Histopathological evaluation of liver fibrosis: quantitative image analysis vs semi-quantitative scores

Pilette, Christophe; Rousselet, Marie Christine; Bédossa, Pierre; Chappard, Daniel; Oberti, Frédéric; Rifflet, H; Maïga, M. Y.; Gallois, Yves; Calès, Paul

doi:10.1016/s0168-8278(98)80318-8

Cited by 190 publications

(161 citation statements)

References 26 publications

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“…The affinity of the sirius red chromophore via its sulphonic acid group for the amino acid composition of collagen confers excellent selectivity of this dye for collagen and has been used previously to quantify tissue collagen by both spectrophotometric and image analysis methods (Chevallier et al, 1994;Pilette et al, 1998). In normal human pancreas, sirius red staining demonstrates collagen around ducts and within the interlobular septae (Bedossa et al, 1989).…”

Section: Resultsmentioning

confidence: 99%

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Neuschwander‐Tetri¹,

Bridle

Wells³

et al. 2000

Laboratory Investigation

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SUMMARY:Pancreatic stellate cells may be a major source of extracellular matrix deposition during injury. This study was undertaken to establish whether pancreatic stellate cells are a source of Type I collagen in vivo and whether they continue to be a source of matrix production in the post-injury fibrotic pancreas. To induce pancreatic fibrogenesis, acute pancreatic injury was induced in mice three times weekly with supraphysiologic doses of cerulein. Animals were treated for 6 weeks and allowed to recover for an additional 6 weeks. Stellate cell activation and pancreatic collagen expression were measured by immunohistochemistry, whole tissue RNA analysis, and in situ hybridization. Histology and digital image analysis demonstrated the development of substantial pancreatic fibrosis after 6 weeks of treatment. During recovery, incomplete resolution of the fibrosis was found. Procollagen ␣ 1 (I) mRNA increased more than15-fold during treatment and continued to be 5-fold elevated during the post-injury phase. In situ hybridization studies demonstrated that collagen gene expression was colocalized to activated pancreatic stellate cells. Collagen expression and fibrosis persisted in focal areas during recovery. These findings show that pancreatic stellate cells are the major source of collagen during repetitive injury in vivo. Additionally, focal areas of sustained pancreatic fibrogenesis persist after cessation of cerulein treatment, and these areas may contribute to sustained total organ collagen expression in the absence of ongoing injury. (Lab Invest 2000, 80:143-150).

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Section: Resultsmentioning

confidence: 99%

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Neuschwander‐Tetri¹,

Bridle

Wells³

et al. 2000

Laboratory Investigation

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“…These include: glycoproteins, such as serum hyaluronate [13][14][15][16][17], laminin [18,19], and YKL-40 [20]; the collagens family, such as procollagen III N-peptide (PIIINP) [13] and type IV collagen [21]; collagenases and their inhibitors, such as matrix metalloproteases (MMP) [22] and tissue inhibitory metalloprotease-1 (TIMP-1) [23].…”

Section: Biological Approach: Serum Fibrosis Biomarkersmentioning

confidence: 99%

Non-invasive assessment of liver fibrosis in chronic hepatitis C

Castéra

2011

Hepatol Int

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“…Although the methodology is not standardized, a number of publications have described methods for quantifying hepatic fibrosis by image analysis, and all appear to yield similar results. 5,[18][19][20][21][22][23][24][25][26][27] The methods are time consuming compared with simple histologic scoring, and the necessary equipment and expertise are not widely available, but in a study to evaluate progression or regression of fibrosis, measuring the amount of fibrosis as precisely as possible seems appropriate.…”

mentioning

confidence: 99%

Progression of fibrosis in advanced chronic hepatitis C: Evaluation by morphometric image analysis

et al. 2007

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Fibrosis progression in chronic liver disease has usually been evaluated by liver biopsy using insensitive semiquantitative numerical scores. An alternative to this is to measure fibrous tissue quantitatively using morphometric image analysis. The aim of this study was to quantify fibrosis progression in a cohort of patients with treatment-refractory chronic hepatitis C enrolled in a placebo-controlled clinical trial of interferon gamma-1b (IFN-␥ 1b) for the treatment of advanced hepatic fibrosis. We used morphometry to quantify the amount of fibrous tissue in liver biopsies performed at baseline and after 48 weeks in 245 patients who had paired unfragmented, adequate-sized specimens and correlated the results with clinical and laboratory parameters. Eighty-seven patients were treated with placebo and 158 with IFN-␥ 1b. No effect of the drug on fibrosis was found in the trial, and so data from all 245 patients were combined for analysis. At baseline, 78% had cirrhosis; 22%, bridging fibrosis. The mean morphometrically determined collagen content increased by 58% between baseline and 48 weeks. There were statistically significant but weak correlations of fibrosis with platelet count, albumin, bilirubin, INR, and hyaluronic acid; however, changes in these did not correlate with or predict changes in fibrosis in the liver biopsy. Conclusion: In advanced chronic hepatitis C, fibrosis increases at a rapid pace that can only be detected by morphometry. This technique can be used in future therapeutic trials of agents to inhibit fibrosis progression. (HEPATOLOGY 2007;45:886-894.)

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Histopathological evaluation of liver fibrosis: quantitative image analysis vs semi-quantitative scores

Cited by 190 publications

References 26 publications

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Repetitive Acute Pancreatic Injury in the Mouse Induces Procollagen α1(I) Expression Colocalized to Pancreatic Stellate Cells

Non-invasive assessment of liver fibrosis in chronic hepatitis C

Progression of fibrosis in advanced chronic hepatitis C: Evaluation by morphometric image analysis

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