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  • Title: [Study of liver glucuronidase function in indirect hyperbilirubinemia and liver cirrhosis].
    Author: Goranov I, Avramova K.
    Journal: Probl Khig; 1975; 1():171-7. PubMed ID: 1235997.
    Abstract:
    A discussion is made of the basic peculiarties and differences in the clinico-laboratory profile in various forms of pre- and postmicrosome jaundice. The importance of direct to total bilirubin ratio, and of quantitative bilirubin and urobilinogen bodies' determination in the urine is stressed. Bile pigments conjugation by the hepatic cells and free bilirubin conversion to glucuronose may be also assayed by resorting to some additional tests. The test with N-acetyl-paraaminophenol (NAPA) provides for an indirect assessment of the liver's glucuronidase function and has a good informative value. It is optimally characterized by the percentage of free (non-conjugated) NAPA with respect to the total. The latter indicator is normal in chronic hepatitis and in Dubin-Johnson's syndrome, and is at the uppermost normal limit in hepatic cirrhosis and cholestatic jaundice. It is strongly increased (in the average three times with respect to normal values) in Gilbert's disease and posthepatitis hyperbilirubinemia (PHHB). It affords some information on the severity of the defect in transport of bile pigments in the mentioned affections. In hemolytic jaundice a normal percentage of free NAPA is usually found. Glucuronose conversion of bilirubin hardly plays an essential role in the pathogenesis of hyperbilirubinemia i the listed above diseases. This is also confirmed by the NAPA test, performed subsequent to novobiocin loading. The percentare of free NAPA under the conditions just outlined is furthermore increased in Gilbert's disease and PHHB, while in hemolytic jaundice it remains within normal limits. In Gibert's disease and PHHB, a strongly pronounced delay in the excretion of substances is noted. Not infrequently, a similar disorder is also observed in hepatic cirrhosis. It is interpreted as an expression of an overall disturbance in hepatic blood flow and function of the heavily affected hepatic parenchyma.
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