Colonic distention is a common cause of ulcerative colitis (UC), an inflammatory disease of the rectum or colon of unknown origin. It mainly involves the rectum, sigmoid colon and descending colon and is characterized by mucosal congestion, edema, multiple superficial ulcers, advanced wall thickening and luminal narrowing with polyp formation. The disease is characterized by persistent diarrhea, mucus stools, bloody or purulent stools, abdominal pain and urgency, and may be accompanied by extraintestinal manifestations such as fever, anemia, arthritis, skin lesions and liver disease. The onset of the disease is rarely acute, but most of them have a slow onset and a long course, often with recurrent episodes of variable length, also known as chronic non-specific ulcerative colitis. In the early stages, abdominal pain, diarrhea and bloody stools may occur. Abdominal pain of varying degrees is caused by spasm of the colonic muscles, distension of the colon and inflammation stimulating local sensory nerves. Abdominal distension is mostly confined to the left lower abdomen or lower abdomen, with paroxysmal mild pain. When the lesion is severe it may present with colic. The etiology is completely clear and may be related to immune, genetic, psychiatric and infectious factors. The disease is often complicated by autoimmune diseases such as hemolytic anemia, arthritis, erythema nodosum, and liver disease during its development, while treatment with adrenocorticosteroids can lead to remission. In some patients, anti-colon epithelial cell antibodies and anti-E. coli O14 antibodies are detected in the serum, and these antibodies react with colonic epithelial cell antigens in an autoimmune reaction, causing mucosal damage. There was lymphocyte infiltration in the diseased colonic tissue, and in tissue culture, lymphocytes from the patient were found to have cytotoxic effects on normal human colonic epithelial cells. The presence of immune complexes with IgG, complement and fibrinogen deposition in the lamina propria of the colonic mucosa was confirmed by fluorescent immunoassay, and this immune complex was experimentally found to have a damaging effect on the colonic mucosa. This suggests that the pathogenesis of the disease is related to the immune response and is therefore considered to be an autoimmune disease. The incidence of the disease is often familial, with a significantly higher incidence in the patient’s family, and there are significant differences in incidence between races, with a significantly higher incidence in Europe and the United States than in Asian countries such as Japan, suggesting that the onset of the disease may be related to genetic factors. In addition, the increased presence of human leukocyte antigens HLA-11 and 7 in patients with this disease also suggests that genetic factors may have a role in the development of the disease. Mental factors and emotional changes cause dysfunction of the vegetative nerves, leading to inflammation of the intestinal wall and promoting the onset of the disease, which are generally considered to be predisposing factors for the onset of the disease. The pathological changes and clinical manifestations of the disease are similar to those of bacterial dysentery, but a possible pathogen has not been identified in the stool. It is thought that dysentery bacilli, intestinal bacterial and viral infections may be associated with the onset of the disease, but are only a predisposing factor.