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Updated: Oct 6, 2026

Creation of Reversible Cholestatic Rat Model
Published on: May 22, 2011
Studies in cholestasis of pregnancy
Forty-one pregnant women with pruritus, in whom cholestasis was verified by the presence in their serum of an abnormal lipoprotein, lipoprotein-X (LP-X), were divided into two clinical groups, pruritus gravidarum (PG) (n=20) and hepatosis of pregnancy (HP) (n=21) in relation to serum bilirubin (below and above 1.2 mg/100 ml, respectively) and/or SGOT, SGPT (below and above 50 units/l, respectively). In HP, but not in PG, serum lipids, i.e. cholesterol, phospholipids, triglycerides, pre-beta-lipoproteins (very-low-density lipoproteins), and low-density lipoproteins were increased and high-density lipoproteins decreased when compared with suitable controls. Serum lipids were elevated in proportion to the derangement in the liver function tests, alkaline phosphatase, SGOT, and SGPT. The occurrence of LP-X was inversely related to HDL cholesterol, suggesting a causal relationship between HDL lipid metabolism and the presence of LP-X. Serum TIBC, Simplastin A, and serum iron were elevated in HP in relation to the degree of deterioration of liver function tests. Some of these changes in serum in cholestatic pregnancy may partially (serum triglycerides and pre-beta-lipoproteins) or completely (TIBC and Simplastin A) be explained by an enhanced estrogen influence in promoting increased liver lipid/protein metabolism.
Forty-one pregnant women with pruritus, in whom cholestasis was verified by the presence in their serum of an abnormal lipoprotein, lipoprotein-X (LP-X), were divided into two clinical groups, pruritus gravidarum (PG) (n=20) and hepatosis of pregnancy (HP) (n=21) in relation to serum bilirubin (below and above 1.2 mg/100 ml, respectively) and/or SGOT, SGPT (below and above 50 units/l, respectively). In HP, but not in PG, serum lipids, i.e. cholesterol, phospholipids, triglycerides, pre-beta-lipoproteins (very-low-density lipoproteins), and low-density lipoproteins were increased and high-density lipoproteins decreased when compared with suitable controls. Serum lipids were elevated in proportion to the derangement in the liver function tests, alkaline phosphatase, SGOT, and SGPT. The occurrence of LP-X was inversely related to HDL cholesterol, suggesting a causal relationship between HDL lipid metabolism and the presence of LP-X. Serum TIBC, Simplastin A, and serum iron were elevated in HP in relation to the degree of deterioration of liver function tests. Some of these changes in serum in cholestatic pregnancy may partially (serum triglycerides and pre-beta-lipoproteins) or completely (TIBC and Simplastin A) be explained by an enhanced estrogen influence in promoting increased liver lipid/protein metabolism.
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