[The pathomorphology and pathogenetic problems of liver involvement in icterohemorrhagic leptospirosis].
Morphologic findings on the liver during different time periods of Leptospira infection suggest the leading role in the pathogenesis of the damaged organ early in the course of the disease of a toxic vascular affection of the microcirculatory bed presenting with hyperpermeability of the vascular wall, interstitial edema, dyscomplexation of the liver crosspieces together with inflow of bile to the sinusoidal capillaries. To a lesser extent jaundice is related to the hepatocyte dystrophic and necrotic changes as evidenced by the absence of marked disturbances in the protein-synthetizing function of the liver and low enzymatic activity. At week 2 to 3 of the illness against the background of diminution of the edema and partial or complete restoration of the liver constitution (especially so in less afflicted peripheral portions of the lobes) jaundice with high bilirubinemia is caused by a toxic affliction of hepatocytes and advancing centrolobular cholestasis. High values for bilirubin might be related not only to grave alternative changes in hepatocytes but to microcirculatory abnormalities as well, which fact accounts for the absence in leptospirosis of a direct relationship of the blood level of bilirubin to the degree of affliction of the hepatic cells.
Anisimova
Iu I
IuI
Matiash
V I
VI
D006801:Humans; D008099:Liver / Q000473:pathology*; D008107:Liver Diseases / Q000209:etiology / Q000473:pathology*; D012157:Mononuclear Phagocyte System / Q000473:pathology; D012189:Retrospective Studies; D013997:Time Factors; D014895:Weil Disease / Q000150:complications / Q000473:pathology*