“…Liver biopsy is invasive and risky, 70 samples only 1/50,000 of the liver, and is prone to considerable sampling error. This is illustrated by a study that compared laparoscopic liver biopsies from the right and the left lobe in patients with hepatitis C. One-third of paired samples differed by at least one out of the four Metavir stages, and 14.5% showed advanced fibrosis in one and cirrhosis in the other lobe (stage F3 versus stage F4).…”
Section: Noninvasive Means To Assess Liver Fibrosis and Fibrogenesismentioning
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
“…Liver biopsy is invasive and risky, 70 samples only 1/50,000 of the liver, and is prone to considerable sampling error. This is illustrated by a study that compared laparoscopic liver biopsies from the right and the left lobe in patients with hepatitis C. One-third of paired samples differed by at least one out of the four Metavir stages, and 14.5% showed advanced fibrosis in one and cirrhosis in the other lobe (stage F3 versus stage F4).…”
Section: Noninvasive Means To Assess Liver Fibrosis and Fibrogenesismentioning
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
“…Poynard et al reported that liver biopsy was responsible for most of the significantly discordant results between liver biopsy and serum markers, as a result of sampling error [29]. In our study, a minimum length of at least 1.0 cm from the liver biopsy and at least six complete portal tracts were required for study inclusion [20]. But Standish et al have suggested a minimum of 11 portal tracts as a requirement to allow for reliable fibrosis estimates especially in patients with hepatitis C [30].…”
Section: Discussionmentioning
confidence: 81%
“…A minimum length of at least 1.0 cm from the liver biopsy and at least six complete portal tracts were required for diagnosis [20]. The mean length of the liver biopsy sample was 12.6 mm (±3.3 mm) and the mean number of portal tracts was 13.2 (±6.3).…”
Background/Aims The majority of non-invasive markers of liver fibrosis have been developed in patients with chronic hepatitis C. We aimed to develop a formula for predicting significant fibrosis in patients with chronic viral hepatitis and to compare the usefulness of published models derived from the data obtained from patients with chronic hepatitis C. Methods Serum markers and the METAVIR stage of fibrosis in liver biopsy specimens were compared prospectively in patients with chronic hepatitis B and C (estimation set, 367; validation set, 159). Results In the estimation set, multiple forward stepwise logistic regression analysis identified c-glutamyl transpeptidase, haptoglobin, a2-macroglobulin, matrix metalloproteinase-2, and tissue inhibitor of metalloproteinase-1 as independent predictors of significant fibrosis. A formula termed the SF index was constructed with the aforementioned five variables. The areas under the receiver operating characteristic curves of the SF index for predicting significant fibrosis were 0.828, 0.776, and 0.827 in the estimation, validation, and total sets, respectively. Using cut-off scores of 2.2 and 3.3, significant fibrosis was predicted with considerable accuracy. The diagnostic performances of the SF index and the Zeng index derived from chronic hepatitis B patients were much better than indices derived from chronic hepatitis C patients, such as the APRI, Forns index, and FIB-4. Conclusions We developed a novel formula for predicting significant fibrosis in patients with chronic viral hepatitis. Serum indices from studies in patients with chronic hepatitis C were less accurate in patients with chronic hepatitis B for predicting significant fibrosis.
“…144 But its use is limited by its invasiveness, risk of complications and its sampling variability. 145 Thus, non-invasive tests of liver fibrosis such as the AST-to-platelet ratio index (APRI), fibroSURE, FibroSCAN etc are being used. However, none of them are validated for clinical use.…”
Section: Role Of Micrornas In Liver Transplantationmentioning
MicroRNAs (miRs) are small non-coding RNAs that negatively regulate gene expression by pairing with partially complementary target sequences in the 3 0 UTRs of mRNAs to promote degradation and/or block translation. Aberrant miR expression is associated with development of multiple diseases including hepatic diseases. The role of miRs in the regulation of gene expression and rapid progress in the field of microRNA research are resulting in momentum toward development of diagnostic markers and novel therapeutic strategies for human liver diseases. Recent studies provide clear evidence that miRs are abundant in the liver and modulate a diverse spectrum of biological functions, thereby supporting an association between alterations of miR homeostasis and pathological liver diseases. Here we review the role of miRs in liver as their physiological and pathological importance has been demonstrated in metabolism, immunity, viral hepatitis, oncogenesis, fatty liver diseases (alcoholic and non-alcoholic), drug-induced liver injury, fibrosis as well as acute liver failure. ( J CLIN EXP HEPATOL 2013;3:231-242)
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