Can ursodeoxycholic acid induce disease remission in primary biliary cirrhosis?

Wolfhagen, Frank H.J.; Buuren, Henk R. van; Schalm, Solko W.; Kate, Fiebo J.W. ten; Hattum, Jan van; Eskens, Fery A.L.M.; Muller, Jannie W. den Ouden; Vries, Richard A. de; Ferwerda, J.; Hoek, Egbert W. van der; Scherpenisse, Joost; Henegouwen, G. P. van Berge

doi:10.1016/0168-8278(95)80297-5

Cited by 10 publications

(3 citation statements)

References 8 publications

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“…39 Whether UDCA has favorable immunomodulatory properties continues to be debated. Some investigators believe that the most efficacious therapy for primary biliary cirrhosis involves a combination of an immunosupressive agent such as prednisone and UDCA 44 or the triple combination of UDCA, prednisone, and azathioprine. 45 Ursodeoxycholic acid therapy has also shown favorable effects in other cholestatic conditions, such as cholestasis associated with pregnancy 46 and cholestasis associated with total parenteral nutrition.…”

Section: Displacement Therapymentioning

confidence: 99%

The Continuing Importance of Bile Acids in Liver and Intestinal Disease

1999

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Bile acids, the water-soluble, amphipathic end products of cholesterol metabolism, are involved in liver, biliary, and intestinal disease. Formed in the liver, bile acids are absorbed actively from the small intestine, with each molecule undergoing multiple enterohepatic circulations before being excreted. After their synthesis from cholesterol, bile acids are conjugated with glycine or taurine, a process that makes them impermeable to cell membranes and permits high concentrations to persist in bile and intestinal content. The relation between the chemical structure and the multiple physiological functions of bile acids is reviewed. Bile acids induce biliary lipid secretion and solubilize cholesterol in bile, promoting its elimination. In the small intestine, bile acids solubilize dietary lipids promoting their absorption. Bile acids are cytotoxic when present in abnormally high concentrations. This may occur intracellularly, as occurs in the hepatocyte in cholestasis, or extracellularly, as occurs in the colon in patients with bile acid malabsorption. Disturbances in bile acid metabolism can be caused by (1) defective biosynthesis from cholesterol or defective conjugation, (2) defective membrane transport in the hepatocyte or ileal enterocyte, (3) defective transport between organs or biliary diversion, and (4) increased bacterial degradation during enterohepatic cycling. Bile acid therapy involves bile acid replacement in deficiency states or bile acid displacement by ursodeoxycholic acid, a noncytotoxic bile acid. In cholestatic liver disease, administration of ursodeoxycholic acid decreases hepatocyte injury by retained bile acids, improving liver tests, and slowing disease progression. Bile acid malabsorption may lead to high concentrations of bile acids in the colon and impaired colonic mucosal function; bile acid sequestrants provide symptomatic benefit for diarrhea. A knowledge of bile acid physiology and the perturbations of bile acid metabolism in liver and digestive disease should be useful for the internist.

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Section: Displacement Therapymentioning

confidence: 99%

The Continuing Importance of Bile Acids in Liver and Intestinal Disease

1999

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“…The criteria for remission of PBC has been defined as follows: (i) a disappearance of pruritus and fatigue (symptomatic remission); (ii) normalization of serum bilirubin, AST and IgM, with ALP < 1.5 × normal (biochemical remission); and (iii) absence or restriction of inflammation to the portal tracts without bile duct destruction and absence of granulomas (histological remission) 15 . Based on the above criteria, Wolfhagen et al reported that treatment with UDCA resulted in the biochemical remission in 11% of their patients with PBC, both biochemical and symptomatic remission in 6%, and complete (symptomatic, biochemical and histological) remission in only 4% of patients 15 . Jorgensen et al also reported normalization of liver biochemical functions in 19% of their patients with PBC 2 years after treatment with UDCA 16 .…”

Section: Discussionmentioning

confidence: 99%

Changes in titers of antimitochondrial and antinuclear antibodies during the course of primary biliary cirrhosis

Masuda

Omagari

Matsuo

et al. 2001

J of Gastro and Hepatol

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A case of primary biliary cirrhosis (PBC) in whom a complete biochemical (serum bilirubin, transaminases and alkaline phosphatase) remission was noted after combination treatment with ursodeoxycholic acid (UDCA) and corticosteroid is reported. The antimitochondrial antibody (AMA) detected by indirect immunofluorescence was initially positive, and the antinuclear antibody (ANA) was negative, but these two antibodies subsequently fluctuated independently (AMA-positive/ANA-negative, AMA-negative/ANA-negative, AMA-negative/ANA-positive, AMA-positive/ANA-positive, and again AMA-negative/ANA-positive) in spite of a lack of histopathological improvement in the liver after treatment. The clinical presentation in our case suggests that in some cases the diagnosis of PBC or so-called autoimmune cholangitis (AIC) might depend on the 'phase' of the same disease. Our results also suggest that detailed immunoreactive profiles against 2-oxo-acid dehydrogenase complex (2-OADC) enzymes by using immunoblotting, together with a serial histological examination, should provide more precise information for a diagnosis of PBC.

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“…The Dutch Multicentre PBC Study Group chose a dose of 10 mg/kg/day. When evaluation revealed that biochemical remission was achieved in 11% of patients and combined clinical, biochemical and histological remission occurred in less than 5%, the question arose as to whether the UDCA dose was too low 15 …”

Section: Introductionmentioning

confidence: 99%