Concept of the pathogenesis and treatment of cholelithiasis

Abstract

Gallstone disease (GD) is a chronic recurrent hepatobiliary disease, the basis for which is the impaired metabolism of cholesterol, bilirubin and bile acids, which is characterized by the formation of gallstones in the hepatic bile duct, common bile duct, or gallbladder. GD is one of the most prevalent gastrointestinal diseases with a substantial burden to health care systems. GD can result in serious outcomes, such as acute gallstone pancreatitis and gallbladder cancer. The epidemiology, pathogenesis and treatment of GD are discussed in this review. The prevalence of GD varies widely by region. The prevalence of gallstone disease has increased in recent years. This is connected with a change in lifestyle: reduction of motor activity, reduction of the physical load and changes to diets. One of the important benefits of early screening for gallstone disease is that ultrasonography can detect asymptomatic cases, which results in early treatment and the prevention of serious outcomes. The pathogenesis of GD is suggested to be multifactorial and probably develops from complex interactions between many genetic and environmental factors. It suggests that corticosteroids and oral contraceptives, which contain hormones related to steroid hormones, may be regarded as a model system of cholelithiasis development in man. The achievement in the study of the physiology of bile formation and the pathogenesis of GD has allowed expanding indications for therapeutic treatment of GD.

Keywords: Gallstone disease: Epidemiology; Pathogenesis of cholesterol stones; Treatment.

Figure 1

Diagram of steroid hormones-induced inhibition of cholesterol catabolism.

Figure 2

Color cathodoluminescence scanning electron microscopy micro images of cholesterol gallstones. The application of the computer program “Adobe Photoshop” (software) and color contrast by the color cathodoluminescence scanning electron microscopy (CCLSEM) technique permitted the determination of cholesterol, bilirubin and protein within the stone. CCLSEM micrographs of cholesterol (A), protein (B), bilirubin (C) were obtained after color separation[100]. The major components of the gallstones under examination were cholesterol (A) and protein (B). They were detected all over the entire surface of the scanned gallstone while rare bilirubin insertions (C) were seen only at the periphery of the gallstone.

Figure 3

Formation of molecular structures in the system containing bile acids, lecithin and cholesterol. Cholesterol-supersaturated vesicles can stick together and agglomerate to form multilayer (liposomal) liquid-crystal structures. When gallbladder contractility is decreased, liposomes may be converted to solid cholesterol monocrystals. BA: Bile acids; L: Lecithin; Ch: Cholesterol.

Figure 4

It shows a diagram of gallstone formation by taking into account the above impaired bile production and excretion processes.

Figure 5

The phase state of the main bile components (cholesterol, phosphatidylcholines, bile acids) in the triangular coordinate system[114].