[Gallstone disease and gallbladder cholesterosis: miscellaneous diseases or various manifestations of a single process]

Abstract

Objective: analysis of literature on the pathogenesis of GSD and GBC.

Results: It is suggested that the GSD and GBC are clinical subfenotypes the same disease, the common factor in the pathogenesis of which are metabolic disorders LP low densities, due to polymorphism of the apoB. The main function of the LP is transport into the cells of the NLC, and PUFA, which perform different functions in the body and transported in different ways. NLC are energy substrate, and are delivered to the cells of liver TG in the CM with the participation of apoB-48 BLK. PUFA determine the functional specificity of biological membranes, transport forms are PL and EHS. APOE determines the transport of the NLC at the stage of enterocytes--CM--hepatocytes--VLDL--BOB. Extension of its already active transport of fatty acids to the cells in the LDL. Consequently, the level of cholesterol in the blood reflects the degree of deficiency in the cells of PUFA. Investigation of polymorphism of apoE suggests that in GSD and GBC identified metabolic disorders as NLC (allele epsilon2) and PUFA (allele epsilon4), but the GBC--more polyunsaturated (with the increase and structural changes in LDL), and at GSD--saturated fatty acids (with an increase VLDL). This fact explains why, in the GSD is often formed cholesterosis, and for GBC--stones.