What causes chronic cholecystitis?
Last reviewed: 17.10.2021
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The causes of chronic cholecystitis in children are not always clear. It is assumed that the disease can be the outcome of acute cholecystitis, but the anamnesis confirms this assumption only in some children. Almost always there are indications of various infectious diseases (chronic tonsillitis, caries, appendicitis, pyelonephritis, intestinal infections, etc.). The risk of chronic cholecystitis in children with pancreatitis is high. Nonspecific ulcerative colitis, Crohn's disease. Although the infection can not be diagnosed, its role in the pathogenesis of chronic cholecystitis is not ruled out. The significance of infection increases in the case of a decrease in bactericidal bile and violations of mechanisms of local nonspecific protection.
The development of chronic cholecystitis causes dysfunction of the gallbladder, bile ducts, sphincter of Oddi. The risk of chronic cholecystitis is high with a close location of the excretory ducts of the pancreatic and common bile duct. The receipt of the secrets of the pancreas into the common bile duct and proximal contributes to the formation of fermentative chronic cholecystitis. The defeat of the gallbladder is possible with allergic, endocrine diseases (obesity), helminthiases, protozoosis. Increased risk of chronic cholecystitis after operations on the abdominal organs, carrying out endoscopic retrograde cholangiopancreatography. Significant role of quantitative and qualitative disorders of nutrition, physical and neuropsychic stress. Sluggish pathological process in the gall bladder develops during sedimentation - "biliary sludge". Nodular periarteritis, Caroli syndrome.
How does chronic cholecystitis develop in children?
The penetration of infection into the gallbladder is possible ascending, hematogenous or lymphogenous, as in acute cholecystitis. The infectious process, as a rule, is localized in the neck of the organ and leads to damage to the anatomical siphon (cervical cholecystitis or siphonopathy). Significance is attached to motor-evacuation disorders, which change the bile passage and cause it to stagnate. Disorders of biochemistry bile (discololia), on the one hand, exacerbate the chronic sluggish inflammatory process, on the other - contribute to the formation of an aseptic process in the mucosa of the gallbladder. Reducing the concentration of bile acids disrupts bactericidal activity of the bile.
In the bile, the content of slgA falls on the background of an increased concentration of IgA and IgM, to a lesser extent IgG. The role of slgA is to prevent the effects of microorganisms and their toxins on the mucosa of the gallbladder. Disturbances facilitate the penetration of various antigens (bacterial, alimentary, xenobiotics, etc.) into the own plate of the mucosa while stimulating the plasmocytes that synthesize IgG. Reduction of the IgM content is interpreted as a compensatory reaction, since according to biological properties this immunoglobulin is close to slgA.
Increasing the concentration of IgA in the bile contributes to the elimination of antigens in the form of immune complexes.
The factors of nonspecific protection (phagocytosis, spontaneous migration, rosette formation) are undergoing changes. The autoimmune component in chronic cholecystitis persists for a long time, contributing to the chronicization of the pathological process and the tendency of the disease to relapse.
Pathomorphology
The main morphological sign of chronic cholecystitis is densification and thickening of the gallbladder wall from 2-3 mm or more. Visually determine the deformation of the bladder, adhesions with neighboring organs, regarded as signs of a slow and prolonged inflammatory process. Microscopic examination allows to establish lymphohistiocytic infiltration of epithelium, submucosal and muscular layers, to see polypoid growths, metaplasia of epithelium according to pyloric or intestinal type. In the case of intestinal metaplasia, the cells become cup-shaped. In the muscle sheath, connective tissue proliferation, focal sclerosis, thickening of myocytes due to hypertrophy are noted. Sinuses of Rokitansky-Ashoff are deep, they often reach the subserous layer, they can contain microabscesses, pseudodiverticles, which create favorable conditions for the formation of a slow inflammatory process. Stroke Lyushka branched, with cystic enlargements, penetrating to the subserous layer, which promotes the spread of the pathological process to the serous membrane, the development of pericholecystitis and deformation of the gallbladder.
Vessels of the own plate of the mucous membrane are full-blooded or narrowed, stasis of erythrocytes in the lumen of the capillaries of the mucous membrane and the muscle layer, diapedesis hemorrhages is possible. As a result of sclerosing the vascular wall and narrowing the lumen of the vessels, ischemia develops, which increases dystrophic processes in the gallbladder and explains the progression of the pathological process. If the disorders are superficial, the functional state of the gall bladder does not change. In the case of pronounced morphological symptoms with the formation of chronic atrophic cholecystitis, there is a violation of the secretory, suction and contractile activity of the organ.