Crohn's disease

Introduction Crohn's disease is also known as "limited enteritis", "segmental enteritis", "chronic full-thickness of the intestinal wall" and so on. Its characteristics are unclear, more common in young people, manifested as granulomatous inflammatory lesions, combined with fibrosis and ulcers. It can invade any part of the gastrointestinal tract, including the mouth and anus. The lesions are segmental or jumping, and can invade the outside of the intestines, especially the skin. The clinical manifestations vary according to the location, extent and extent of the lesion, which can be manifested as abdominal pain, diarrhea, abdominal mass, fistula formation and intestinal obstruction, accompanied by fever and anemia. The course of the disease is slow and easy to relapse. Causes (1) The cause of the disease has not been determined so far. Recent studies have tended to suggest that the disease may be the result of a combination of genetic susceptibility and a variety of exogenous factors. 1. Genetic susceptibility (1) Genetic factors: A large number of data indicate that Crohn's disease is related to genetic factors. The study found that the coincidence rate of Crohn's disease among twins with single egg development was significantly higher, at 67%, while the twins of twins had a coincidence ratio of only 8%. At the same time, it was found that patients with Crohn's disease showed inconsistency with their spouses and did not differ from the general population. The above indicates that the disease has family aggregation. It has also been reported that the Jewish family has a high incidence of the disease in the Jewish family compared with non-Jewish people and finds mainly those of the Ash Kenazi race. The survey of Askenazi people scattered around the world has a higher incidence of Crohn's disease than those of non-Askens children living in the same area. Perhaps the Askenaz Jews represent humans. People with genetic susceptibility. It has also been reported that patients with Crohn's disease are more associated with HLA-DR4 type serum antigens. How genetic factors affect the occurrence of this disease is unclear. Some people think that genetics determine the body's immune response. The genetic factors of patients with inflammatory bowel disease determine that they have an excessive immune response to some antigenic substances in the intestinal lumen. (2) Changes in susceptibility: At present, most scholars believe that the occurrence of Crohn's disease may be related to the abnormal immune response of the body to various antigens stimulated in the intestine. A growing body of evidence suggests increased T cell activation in the lamina propria of Crohn's disease, including increased expression of surface markers for T cell activation, increased production of T cell cytokines, and increased cytotoxic T cell function. This increase in T cell activation leads to aggregation of effector cells such as neutrophils. Subsequent synthesis of destructive substances (such as proteases and reactive oxygen metabolites) results in intestinal damage in Crohn's disease. The triggering mechanism of T cell activation is unclear. In the past, there was some conviction that it was caused by chronic mycobacterial infection, but there is no reliable evidence. It is currently believed that it may not be singular and is more likely to be activated by a number of widely occurring triggering substances. The fundamental defect of Crohn's disease leads to the permanent activation of T cells, a defect that is currently being explored. It may be a foreign antigen, increased antigen delivery (increased intestinal permeability), and a genetically predisposed mucosal immune disorder. The result of a complex interaction. Current research indicates that the view that this disease was once considered an autoimmune disorder is inaccurate. In fact, there is no credible evidence that there is an immune response directly associated with any autoantigen that can cause the inflammatory process observed in Crohn's disease. 2. Exogenous factors (1) Infectious factors: In early years, the pathological manifestations of Crohn's disease were similar to those of non-calcified tuberculosis. It was suspected that the disease was caused by Mycobacterium tuberculosis, but the pathogen was not isolated by various methods. In the late 1970s and early 1980s, there were reports of mycobacteria of Kansasii or mycobacteria similar to Mycobacterium tuberculosis in the intestinal segment and mesenteric lymph nodes excised from Crohn's disease. Studies have found that these mycobacteria inoculated in the peritoneal cavity of mice can cause granuloma in the liver and spleen and develop acid-fast bacilli. These acid-fast bacilli are then administered orally to the dairy sheep, and non-caseal granuloma can occur at the end of the ileum of the sheep after several months. It is believed that mycobacteria may be the cause of Crohn's disease. However, some authors have observed that these mycobacteria are also present in some non-inflammatory bowel diseases or normal human intestinal tissues, and it has been reported that Streptococcus faecalis can cause local granuloma in the intestinal wall of rabbits, so these branches are not certain. Bacilli is the exact cause of the disease. It has also been suspected that the cause of Crohn's disease is a virus. In 1970, Mitchell and Rees inoculated mesenteric lymph nodes and tissue homogenates from patients with Crohn's disease through a 220 nm filter screen and inoculated on the toes of rats. After 6-24 months, epithelioid cell granuloma and giant cell granuloma occurred on the toes of rats. In the same way, granuloma can occur in the ileum of rabbits. Immunosuppressive drugs have no effect on the pathogenesis, suggesting that there may be an infectious microorganism that may be a virus. However, the results of this experiment have not been repeated. It is also believed that Crohn's disease is associated with viral infections such as measles and influenza. However, the true virus particles have not been isolated from the intestinal tissue of Crohn's disease patients, so the cause of this disease cannot be confirmed as a virus. (2) Environmental factors: The incidence of urban residents is higher than that of rural people. This difference also exists in Sweden, where rural health care is high, which may be related to social and economic status. Some studies have shown that oral contraceptives increase the risk of inflammatory bowel disease. But other studies have failed to confirm. Numerous studies have shown that smokers are at increased risk of Crohn's disease. And smoking can increase the likelihood of recurrence of Crohn's disease. The mechanism is still unclear. Some potential environmental factors can trigger the development of Crohn's disease. The increase in edible refined sugar has been identified as a disadvantage. An ordinary period of birth can also be used as a stimulating factor to cause some pregnant women to develop Crohn's disease after childbirth. (B) the pathogenesis 1. Distribution of lesions The disease can be affected from any part of the gastrointestinal tract from the mouth to the anus, the lesions are leaping or segmental distribution. Simultaneous involvement of the small intestine and colon is the most common, accounting for 40% to 60%; limited to 30% to 40% of the small intestine, mainly in the terminal ileum; lesions occurring in the anus or rectum alone are rare, accounting for 3%, mostly with the small intestine and Colonic lesions are present in combination; colons are less common, accounting for 5% to 20%. The stomach or duodenum, esophagus, and oral lesions account for about 10% or less. 2. The early pathological changes of the general pathology are small ulcers of the mouth ulcers, ranging in size. The smallest is the tip of the needle, accompanied by bleeding; the larger one is clearly shallow and the bottom is white. If a small lesion is missed during surgical resection, it can recur from there. Typical ulcers are longitudinal or limp, discontinuous, and vary in size. Cobblestone-like changes are present in approximately 1/4 of the cases. Thickening of the intestinal wall and intestinal stenosis are more common. About 95% of surgical cases have stenosis. Some Crohn's disease can be seen with multiple inflammatory polyps. 3. Microscopically, the lesions under the microscope are found in the intestinal mucosa, submucosa and serosal layer, mainly the submucosa. Common lymphocyte aggregation can have a germinal center. The location of lymphocyte aggregation is closely related to blood vessels and dilated lymphatic vessels. Lymphocyte aggregation of the serosa layer can form a rosette-like pattern. Plasma cells, multinucleated cells, and eosinophils can also be seen. A mucosal layer can be seen in the sac abscess. Non-case granuloma is one of the important features of this disease. It consists of epithelioid cells and giant cells. There is no cheese necrosis in the center, which is uncommon. It is only found in about 50% of cases. It should be noted that granulomas can also be found in Yersinia infection or Chlamydia infection, which can be identified by an experienced pathologist. Glassy and adenoid inclusions are seen in 5% of cases, as seen in sarcoidosis and tuberculosis. Granuloma is often very atypical and has a distinct boundary formed by lymphocytes. It can be seen in the whole layer of the intestinal wall, but the submucosa and serosal layer are most likely to appear. In addition to the intestinal wall, granulomas can also be found in local lymph nodes. The fissure ulcer of the intestinal wall extends deep into the muscularis propria. Transmural penetration is the basis for the formation of internal fistulas and cutaneous fistulas and abscesses. The fracture under the naked eye is linear and may have branches, surrounded by edema and island-like mucosa. In the cross section, the fissure branches appear as intramural abscesses. Due to edema and lymphatic vessel expansion and an increase in the number of collagen fibers, the submucosa is widened and the intestinal wall is thickened. Symptoms Clinical manifestations of Crohn's disease are insidious onset, often asymptomatic in the early stages, or mild in symptoms and easily overlooked. From symptomatic to confirmed diagnosis, it usually averages 1 to 3 years. The course of the disease is often chronic and recurrent. More common in young people, women are slightly more than men. 1. Common symptoms (1) Systemic manifestations: weight loss, increasing weight loss is the most common symptom. About one-third of patients have low or moderate fever, without chills. At this time, there are often active lesions or complications. (2) Abdominal pain: the most common symptom, intermittent attack. Lighter only has bowel and abdominal discomfort, and severe cases can be severe colic. Eating foods containing more cellulose often causes episodes of abdominal pain. Colonic lesions often have diarrhea and abdominal pain, and abdominal pain can be relieved after defecation or deflation. Sudden abdominal pain can occur at the end of the ileum due to lesions, which is caused by lesions in the visceral or peritoneal nerve endings. When the lesion invades the stomach and duodenum, abdominal pain is similar to peptic ulcer, and often accompanied by pyloric and duodenal obstruction. When the lesion invades the ileocecal area. Pain often occurs in the umbilical cord and is later confined to the lower right abdomen. Some cases have no obvious symptoms and sudden abdominal pain. Similar to acute appendicitis or intestinal perforation, it is the first symptom of this disease. Therefore, it is often misdiagnosed as acute appendicitis or intestinal perforation. Crohn's disease is only found when open. The lesion invades the jejunum and can be manifested as upper abdominal pain. When it develops into a granulomatous abscess and extensive mesenteric damage, it is often misdiagnosed as a bone or kidney lesion with back pain. (3) Defecation changes: Most patients have diarrhea, mostly intermittent seizures, and the number of stools is related to the extent of the lesion. 2 to 3 times a day to 10 times, or even dozens of times. For soft stools or loose stools, no pus or mucus. A wide range of diffuse small bowel lesions can have watery stools or fat stools. The onset of diarrhea is often associated with eating foods rich in cellulose. Emotional or nervous can also induce diarrhea, but unlike mental diarrhea, nighttime can be awakened by a sense of defecation. Patients with distal colon involvement may have symptoms such as urgency, urgency, or constipation, and difficulty in defecation. (4) Nausea and vomiting: When the lesion invades the stomach and the duodenum, jejunum, ileum, or forms part of intestinal obstruction caused by intestinal stenosis, symptoms such as nausea, vomiting, and abdominal pain occur. (5) Nutritional deficiency: A wide range of intestinal lesions can cause a decrease in the absorption area, dysbacteriosis, resulting in diarrhea, anorexia, and reduced food intake, resulting in varying degrees of malnutrition. The extent of malnutrition is closely related to the extent and location of the lesion. It is characterized by anemia, hypoproteinemia, vitamin deficiency, electrolyte imbalance and so on. Due to calcium deficiency, osteoporosis is seen and the trunk is painful. Young and pre-pubertal patients may experience growth retardation due to malnutrition and delayed maturity. It can be improved after surgery. (6) Relationship with pregnancy in women: Pregnancy can make the condition worse or worse. If the disease occurs during pregnancy, it will pose a threat to the fetus and mother, prone to stillbirth, miscarriage, premature delivery, fetal malformation. (7) Extra-gastrointestinal manifestations: This disease may be associated with multiple arthritis. When the lesion is relieved or surgically removed, the joint symptoms disappear. The skin may have urticaria, erythema multiforme, nodular erythema, and the like. In addition, conjunctivitis, iridocyclitis, corneal ulcer, keratitis can occur. Fatty liver, amyloidosis, cirrhosis, primary sclerosing cholangitis, etc. can also occur. (8) Anal and rectal lesions: abscess around the anus or around the rectum. Sinus and fistula are the more common manifestations of Crohn's disease. Crohn et al reported that the incidence of fistula was 14.2%, and it was reported that the incidence rate was 81%. Infections around the rectum and anus can develop into rectal abscesses, rectal vaginal fistulas. Extensive ulcers and granulomatous lesions can be found around the anus and on the buttocks. Individual patients with anal fistula are the first sign of the disease. (9) Common signs: The parts of the lesions are different, and their signs are also different. The mass can be touched at the site of the lesion, and there is local tenderness. The lower right abdominal mass is more common, the shape is sausage-like, the boundary is unclear, and it is relatively fixed. Intestinal obstruction often has bloating, and the intestinal type and the dilated bowel can be seen. Ulcers, sinus or fistulas can be seen around the anus. In some cases, clubbing, liver palm, and nodular erythema (mostly occurring in front of the sputum). Occasionally hepatosplenomegaly. 2. Classification of disease activity Due to the large difference in the condition of the disease, the disease activity index is currently graded internationally using the disease activity index. The following two methods for calculating the scores are commonly used: (1) The activity index of Crohn's disease is counted according to the eight variables of the disease proposed by Best and Singbton of the Crohn disease collaboration group in the United States (Crohn's Read more...