Gallstone dissolution with ursodeoxycholic acid in patients with chronic active hepatitis and two years follow-up

Leuschner, U.; Leuschner, M.; Sieratzki, J.; Kurtz, W; Hübner, K.

doi:10.1007/bf01308413

Cited by 165 publications

(62 citation statements)

References 28 publications

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“…Leuschner et al (38) found that ursodeoxycholic acid (UDCA) administration reversed hepatotoxicity, and UDCA treatment is used to ameliorate primary biliary cirrhosis (39,40). Similarly, chenodeoxycholic acid-or deoxycholic acid-induced rodent liver hepatotoxicity can be reversed by co-administration of less detergent bile acids such as UDCA or tauroursodeoxycholic acid (TUDCA) (41).…”

Section: Discussionmentioning

confidence: 99%

Disrupted Bile Acid Homeostasis Reveals an Unexpected Interaction among Nuclear Hormone Receptors, Transporters, and Cytochrome P450

Schuetz

Strom

Yasuda

et al. 2001

Journal of Biological Chemistry

359

310

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Sister of P-glycoprotein (SPGP) is the major hepatic bile salt export pump (BSEP). BSEP/SPGP expression varies dramatically among human livers. The potency and hierarchy of bile acids as ligands for the farnesyl/ bile acid receptor (FXR/BAR) paralleled their ability to induce BSEP in human hepatocyte cultures. FXR:RXR heterodimers bound to IR1 elements and enhanced bile acid transcriptional activation of the mouse and human BSEP/SPGP promoters. In FXR/BAR nullizygous mice, which have dramatically reduced BSEP/SPGP levels, hepatic CYP3A11 and CYP2B10 were strongly but unexpectedly induced. Notably, the rank order of bile acids as CYP3A4 inducers and activators of pregnane X receptor/steroid and xenobiotic receptor (PXR/SXR) closely paralleled each other but was markedly different from their hierarchy and potency as inducers of BSEP in human hepatocytes. Moreover, the hepatoprotective bile acid ursodeoxycholic acid, which reverses hydrophobic bile acid hepatotoxicity, activates PXR and efficaciously induces CYP3A4 (a bile-metabolizing enzyme) in primary human hepatocytes thus providing one mechanism for its hepatoprotection. Because serum and urinary bile acids increased in FXR/BAR ؊/؊ mice, we evaluated hepatic transporters for compensatory changes that might circumvent the profound decrease in BSEP/SPGP. We found weak MRP3 up-regulation. In contrast, MRP4 was substantially increased in the FXR/ BAR nullizygous mice and was further elevated by cholic acid. Thus, enhanced hepatocellular concentrations of bile acids, due to the down-regulation of BSEP/SPGPmediated efflux in FXR nullizygous mice, result in an alternate but apparent compensatory up-regulation of CYP3A, CYP2B, and some ABC transporters that is consistent with activation of PXR/SXR by bile acids.

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Section: Discussionmentioning

confidence: 99%

Disrupted Bile Acid Homeostasis Reveals an Unexpected Interaction among Nuclear Hormone Receptors, Transporters, and Cytochrome P450

Schuetz

Strom

Yasuda

et al. 2001

Journal of Biological Chemistry

359

310

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“…Several reports have confirmed that UDCA improves the hepatic tests in patients with chronic hepatic disease (10,26). However, the exact mechanism of this action is not understood.…”

Section: Discussionmentioning

confidence: 87%

“…It is observed, however, that most of these individuals are not able to reach this objective in a consistent way, needing a more effective treatment (5,12,26). In studies of isolated cases (11) or in uncontrolled studies (12) a histological and biochemical improvement of NAFLD was observed after one year of treatment with UDCA.…”

Section: Discussionmentioning

confidence: 92%

A randomized double-blind study of the short-time treatment of obese patients with nonalcoholic fatty liver disease with ursodeoxycholic acid

Santos

Lanzoni

Szejnfeld

et al. 2003

Braz J Med Biol Res

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In order to determine the effect of ursodeoxycholic acid on nonalcoholic fatty liver disease, 30 patients with body mass indices higher than 25, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) or γ-glutamyltransferase (γ-GT) at least more than 1.5 times the upper limit of normality, and hepatic steatosis demonstrated by ultrasonography were randomized into two groups of 15 patients to receive placebo or 10 mg kg -1 day -1 ursodeoxycholic acid for three months. Abdominal computed tomography was performed to quantify hepatic fat content, which was significantly correlated with histological grading of steatosis (r s = -0.83, P < 0.01). Patient body mass index remained stable for both groups throughout the study, but a significant reduction in mean (± SEM) serum levels of ALT, AST and γ-GT was observed only in the treated group (ALT = 81.2 ± 9.7, 44.8 ± 7.7, 48.1 ± 7.7 and 52.2 ± 6.3 IU/l at the beginning and after the first, second and third months, respectively, N = 14, P < 0.05). For the placebo group ALT values were 66.4 ± 9.8, 54.5 ± 7, 60 ± 7.6 and 43.7 ± 5 IU/l, respectively. No alterations in hepatic lipid content were observed in these patients by computed tomography examination (50.2 ± 4.2 Hounsfield units (HU) at the beginning versus 51.1 ± 4.1 HU at the third month). These results show that ursodeoxycholic acid is able to reduce serum levels of hepatic enzymes in patients with nonalcoholic fatty liver disease, but this effect is not related to modifications in liver fat content.

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“…oraz Yamanaka (dwie prace z 1976 r.). W medycynie zachodniej kwasu tego użyto prawie 10 lat później -najpierw w celu rozpuszczania cholesterolowych złogów żółciowych [2,3], a później w leczeniu pierwotnej marskości żółciowej (primary biliary cirrhosis -PBC).…”

Section: Wstępunclassified

Ursodeoxycholic acid in liver diseases

Juszczyk¹

2012

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Gallstone dissolution with ursodeoxycholic acid in patients with chronic active hepatitis and two years follow-up

Cited by 165 publications

References 28 publications

Disrupted Bile Acid Homeostasis Reveals an Unexpected Interaction among Nuclear Hormone Receptors, Transporters, and Cytochrome P450

Disrupted Bile Acid Homeostasis Reveals an Unexpected Interaction among Nuclear Hormone Receptors, Transporters, and Cytochrome P450

A randomized double-blind study of the short-time treatment of obese patients with nonalcoholic fatty liver disease with ursodeoxycholic acid

Ursodeoxycholic acid in liver diseases

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