Silymarin decreases type I procollogen mRNA levels in rats with secondary biliary cirrhosis

Jia, Jidong; Boigk, G.; Bauer, M.; Strefeld, Thomas; Ruhl, Michael; Riecken, E. O.; Schuppan, Detlef

doi:10.1016/s0016-5085(98)85136-6

Cited by 3 publications

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“…4, 1999 of activated stellate cells 48 and a greater than 50% reduction of both procollagen I and tissue inhibitor of metalloproteinase messenger RNA, both being major effectors of fibrogenesis. 49 These data have spawned randomized, placebocontrolled studies of silymarin in patients with chronic viral hepatitis that include follow-up biopsies and a panel of serum markers of liver fibrosis. 50 Picroliv.…”

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confidence: 99%

Herbal products for liver diseases: A therapeutic challenge for the new millennium

et al. 1999

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Section: -1981 Amanita Phalloides Antidote In Clinical Studiesmentioning

confidence: 99%

Herbal products for liver diseases: A therapeutic challenge for the new millennium

et al. 1999

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“…PBC, the study may be informative in that the antifibrotic action of silymarin was unaccompanied by decreases in either bilirubin or liver enzymes. This finding may be attributable to the fact that silymarin appears to act on activated hepatic stellate cells and myofibroblasts, [9][10][11][12] with only indirect effects on hepatocytes.…”

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Clinical Studies With Silymarin: Fibrosis Progression Is the End Point

Schuppan

Hahn

2001

Hepatology

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We read with interest the report by Angulo et al. 1 on 27 patients with primary biliary cirrhosis (PBC) who did not respond biochemically to ursodeoxycholic acid (UDCA). In a noncontrolled one-armed study the authors investigated the effect of adding oral silymarin for 1 year to the standard regimen with UDCA. Since silymarin did not alter alkaline phosphatase, bilirubin, aspartate transaminase, albumin, or the Mayo risk score, they concluded that silymarin is not effective in patients with PBC who do not respond to UDCA and that further controlled trials of silymarin in PBC are not warranted. We would take issue with several aspects of the study. 1. The patients were at an early clinical stage of the disease, in which the Mayo score has limited prognostic value. In addition, a treatment time interval of 1 year is generally too short to assess disease progression, with or without medication. 2-7 If one chooses to argue that 1 year is sufficient, then the finding of no progression of disease could be interpreted as evidence for a beneficial effect of silymarin. 2. The outcome parameters for the efficacy of silymarin (alkaline phosphatase, aspartate transaminase, albumin, bilirubin, and the Mayo risk score) are, at best, indirect measures of disease progression and unreliable as predictors of fibrosis, particularly in patients receiving UDCA. 2-7 Since progression of fibrosis ultimately determines the prognosis of PBC, fibrosis-related parameters should be monitored, including sequential histology, aminoterminal procollagen type III peptide, collagen IV, hyaluronic acid, and others. 8 3. The authors failed to note a large experimental study of secondary biliary fibrosis in rats, which showed a highly significant antifibrotic effect of silymarin in early as well as advanced disease. 9 Although not using an exact model of human

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“…9 Although not using an exact model of human PBC, the study may be informative in that the antifibrotic action of silymarin was unaccompanied by decreases in either bilirubin or liver enzymes. This finding may be attributable to the fact that silymarin appears to act on activated hepatic stellate cells and myofibroblasts, [9][10][11][12] with only indirect effects on hepatocytes.…”

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confidence: 99%