The pathogenesis of intrahepatic cholestasis of pregnancy (ICP) is still unknown, although it is currently accepted that the disease represents an abnormal reaction of genetically predisposed maternal liver, to estrogen hormones. To gain a better insight into the hepatic handling of cholephilic anions outside of pregnancy itself, we determined, using the perfusion technique of Wheeler et al. (1960), the hepatic maximum excretory rate (Tm) and the storage capacity (S) of sulfobromphthalein (BSP) in 6 women with a past history of ICP and in 6 controls, matched for age and parity, but with no history of ICP or other liver disease. The BSP Tm in the group with previous ICP did not differ significantly from that measured in the control group (9.22 +/- 2.37 vs 7.92 +/- 1.20). By contrast, BSP S values in the 'previous ICP' group was critically higher than that of the controls (120.43 +/- 55.89 vs 39.15 +/- 16.17: t-test p less than 0.005, U-test p less than 0.001). A possible explanation for this result could be the existence of a metabolic defect responsible for an increased intrahepatic concentration of the cholephilic substances inside the liver cells.

Alteration in sulfobromophthalein hepatic storage capacity (S) in non-pregnant women previously affected with intrahepatic cholestasis of pregnancy.

POZZATO, GABRIELE;
1986-01-01

Abstract

The pathogenesis of intrahepatic cholestasis of pregnancy (ICP) is still unknown, although it is currently accepted that the disease represents an abnormal reaction of genetically predisposed maternal liver, to estrogen hormones. To gain a better insight into the hepatic handling of cholephilic anions outside of pregnancy itself, we determined, using the perfusion technique of Wheeler et al. (1960), the hepatic maximum excretory rate (Tm) and the storage capacity (S) of sulfobromphthalein (BSP) in 6 women with a past history of ICP and in 6 controls, matched for age and parity, but with no history of ICP or other liver disease. The BSP Tm in the group with previous ICP did not differ significantly from that measured in the control group (9.22 +/- 2.37 vs 7.92 +/- 1.20). By contrast, BSP S values in the 'previous ICP' group was critically higher than that of the controls (120.43 +/- 55.89 vs 39.15 +/- 16.17: t-test p less than 0.005, U-test p less than 0.001). A possible explanation for this result could be the existence of a metabolic defect responsible for an increased intrahepatic concentration of the cholephilic substances inside the liver cells.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11368/2559434
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