Intestinal Crohn’s disease, also known as clonorchiasis, restrictive enteritis, granulomatous ileitis, etc. It is a granulomatous inflammatory disease of the gastrointestinal tract of unknown etiology and belongs to the same category of inflammatory bowel disease (IBD) as ulcerative colitis. Recent studies suggest that the pathogenic factors are due to the invasion of certain pathogens into the intestinal epithelium and the subsequent autoimmune response of the body, among which Mycobacterium avium subspecies paratuberculosis, measles virus, and invasive Escherichia coli infection may be associated with the development of the disease. The lesions are characterized by segmental or jumping ulcerative lesions that can occur in any part of the gastrointestinal tract, with the ileocecal region being the most common. The disease is more common in males. The onset is more frequent in young adults aged 15 to 40 years. The intestine is the main means of detecting Crohn’s disease. About the diagnosis: The disease starts insidiously and has a chronic course, with alternating periods of activity and remission, and patients often present with abdominal pain and diarrhea. The abdominal pain is mostly located in the right lower abdomen or around the umbilicus, often in spasmodic paroxysms with abdominal tinnitus, aggravated by meals, and relieved by defecation and exhaustion. Diarrhea is mostly burnt, and pus, blood or mucus stools are rare. A more fixed mass may be found in the right lower abdomen or around the umbilicus. The diagnosis of CD requires a comprehensive analysis in close combination with clinical, endoscopic, imaging, and tissue biopsy, and reliance on one test alone may lead to misdiagnosis. Because the terminal ileum is the preferred site of lesions, endoscopy should generally be inserted into the terminal ileum as far as possible in patients suspected of having this disease. Segmental ulcerative lesions mainly in the right hemicolectum can be considered. Capsule endoscopy or small bowel microscopy can help confirm the diagnosis if similar ulcerative lesions are found in the small intestine. The main diseases to be differentiated are intestinal tuberculosis, Campylobacter enteritis, Yersinia enterocolitica, malignant lymphoma, intestinal leukoaraiosis, ulcerative colitis, ileocecal tumors, amebic enteropathy, and ischemic enterocolitis. Approximately 10% of IBDs cannot be distinguished as CD or ulcerative nodes and are called undefined colitis (IDC). The severity of the disease can be determined clinically by referring to the activity criteria and classifying those without systemic symptoms, abdominal pain, masses and obstruction as mild; those with significant abdominal pain, diarrhea, systemic symptoms and their complications as severe; and those in between as moderate. The extent of lesions is determined with reference to imaging and endoscopic findings, such as intestinal lesions can be classified as small intestine, colon and ileocolon. Complications include intestinal obstruction, fistula, inflammatory mass or abscess, hemorrhage, intestinal perforation, etc. Treatment: The principles of treatment for this disease are to enhance supportive symptomatic treatment, control acute attacks, relieve symptoms, and reduce recurrence. Since the disease is a total proliferative inflammatory lesion, treatment differs from ulcerated nodes, emphasizing the application of hormones, immunosuppressive agents, and biological agents. In mild cases, salicylic acid preparations are the mainstay, but additional glucocorticoid drugs are usually required. Immunosuppressive agents are used in combination with poor results or if they are not tolerated. In severe lesions with poor treatment or fistulae, biological agents may be used. At the same time, systemic nutrition and symptomatic treatment should be enhanced, water-electrolyte balance should be maintained, blood and albumin transfusions should be given, and TPN or elemental diet should be given in severe cases. Glucocorticosteroids are effective drugs for controlling disease activity and are suitable for treatment of active lesions, but are ineffective for resting disease and do not prevent recurrence, so they are not suitable for long-term maintenance treatment. The dose of prednisone is 1 mg per kg of body weight per day, which can be increased to 60 mg/d in heavy cases, and the dose should be reduced only after the disease has reached remission. For those who cannot tolerate oral administration or acute severe cases, hydrocortisone 200-300mg/d can be administered orally for 1 week until remission. After remission, the dose is gradually reduced to discontinuation at a rate of 5 mg per week. Budesonide may also be used at a dose of 9 mg/d. Compared with prednisone, the efficacy of the two drugs differs in CD at different sites of involvement: in lesions located in the right hemicolectum, budesonide is comparable to prednisone in efficacy, but with significantly fewer side effects. In lesions involving the whole colon, prednisone was significantly more effective than budesonide. Biologic therapy is the most effective treatment for refractory lesions or fistulae, and currently the main monoclonal antibody against TNF, Infliximab, is available in the form of 100mg/vial. The usual dose is 5mg/kg given at weeks 0, 2, 6 and then every 8 weeks. However, it is very expensive and a few patients may have adverse reactions such as urticaria, dyspnea or hypotension during the infusion.