Transforming Growth Factor-β1 as a Surrogate Marker of Hepatic Dysfunction in Chronic Liver Diseases

Flisiak, Robert; Prokopowicz, D

doi:10.1515/cclm.2000.170

Cited by 13 publications

(10 citation statements)

References 17 publications

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“…These findings are in agreement with the results of Hussein et al [16] and Flisiak and Prokopovicz [17] , who reported that plasma TGF-β1 was elevated in patients with a higher Child score and also stated that elevated plasma TGF-β1 levels in patients with chronic liver disease might be caused by decreased clearance.…”

Section: In O Ur Stu Dy We De M O Nst R Ate D Si Gni F I C Ant Lysupporting

confidence: 93%

Association of serum levels of transforming growth factor b1 with disease severity in patients with hepatocellular carcinoma

Kohla¹,

Attia²,

Darwesh³

et al. 2017

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Aim: Transforming growth factor (TGF) is overexpressed by tumor cells like other proteins and growth factors. TGF-β1 is then activated in the extracellular compartment but is unable to control cell proliferation because of the absence or low level of TGF-β1 receptors on the plasma membrane of malignant hepatocytes. This potential mechanism might interrupt the autocrine regulation loop of TGF-β1 and its blocking effect on cell proliferation. TGF-β1 is a multifunctional cytokine involved in the regulation of growth and differentiation of both normal and transformed cells. This study aimed to evaluate the association of serum levels of TGF-β1 with disease severity. Methods: A total of 180 subjects were classified into 6 groups according to Barcelona clinic liver cancer (BCLC) classification, 30 patients each: early (BCLC 0 and A), intermediate (BCLC B), advanced stage (BCLC C), and terminal stage (BCLC D) of hepatocellular carcinoma as well as 1 group of patients with cirrhosis only and 1 control group. Serum levels of TGF β1 were measured. Results: Serum levels of TGF-β1 were significantly higher in patients with HCC (1,687.47 ± 1,462.81 pg/mL) than cirrhotics (487.98 ± 344.23 pg/mL, P < 0.001) and controls (250.16 ± 284.61 pg/mL, P < 0.001). Conclusion: TGF-β1 may have a role in tumor growth and progression.

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Section: In O Ur Stu Dy We De M O Nst R Ate D Si Gni F I C Ant Lysupporting

confidence: 93%

Association of serum levels of transforming growth factor b1 with disease severity in patients with hepatocellular carcinoma

Kohla¹,

Attia²,

Darwesh³

et al. 2017

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“…This might allow estimation of liver insufficiency, fibrogenesis, malignancy, and immunosuppressive drug treatment in liver transplant patients. Indeed, studies have reported elevated concentrations of plasma TGF-beta 1 in patients with chronic active hepatitis B and C, HBV related and alcoholic liver cirrhosis (122). The degree of elevation could be correlated with scores of the Child-Pugh classification (123) and a number of biochemical liver function tests (124) in cirrhotic patients.…”

Section: The Potential Of Circulating Tgf-beta As a Diagnostic Toolmentioning

confidence: 95%

Roles of TGF-beta in hepatic fibrosis

Axel¹

2002

Front Biosci

485

187

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TGF-beta has multiple profibrogenic but also anti-inflammatory and immunosuppressive effects. The balance of these actions is required for maintaining tissue homeostasis and an aberrant expression of TGF-beta is involved in a number of disease processes in the liver. In addition to its fibrogenic action leading to transdifferentiation of hepatic stellate cells into myofibroblasts, TGF-beta is also an important negative regulator of proliferation and an inducer of apoptosis. The major portion of TGF-beta is secreted as part of an inactive complex and the details of the activation process in liver have not yet been elucidated. The initially striking simplicity of the core TGF-beta/Smad signaling pathways is rapidly giving way to a much more complex view of intracellular signal transduction mechanisms and recent work has demonstrated the importance of cross-talk among different signaling pathways to either specify, enhance, or inhibit TGF-beta responses. The ubiquitous pathophysiologic relevance of TGF-beta suggests its measurement in blood as a diagnostic tool. Other strategies aim at inhibition of TGF-beta1 function or synthesis as a primary target for the development of antifibrotic strategies and recent advances in cell biology have opened several ways to approach the inhibition of TGF-beta action.

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“…As a result, TGF‐β concentrations in plasma were analysed to estimate their diagnostic significance. The concentrations are elevated in and correlated with the severity of liver diseases suggesting this cytokine as a non‐invasive biomarker of hepatic dysfunction in chronic liver diseases [47], and possibly of hepatic fibrosis progression [48]. The significant correlation with aspartate‐aminotransferase (AST) and alanin‐aminotransferase (ALT) activity in serum [49] and the pathobiochemical finding that hepatocytes contain substantial amounts of TGF‐β, which is released into the medium if hepatocytes are damaged [50], proposes that the elevation of this cytokine in serum is due to necrosis instead of fibrogenesis.…”

Section: Class I Biomarkers Of Fibrosismentioning

confidence: 99%

Biomarkers of hepatic fibrosis, fibrogenesis and genetic pre‐disposition pending between fiction and reality

Gressner

Weiskirchen

Gressner

2007

J Cellular Molecular Medi

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Fibrosis is a frequent, life-threatening complication of most chronic liver diseases. Despite major achievements in the understanding of its pathogenesis, the translation of this knowledge into clinical practice is still limited. In particular, non-invasive and reliable (serum-) biomarkers indicating the activity of fibrogenesis are scarce. Class I biomarkers are defined as serum components having a direct relation to the mechanism of fibrogenesis, either as secreted matrix-related components of activated hepatic stellate cells and fibroblasts or as mediators of extracellular matrix (ECM) synthesis or turnover. They reflect primarily the activity of the fibrogenic process. Many of them, however, proved to be disappointing with regard to sensitivity and speci-ficity. Up to now hyaluronan turned out to be the relative best type I serum marker. Class II biomarkers comprise in general rather simple standard laboratory tests, which are grouped into panels. They fulfil most criteria for detection and staging of fibrosis and to a lesser extent grading of fibrogenic activity. More than 20 scores are currently available, among which Fibrotest™ is the most popular one. However, the diagnostic use of many of these scores is still limited and standardization of the assays is only partially realized. Combining of panel markers in sequential algorithms might increase their diagnostic validity. The translation of genetic pre-disposition biomarkers into clinical practice has not yet started, but some polymorphisms indicate a link to progression and outcome of fibrogenesis. Parallel to serum markers non-invasive physical techniques, for example, transient elastography, are developed, which can be combined with serum tests and profiling of serum proteins and glycans.

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Transforming Growth Factor-β1 as a Surrogate Marker of Hepatic Dysfunction in Chronic Liver Diseases

Cited by 13 publications

References 17 publications

Association of serum levels of transforming growth factor b1 with disease severity in patients with hepatocellular carcinoma

Association of serum levels of transforming growth factor b1 with disease severity in patients with hepatocellular carcinoma

Roles of TGF-beta in hepatic fibrosis

Biomarkers of hepatic fibrosis, fibrogenesis and genetic pre‐disposition pending between fiction and reality

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