Causes and mechanisms of development
The etiology of ulcerative colitis is not fully understood. The role of specific bacteria or parasites has not been proven, but genetic predisposition is supported by familial cases.
The autoimmune theory is considered leading. It is hypothesized that the key pathogenetic mechanism is T-lymphocyte dysfunction, which exerts a direct cytotoxic effect on the colonic mucosa. This theory is also supported by frequent systemic (extraintestinal) manifestations of the disease, such as erythema nodosum, arthritis, and hemolysis.
Pathomorphology
The inflammatory process in UC always begins in the rectum and gradually spreads proximally to other parts of the large intestine. Total colonic involvement is observed in 25% of cases.
During an exacerbation, the mucosa becomes edematous and hyperemic, with multiple erosions and coalescing irregular ulcers appearing. The process may involve the submucosal and muscular layers, which carries a risk of perforation and bleeding. The bowel wall is infiltrated by lymphocytes, plasma cells, and eosinophils, and small abscesses are formed.
The outcome of inflammation is scarring: strictures (narrowing of the lumen) develop, the mucosa atrophies, and multiple pseudopolyps appear.
Clinical presentation
The disease has a chronic, prolonged course with alternating phases of exacerbations and remissions (which can last up to 10–15 years). Females are affected more frequently.
- Onset: the appearance of bright red blood in the stool is often the first sign.
- Leading symptom: frequent loose stools mixed with blood, mucus, and pus.
- Pain syndrome: discomfort, abdominal pain, and painful false urges (tenesmus) accompanied by cramps.
- General toxic syndrome: progressive weakness, loss of appetite, fever, weight loss.
Particular attention should be paid to systemic manifestations, which reflect the autoimmune nature of the disease. These include polyarthritis, erythema nodosum, pyoderma, uveitis, stomatitis, phlebitis, thrombosis, nephritis, and hepatobiliary system involvement. Metabolic disorders are also observed: muscle wasting, electrolyte imbalance, vitamin deficiencies, and growth retardation in children.
Diagnostics
The diagnosis of UC is established based on a comprehensive examination:
- Laboratory findings: blood tests reveal anemia (due to blood loss and malabsorption), leukocytosis, elevated ESR, dysproteinemia, hypoalbuminemia, and electrolyte shifts. Stool test (coprogram) shows clusters of leukocytes, erythrocytes, and epithelial cells. Bacteriological culture at the onset of the disease shows no pathogenic flora (important for ruling out infections).
- Endoscopy (colonoscopy): visualization shows the disappearance of normal folds, hyperemia, edema, specific multiple hemorrhages, and in severe cases, ulcer defects. Exudate (mucus, pus, blood) is detected in the lumen.
- Biopsy: necessary for differential diagnosis, primarily with Crohn's disease and specific infections.
- X-ray examination (barium enema): shows smoothing of the mucosal relief, ulcers, pseudopolyps, and loss of haustration («lead pipe» sign).
Complications and treatment principles
UC complications can be life-threatening. In acute severe forms (Colitis gravis), toxic megacolon may develop—significant dilation of the bowel lumen due to smooth muscle paralysis. Surgical complications include ulcer perforation with peritonitis, profuse bleeding, and stricture formation. There is also an increased risk of colorectal cancer, which rises with disease duration.
Treatment is divided into:
- Conservative: sulfasalazine drugs as baseline therapy; glucocorticoids are prescribed for severe forms, extensive involvement, and systemic manifestations.
- Surgical: used when severe complications develop or conservative therapy is ineffective.
Briefly: answers to topical questions
What classes of medications are used for the conservative treatment of ulcerative colitis?
The following drug therapy groups are indicated in the literature for the conservative treatment of ulcerative colitis:
- 5-Aminosalicylic acid (5-ASA) preparations — baseline drugs for UC treatment; include mesalazine, as well as sulfasalazine as a prodrug releasing 5-ASA in the colon.
- Glucocorticoids — used as intensive therapy for extensive involvement, marked metabolic shifts, and systemic manifestations.
- Biological therapy / bDMARDs in case of ineffectiveness of glucocorticoids within 2 weeks: TNF-alpha inhibitors (infliximab, adalimumab, golimumab), selective immunosuppressant vedolizumab, interleukin inhibitor ustekinumab.
- Targeted synthetic selective immunosuppressants (tsDMARDs): tofacitinib, upadacitinib, ozanimod.
What local surgical complications can occur in ulcerative colitis?
Local surgical complications of ulcerative colitis include toxic megacolon, perforation, bleeding, and strictures.
- Toxic megacolon — a specific complication of acute severe ulcerative colitis (Colitis gravis); associated with paralytic changes in the smooth muscle cells of the bowel wall and manifests as significant dilation of the colonic lumen.
- Ulcer perforation — leads to peritonitis; the following chain is also described: bowel segment atonia → sharp distension → perforation → peritonitis.
- Profuse bleeding.
- Strictures — cicatricial and inflammatory narrowing of the bowel lumen.
What changes are detected in complete blood counts and biochemical blood tests during an exacerbation of ulcerative colitis?
Blood tests during an exacerbation of ulcerative colitis reveal signs of inflammation, anemia, and metabolic disorders. In the complete blood count:
- Anemic syndrome — post-hemorrhagic anemia due to blood loss and deficiency anemia due to impaired absorption of iron, vitamin B12, and folic acid.
- Inflammatory syndrome — leukocytosis and elevated ESR are characteristic.
In the biochemical blood test:
- Dysproteinemia — manifested by an increase in alpha-1 and alpha-2 globulins.
- Metabolic disorders — hypoalbuminemia and hypocholesterolemia are detected.
- Electrolyte shifts — decreased potassium (hypokalemia) and magnesium (hypomagnesemia) levels.
Which intestinal infectious diseases require differential diagnosis with ulcerative colitis?
Differential diagnosis of ulcerative colitis among intestinal infections is primarily performed with the following specific infections:
- amebiasis;
- schistosomiasis;
- intestinal tuberculosis.
Bacteriological examination is used for differential diagnosis with infections: in ulcerative colitis, the absence of pathogenic flora at the onset of the disease is noted. If differentiation from amebiasis is required, colonoscopy with mucosal biopsy is indicated, followed by parasitological examination of the biopsy specimen, as well as the contents and discharge of erosions and ulcers.
To memorize the exudate triad in UC endoscopy, use the mnemonic «M-P-B»: Mucus, Pus, Blood.
Class and exam questions
What is the difference in localization between UC and Crohn's disease?
In ulcerative colitis, the rectum is always affected, and the process spreads only along the large intestine, mainly involving the mucosa. Crohn's disease can affect any part of the gastrointestinal tract through the entire thickness of the wall.
What is toxic megacolon?
This is a severe complication of UC, in which significant dilation of the colonic lumen occurs due to paralytic changes in the smooth muscle cells of the wall. It is associated with a high risk of mortality.
What systemic (extraintestinal) manifestations are characteristic of UC?
These include joint lesions (polyarthritis), skin lesions (erythema nodosum), eye lesions (uveitis), oral mucosal lesions (stomatitis), as well as vascular, renal, and hepatic involvement.
What else to study on this topic
- Mechanisms of anemic syndrome development in UC
- Differential diagnosis of UC and infectious colitis
- Histological picture of the biopsy sample in UC
- Metabolic shifts and their correction in severe course
- Indications and methods of surgical treatment for ulcerative colitis
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