Intestinal wall edema and thickening
Introduction
Introduction Clinical manifestations of connective tissue enteritis can be seen by the naked eye with edema and thickening of the intestine. Connective tissue enteritis is a connective tissue disease involving the gastrointestinal tract with scleroderma, systemic lupus erythematosus, nodular polyarteritis, dermatomyositis, rheumatoid arthritis, and the like. Among them, scleroderma is the most prominent. Scleroderma is a systemic connective tissue disease. The cause is related to genetic and immune abnormalities, and occurs mostly in women of childbearing age. Clinically characterized by localized or diffuse skin thickening and fibrosis, and involving connective tissue diseases of the internal organs such as heart, lung, kidney, and digestive tract. According to the degree of skin lesions and the sites involved in the lesions, they can be divided into two types: localized and systemic. Localized scleroderma is mainly characterized by skin sclerosis; systemic scleroderma, also known as systemic sclerosis, can affect the skin, synovium and internal organs, especially the gastrointestinal tract, lungs, kidneys, heart, blood vessels, skeletal muscles. The system, etc., causes the function of the corresponding organ to be incomplete.
Cause
Cause
1. 57% of patients with scleroderma have intestinal involvement, pathological changes in the small intestine have smooth muscle atrophy, patchy collagen fibers in the submucosal, muscular and serosal layers, and chronic inflammatory cell infiltration in the mucosal lamina propria.
2. In the dermatomyositis, the small intestine has different degrees of expansion and sectional changes, with low power and prolonged passage. Intestinal wall edema and thickening can be seen with the naked eye. Microscopic examination revealed multiple mucosal erosions, submucosal edema, muscular atrophy, and fibrosis with lymphatic and plasma cell infiltration. Intestinal submucosal to serosal small artery, venule intima thickening is prone to thrombosis and luminal occlusion.
3. Intestinal damage of systemic lupus erythematosus is mainly the result of vasculitis, which is characterized by fibrinoid degeneration, thrombosis, hemorrhage and ischemia, mainly invading the inferior intestinal mucosa, muscular layer and mesenteric arterioles and venules.
4. Nodular polyarteritis may involve any part of the intestine, but mainly invades the mesenteric mesenteric and submucosal and muscular layer arterioles, followed by venules. The damage is segmental and the layers of the wall are involved. Histological features are fibrin-like degeneration, necrosis and thrombosis with inflammatory cell infiltration.
5. Rheumatoid arthritis can also be complicated by intestinal malabsorption, steatorrhea and selective lactose intolerance. Malabsorption is caused by concurrent amyloidosis of the small intestine and may be accompanied by loss of protein in the gastrointestinal tract.
Examine
an examination
Related inspection
Gastrointestinal CT examination of gastrointestinal diseases by ultrasound examination of gastrointestinal imaging
Immunological examination: ANA positive rate >90%, mainly spot type and nucleolar type, about 20% anti-RNP antibody positive, 50% ~ 90% CREST patients anti-centromere antibody (ACA) positive, (labeled antibody), 20% to 40% of patients with systemic sclerosis were positive for serum SCL-70 antibody (labeled antibody), 30% of cases had RF, and the total number of peripheral blood T cells was normal or slightly lower, with T helper cells increasing and T suppressing cells decreasing.
Diagnosis
Differential diagnosis
Mainly differentiated from bacterial dysentery, viral enteritis, cholera, and intestinal amoeba.
Intestinal wall edema thickening: dermatomyositis has different degrees of dilatation and segmental changes, with low power and prolonged passage. Intestinal wall edema and thickening can be seen with the naked eye. Microscopic examination revealed multiple mucosal erosions, submucosal edema, muscular atrophy, and fibrosis with lymphatic and plasma cell infiltration. Intestinal submucosal to serosal small artery, venule intima thickening is prone to thrombosis and luminal occlusion.
Intestinal wall fibrosis: schistosomiasis granuloma in the ileocecal area is the venous oocysts that swell into the intestinal wall tissue around the blood vessels, especially the submucosa. Insect eggs cause leukocyte infiltration in the intestinal wall, pseudo nodules are formed, fibrous tissue is proliferated, late intestinal wall fibrosis is thickened, and mucosal proliferation forms granuloma.
Intestinal wall necrosis: It is a simple mechanical intestinal obstruction because it is blocked by intestinal contents such as mites, gallstones, feces or other foreign bodies. More common is that the aphids clump together and cause local intestinal fistulas and block the intestinal lumen. Most common in children, the incidence rate in rural areas is high. The clinical manifestations are paroxysmal abdominal pain and vomiting around the umbilicus, which may have a history of aphids or spit mites.
