Extrahepatic Cholestasis Increases Liver Stiffness (Fibroscan®) Irrespective of Fibrosis

Millonig, Gunda; Reimann, Frank; Friedrich, Stefanie; Fonouni, Hamidreza; Mehrabi, Atefeh; Büchler, Markus W.; Seitz, Helmut K.; Mueller, Sebastian

doi:10.1055/s-0029-1191982

Cited by 132 publications

(180 citation statements)

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“…Indeed, as previously mentioned, the extent of necro-inflammatory activity has been shown to influence TE measurements in patients with viral hepatitis with a steady increase of liver stiffness values in parallel with the degree of histological activity [66,70,100]. Consistent with these results, the risk of overestimating liver stiffness values has been reported in case of ALT flares in patients with acute viral hepatitis or chronic hepatitis B [101][102][103], as well as in cases of extrahepatic cholestasis [104] or congestive heart failure [105].…”

Section: Limitationssupporting

confidence: 71%

Non-invasive assessment of liver fibrosis in chronic hepatitis C

Castéra

2011

Hepatol Int

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Section: Limitationssupporting

confidence: 71%

Non-invasive assessment of liver fibrosis in chronic hepatitis C

Castéra

2011

Hepatol Int

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“…In addition, severe inflammation and mechan-ical cholestasis can significantly increase hepatic stiffness, thus confounding the fibrosis readout. [104][105][106] Nonetheless, ultrasound elastography should prove useful for stratification of patients for inclusion into treatment studies.…”

Section: Noninvasive Means To Assess Liver Fibrosis and Fibrogenesismentioning

confidence: 99%

Targeting liver fibrosis: Strategies for development and validation of antifibrotic therapies

2009

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We have made striking progress in our understanding of the biochemistry and cell biology that underlies liver fibrosis and cirrhosis, including the development of strategies and agents to prevent and reverse fibrosis. However, translation of this knowledge into clinical practice has been hampered by (1) the limitation of many in vitro and in vivo models to confirm mechanisms and to test antifibrotic agents, and (2) the lack of sensitive methodologies to quantify the degree of liver fibrosis and the dynamics of fibrosis progression or reversal in patients. Furthermore, whereas cirrhosis and subsequent decompensation are accepted hard clinical endpoints, fibrosis and fibrosis progression alone are merely plausible surrogates for future clinical deterioration. In this review we focus on an optimized strategy for preclinical antifibrotic drug development and highlight the current and future techniques that permit noninvasive assessment and quantification of liver fibrosis and fibrogenesis. The availability of such noninvasive methodologies will serve as the pacemaker for the clinical development and validation of potent antifibrotic agents. (HEPATOLOGY 2009;50:1294-1306

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“…5 However, several confounders of LSM have also been identified. [6][7][8][9][10] Among them, major changes in transaminases have been demonstrated as a significant in overestimating factor in liver fibrosis. 9,10 In cases with more than 10 valid measurements, the validity of LSM is generally determined by two parameters: a success rate of at least 60% and an interquartile range (IQR) for all successful measurements of less than 30% of the median value according to the manufacturer's recommendations.…”

Section: Introductionmentioning

confidence: 99%