circular or sectoral narrowing, or a broad-based tumor.

** Dysplastic polyps can be treated endoscopically without any fear, provided that the adjacent mucosa is not dysplastic.

Information

Sources and literature

1. "ASGE (American Society for Gastrointestinal Endoscop.) guideline: endoscopy in the diagnosis and treatment of inflammatory bowel disease", Gastrointest Endosc 2006 Apr;63(4):558-65
2. "Colonoscopic surveillance for prevention of colorectal cancer in people with ulcerative colitis, Crohn's disease or adenomas" National Institute for Health and Clinical Excellence, 2011
3. "Diagnosis and Management of Polyps in Inflammatory Bowel Disease" Robert D. Odze, M.D., F.R.C.P.C. Chief, GI Pathology Service Associate Professor of pathology Brigham & Women’s Hospital Harvard Medical School Boston, MA
4. "Elevated serum values ​​of procollagen III peptide (PIIIP) in patients with ulcerative colitis who will develop pseudopolyps", World J Gastroenterol, 2003 Mar 15 ;9(3): 619-621
   1. Žarko Babić, Vjekoslav Jagić, Zvonko Petrović, Ante Bilić, Kapetanović Dinko, Goranka Kubat, Rosana Troskot, Mira Vukelić
5. "Ulcerative Colitis" Richard Farrell, Mark Peppercorn, Department of Gastroenterology, Center for Inflammatory Bowel Diseases, Bethe Israel Deaconess Medical Center, "International Medical Journal", No. 1, 2003
6. http://www.pathologyoutlines.com/topic/colontumorinflammatory.html
7. wikipedia.org (Wikipedia)
   1. http://ru.wikipedia.org/wiki/Colonoscopy -

Information

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The development of pseudopolyps in nonspecific ulcerative colitis is described by many authors with different frequencies: 23.7% - V.K. Karnaukhov (1973), 18% - Brown (1950) and 65% - Goldgraber (I960). As Watkinson (1970) points out, pseudopolyps are most often formed in the sigmoid colon and in the left half of the colon. The predominant localization of pseudopolyps in the areas of the earliest and most severe lesions is quite understandable, given that the origin of pseudopolyps is associated with destructive and regenerative processes in the intestinal wall.

In our material, out of 71 patients with a chronic form of ulcerative colitis, pseudopolyposis was detected in 44 (62%) patients. Pseudopolyps are very diverse in their morphology. As a rule, they are quite large - from 0.5 to 1-1.5 cm in diameter, have a mushroom shape or resemble a mulberry, and are located on a wide base. Sometimes pseudopolyps are long, finger-shaped, 3-5 and even 7 cm long, hang freely into the intestinal lumen or spread over the ulcerated surface in the form of bridges. Histologically, similar pseudopolyps are islands of the mucous membrane, sometimes submucosal, preserved during the destructive and ulcerative process. Their formation is completed by the proliferation of glandular epithelium, which surrounds the pseudopolyps on all sides. Thus, the origin of these pseudopolyps is associated with destructive and regenerative processes in the intestinal wall. We call them chronic destructive pseudopolyps.

Another form of pseudopolyps are small (2X3 mm in size), often tightly adjacent formations, built from overgrown adenomatous or granulation tissue. According to their histological structure, they belong to typical regenerative pseudopolyps. In adenomatous pseudopolyps, the glands are irregularly shaped, branched, cystically dilated, and sometimes contain many goblet cells that abundantly secrete mucin. In other cases, mucin secretion is insignificant, the epithelium is low and flattened. Pseudopolyps, built from granulation tissue, are small and red in color; histologically they consist of granulation tissue of varying degrees of maturity, always abundantly infiltrated with leukocytes, plasma cells and neutrophilic leukocytes.

We join the opinion of Zh. M. Yukhvidova (1969) and consider pseudopolyposis as one of the morphological manifestations of the disease, which often occurs as a result of deep destruction and regenerative process in the intestinal wall. There is even an opinion that the development of pseudopolyposis is a favorable sign indicating an upcoming recovery. There is another point of view, according to which pseudopolyposis is classified as a precancerous condition. Thus, according to Scarborough (1955) and Kloin (1955), in patients with ulcerative colitis, cancer developed against the background of pseudopolyposis in 27% of cases. Other authors did not observe signs of malignancy of the glandular elements of pseudopolyps. We also failed to note malignancy in patients with a chronic form of ulcerative colitis, despite the fairly high frequency of pseudopolyposis.

Pathological anatomy. Pathological changes reflect the main feature of the course of nonspecific ulcerative colitis - alternating periods of exacerbation and remission. Ulceration and inflammation of the mucous membrane of the colon with the formation of pus are replaced by healing, and then exacerbation again, etc.

In the pathological picture of nonspecific ulcerative colitis, changes characteristic of the acute progressive and chronic course of the pathological process should be distinguished (T. F. Kogoi, 1963; Jones, 1961).

In an acute progressive process, macroscopically the wall of the colon is swollen, hyperemic, and easily ruptures; There are multiple erosions and ulcers on the full-blooded mucous membrane. The latter rarely penetrate deeper than into the submucosa. However, sometimes the process spreads to a deeper layer of the intestinal wall and causes perforation. Ulcers tend to merge, and then the entire surface of the mucous membrane of the colon is one extensive ulcerative surface. Fibrinoid necrosis of the vessel wall may occur at the bottom of the ulcers. When exposed to erosion, such vessels become a source of bleeding.

Due to the addition of a secondary infection, the walls of the affected intestine become covered with mucopurulent loose plaque. Characterized by multiple small pustules - crypt abscesses - and larger abscesses of lymphoid follicles, the intestinal lumen contains bloody-purulent fluid.

In the chronic course of nonspecific ulcerative colitis, pathological changes depend both on the phase of the disease and on the depth of damage to the mucous membrane. In the acute phase, changes in the mucous membrane are similar to those in the acute form of the disease. The difference is the appearance of signs of inflammation against the background of previously existing structural changes in the mucous membrane. As the exacerbation subsides, bleeding decreases, and erosions become epithelialized. In the remission phase, changes are determined due to the development of sclerosis of the intestinal wall and atrophy of the mucous membrane.

For superficial lesions limited to the own layer of the mucous membrane without disruption of the crypt apparatus, the development of atrophy is characteristic. The latter becomes very thin, pale beyond exacerbation, and may appear normal macroscopically.

With deep damage to the mucous membrane of the colon, lush granulation tissue forms at the site of the ulcers, and then cicatricial retraction. The intestinal wall thickens due to edema and fibrosis of the submucosal layer, the intestine shortens and its lumen narrows, and the haustra disappear. As a result of a combination of destructive and reparative processes, the relief of the mucous membrane changes, protrusions of various shapes and sizes appear, which are combined under the term “pseudopolyposis”. Pseudopolyps consist of areas of mucous membrane preserved in the area of ​​extensive ulceration, or of granulation tissue that has arisen at the site of former ulcers; Mixed pseudopolyps are also found. In the phase of exacerbation of the disease, pseudopolyps swell and increase in size, in the remission phase they flatten and decrease. With the development of excessive epithelial regeneration, individual pseudopolyps may acquire the morphological features of a true adenomatous polyp; such polyps do not tend to shrink when the inflammatory process subsides. Cases of the development of colon cancer against the background of long-term (over 10 years) nonspecific ulcerative colitis with pseudopolyposis are described.

In the study of histological changes in the mucous membrane of the colon, great success has been achieved due to the introduction into clinical practice of the aspiration biopsy method, which allows for repeated intravital studies of the mucous membrane of the distal colon in various phases of the disease (P. P. Menshikov et al., 1969; A G. Sahakyan, 1968; Kirsner, 1961; Lumb, 1961, etc.). In Fig. 36 shows a histological picture of the mucous membrane of a healthy person according to aspiration biopsy.

The acute phase of the disease is characterized by stasis and marginal standing of leukocytes in the vessels, thickening of the vascular endothelium and the basement membrane of the epithelium, pronounced lymphoplasmic infiltration of the stroma, groups of segmented leukocytes are found, the epithelium between the crypts, and to a lesser extent the crypt epithelium loses the ability to form mucus and differentiate, abscesses occur crypt (Fig. 37).

In the phase of subsiding exacerbation, changes in the vessels decrease, a gradual restoration of the epithelium occurs, starting from the deep parts of the crypts to the surface epithelium, its ability to form mucus is restored while maintaining the normal chemistry of mucus, lymphoplasmic infiltration remains very intense, in some cases with a large number of eosinophils (Fig. 38). In the remission phase, the epithelium hypersecretes mucus, the connective tissue connecting the mucous itself with the submucosal layer is more clearly visible, the thickness of the mucous layer itself is reduced, the number of crypts is reduced, they are deformed, branched, and form cysts (Fig. 39).

In all phases of the disease, attention is drawn to the preservation of the high ability of the epithelium to regenerate: even in the acute phase, it performs its covering function, transforming into a flat one (Fig. 40). Signs of a high ability to regenerate in the phase of subsiding exacerbation include the appearance of epithelial outgrowths inside the glands (“gland in the gland”) and papillary growths of the integumentary epithelium (Fig. 41). The epithelium of the basal sections of the crypts contains a large amount of proteins and nucleic acids, which indicates more intense metabolic processes than normal.

Rice. 36. The mucous membrane of the colon of a healthy person.
1 - integumentary epithelium; 2 - goblet cells; 3 - crypts; 4 - stroma of the mucous membrane. Microphoto, uv. 56.
Rice. 37. Crypt abscess. Microphoto, uv. 280.
Rice. 38. Chronic recurrent nonspecific ulcerative colitis in the reverse development phase.
1 - abundant cellular infiltration of the mucous membrane; 2 - proliferation of connective tissue in the submucosal and muscular layers of the mucous membrane. Microphoto, uv. 56.
1 - crypts of irregular shape, Microphoto, uv, 56.
Rice. 39. Chronic recurrent nonspecific ulcerative colitis in remission.
Rice. 40. Nonspecific ulcerative colitis in the acute phase. The epithelium is transformed into flat.
Rice. 41. Nonspecific ulcerative colitis in the subsiding phase
exacerbations. 1 - papillary proliferation of the integumentary epithelium.

Histological examination of pseudopolyp tissue showed the presence of similar changes. Histological signs that can be considered characteristic of foci of proliferation in simple adenomatous polyps (higher, darker and narrower epithelium with rod-shaped hyperchromic nuclei located at different levels relative to each other) are very rare, observed in cases where the pseudopolyp is not tends to decrease as the exacerbation of inflammation subsides.

Intestinal damage in nonspecific ulcerative colitis involves either the entire colon or part of it. According to our data, the majority (59.8%) are patients with damage to the left part of the colon, i.e. the descending, sigmoid and rectum; total damage occurs in 21.3% of patients; in these cases, the small intestine is usually affected, but without the formation of ulcers. In 18.9% of cases, the process involves the left section and transverse colon (Fig. 42). We have not encountered any cases of an isolated right-sided process described in the literature.

Rice. 42. Frequency of varying extent of damage to the colon in nonspecific ulcerative colitis.

Pseudopolyp- this is a thickened area of ​​the mucous membrane, localized in the area of ​​\u200b\u200ban ulcer or scar. Pseudopolyps are easily vulnerable, hyperemic growths of the mucous membrane that occur against the background of inflammatory bowel diseases.

Etiology of pseudopolyps

Pseudopolyposis is not a separate disease. This is a sign of a strong inflammatory process, which in most cases is characteristic of ulcerative colitis (22-64% of all cases). During the course of the disease, a restructuring of the intestinal mucosa occurs, in other words, tissue dysplasia occurs. Pseudopolyps are not malignant tumors, but the risk of colon cancer exists, which is associated with the underlying disease. Diseases predisposing to pseudopolyposis are ulcerative colitis, Crohn's disease, dysentery, proctosigmoiditis. If one of these diseases or a group of them is present, they speak of secondary pseudopolyposis. The causes of primary (idiopathic) pseudopolyposis are not known.

Localization

A typical place for pseudopolyps to occur is the left colon or the entire rectum. They are located along with true polyps and have a common nature: both polyps and pseudopolyps are islands of the mucous membrane with inflammatory changes. They differ from true polyps by the absence of a stalk, easy bleeding and prompt disappearance after treatment.

Diagnostics

Pseudopolyps are identified during examination using a sigmoidoscope or colonoscope. Using the same devices, tissue is collected for microscopic examination. Differentiation of pseudopolyps from true polyps is made as a result of studying the structure of the neoplasm and analyzing their structure.

Treatment of pseudopolyps

To treat pseudopolyps, both conservative therapy (as a treatment for the underlying disease) and radiosurgery methods (removal with the Surgitron apparatus) are used with equal success. The latter method is used in cases where the pseudopolyp bleeds profusely and actively secretes mucus. This can happen during every bowel movement. In the absence of a pronounced symptomatic picture, the patient is recommended to eat a diet based on fiber-rich foods, a course of probiotics, and