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What causes chronic cholecystitis?
Medical expert of the article
Last reviewed: 04.07.2025
The causes of chronic cholecystitis in children are not always clear. It is assumed that the disease may be the outcome of acute cholecystitis, but the anamnesis data confirm this assumption only in some children. There are almost always indications of various infectious diseases (chronic tonsillitis, caries, appendicitis, pyelonephritis, intestinal infections, etc.). The risk of chronic cholecystitis is high in children with pancreatitis, nonspecific ulcerative colitis, Crohn's disease. Although the infection may not be diagnosed, its role in the pathogenesis of chronic cholecystitis cannot be ruled out. The significance of infection increases in the case of a decrease in the bactericidal activity of bile and a violation of the mechanisms of local nonspecific protection.
Chronic cholecystitis development is caused by dysfunctions of the gallbladder, bile ducts, and sphincter of Oddi. The risk of chronic cholecystitis is high with close location of the excretory ducts of the pancreatic and common bile ducts. The entry of pancreatic secretions into the common bile duct and proximally contributes to the formation of enzymatic chronic cholecystitis. Gallbladder damage is possible with allergic, endocrine diseases (obesity), helminthiasis, protozoa. The risk of chronic cholecystitis is increased after surgery on the abdominal organs, endoscopic retrograde cholangiopancreatography. The role of quantitative and qualitative nutritional disorders, physical and neuropsychic overstrain is significant. A sluggish pathological process in the gallbladder develops with sediment - "biliary sludge". periarteritis nodosa, Caroli syndrome.
How does chronic cholecystitis develop in children?
Infection may penetrate the gallbladder by ascending, hematogenous or lymphogenous routes, as in acute cholecystitis. The infectious process is usually localized in the neck of the organ and leads to damage to the anatomical siphon (cervical cholecystitis or siphonopathy). Motor-evacuation disorders that change the passage of bile and cause its stagnation are of importance. Disturbances in the biochemistry of bile (dyskholia), on the one hand, aggravate the chronic sluggish inflammatory process, on the other hand, contribute to the formation of an aseptic process in the mucous membrane of the gallbladder. A decrease in the concentration of bile acids disrupts the bactericidal properties of bile.
The content of slgA in bile decreases against the background of an increase in the concentration of IgA and IgM, to a lesser extent IgG. The role of slgA is to prevent the impact of microorganisms and their toxins on the mucous membrane of the gallbladder. Disturbances facilitate the penetration of various antigens (bacterial, alimentary, xenobiotics, etc.) into the proper plate of the mucous membrane with simultaneous stimulation of plasma cells synthesizing IgG. A decrease in the content of IgM is interpreted as a compensatory reaction, since this immunoglobulin is close to slgA in its biological properties.
An increase in the concentration of IgA in bile promotes the elimination of antigens in the form of immune complexes.
Non-specific defense factors (phagocytosis, spontaneous migration, rosette formation) undergo changes. The autoimmune component in chronic cholecystitis persists for a long time, contributing to the chronicity of the pathological process and the tendency of the disease to relapse.
Pathomorphology
The main morphological sign of chronic cholecystitis is compaction and thickening of the gallbladder wall by 2-3 mm or more. Visually, deformation of the bladder and adhesions with adjacent organs are determined, which are regarded as signs of a sluggish and prolonged inflammatory process. Microscopic examination allows us to establish lymphohistiocytic infiltration of the epithelium, submucosal and muscular layers, to see polypoid growths, metaplasia of the epithelium according to the pyloric or intestinal type. In case of intestinal metaplasia, the cells become goblet-shaped. In the muscular membrane, there is proliferation of connective tissue, focal sclerosis, thickening of myocytes due to hypertrophy. Rokitansky-Ashoff sinuses are deep, often reaching the subserous layer, may contain microabscesses, pseudodiverticula, creating favorable conditions for the formation of a sluggish inflammatory process. Luschka's passages are branched, with cystic expansions penetrating to the subserous layer, which contributes to the spread of the pathological process to the serous membrane, the development of pericholecystitis and deformation of the gallbladder.
The vessels of the lamina propria of the mucous membrane are full-blooded or narrowed, erythrocyte stasis in the lumen of the capillaries of the mucous membrane and muscular layer, diapedetic hemorrhages are possible. Due to sclerosis of the vascular wall and narrowing of the lumen of the vessels, ischemia develops, which intensifies the degenerative processes in the gallbladder and explains the progressive nature of the pathological process. If the disorders are superficial, the functional state of the gallbladder does not change. In the case of pronounced morphological symptoms with the formation of chronic atrophic cholecystitis, the secretory, absorption and contractile activity of the organ is disrupted.