<i>Silybum marianum</i> (milk thistle) and indinavir: an RCT and meta‐analysis

Mills, Ed; Wilson, Kumanan; Foster, Brian; Phillips, Elizabeth; Walker, Scott; Rachlis, Beth; Montori, VM; Sp, Myers; Clarke, Mike; Gallicano, S

doi:10.1111/j.2042-7166.2004.tb04536.x

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“…With therapeutic silibinin peak plasma concentrations of 0.6 µM and biliary concentrations up to 200 µM it was concluded [14] that metabolic interactions with xenobiotics metabolised by CYP3A4 or CYP2C9 cannot be excluded, a view not shared by others [17]. No interactions have been described in humans so far; silymarin 160 mg tid (3 × daily) had no apparent effect on indinavir plasma concentrations, a potent inhibitor of CYP3A3/4 [18,19] with the possible exception of a 25% decrease of mean trough levels [20]. In a recent study [21], 200 mg silymarin tid, for 14 consecutive days, did not affect the function of CYP3A4 and UGT1A1 in cancer patients treated with irinotecan.…”

Section: Pharmacokinetics Of Silymarinmentioning

confidence: 99%

An Updated Systematic Review with Meta-Analysis for the Clinical Evidence of Silymarin

Saller

Brignoli

Melzer

et al. 2008

Forsch Komplementärmed

190

138

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Background: The potential benefit of silymarin (special extract from the fruits of Silybum marianum) in the treatment of liver diseases remains a controversial issue. Methods: For this systematic review electronic databases identified 65 papers for the search terms silymarin, silibinin, silicristin or milk thistle and clinical trial. Only 19 complied with the criteria ‘double-’ or ‘single-blind’. These publications were analysed from a clinical point of view and meta-analytic calculations were performed. Results: The clinical evidence of a therapeutic effect of silymarin in toxic liver diseases is scarce. There is no evidence of a favourable influence on the evolution of viral hepatitis, particularly hepatitis C. In alcoholic liver disease, comparing with placebo, aspartate aminotransferase was reduced in the silymarin-treated groups (p = 0.01) while alkaline phosphatase was not. In liver cirrhosis, mostly alcoholic, total mortality was 16.1% with silymarin vs. 20.5% with placebo (n.s.); liver-related mortality was 10.0% with silymarin vs. 17.3% with placebo (p = 0.01). Conclusions: Based on the available clinical evidence it can be concluded - concerning possible risks / probable benefits - that it is reasonable to employ silymarin as a supportive element in the therapy of Amanita phalloides poisoning but also (alcoholic and grade Child ‘A’) liver cirrhosis. A consistent research programme, consolidating existing evidence and exploring new potential uses, would be very welcome.

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