Direct and indirect evidence for the reversibility of cirrhosis

Serpaggi, Jeanne; Carnot, Françoise; Nalpas, Bertrand; Canioni, D.; Guéchot, Jérôme; Lebray, Pascal; Vallet-Pichard, Anaı̈s; Fontaine, Hélène; Bédossa, Pierre; Pol, Stanislas

doi:10.1016/j.humpath.2006.07.007

Cited by 97 publications

(56 citation statements)

References 47 publications

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“…Although sampling error is a well-known problem with biopsy interpretation, taken in aggregate these results are convincing and support the emerging concept of the reversibility of even advanced stages of liver fibrosis [9]. Moreover, the results support the often challenging but fundamental tenets of NASH management to advise aggressive lifestyle changes with the encouragement of weight loss through dietary changes and exercise [10].…”

supporting

confidence: 64%

Reversing Advanced Hepatic Fibrosis in NASH: Clearly Possible, but Widely at Hand?

Caldwell

Argo

2015

Dig Dis Sci

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supporting

confidence: 64%

Reversing Advanced Hepatic Fibrosis in NASH: Clearly Possible, but Widely at Hand?

Caldwell

Argo

2015

Dig Dis Sci

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“…Entretanto, alguns autores encontraram redução dos valores do AH mais evidente nos pacientes que apresentaram resposta virológica sustentada e naqueles com reversão da fibrose (25,29) .…”

Section: Discussionunclassified

Valor preditivo de marcadores séricos de fibrose hepática em pacientes portadores de hepatite crônica viral C

Lima¹,

Martins

Nader

et al. 2008

J. Bras. Patol. Med. Lab.

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Introdução: Os marcadores séricos têm sido empregados na avaliação da fibrose hepática em pacientes portadores de hepatite crônica C (HCC). Objetivos: Avaliar a capacidade do índice aspartato aminotransferase (AST)/alanina aminotransferase (ALT), dos níveis séricos de gama-glutamiltransferase (GGT), contagem de plaquetas, do índice AST/plaquetas (APRI) e do ácido hialurônico (AH) em predizer a intensidade da fibrose hepática na HCC e a variação desses marcadores após tratamento com interferon. Pacientes e métodos: Em 72 pacientes portadores de hepatite C determinamos no soro o índice AST/ALT, GGT, plaquetas, índice APRI (obtido pelo quociente AST/plaquetas) e o AH, que foram comparados ao estadiamento histológico, segundo os critérios de METAVIR. Receberam tratamento com interferon e ribavirina 65 pacientes. Os indivíduos que concluíram o tratamento (n = 33) realizaram nova dosagem dos marcadores séricos de fibrose para comparar com os níveis pré-tratamento. Resultados: Observamos que a GGT, a contagem de plaquetas, o índice APRI e o AH se correlacionaram com estádio de doença hepática (p < 0,01), exceto o índice AST/ALT. A análise das áreas sob as curvas ROC (AUC) evidenciaram que a melhor associação com estadiamento hepático foi para o índice APRI e a dosagem sérica do AH: AUC (APRI) = 0,85 e AUC (AH) = 0,86. Na avaliação pós-terapia com interferon, apenas a GGT e o índice APRI apresentaram redução de seus níveis (p < 0,05). Conclusão: O AH e o índice APRI apresentaram maior acurácia no estadiamento da fibrose, podendo ser aplicados como métodos diagnósticos alternativos na HCC. abstract resumo Introduction: Serum markers have been used in the assessment of liver fibrosis in patients with chronic hepatitis C (CHC). Aims: We evaluated the capacity of aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, gama-glutamyltransferase (GGT) levels, platelet count, the AST to platelet ratio index (APRI) and serum hyaluronic acid (HA) to predict the intensity of hepatic fibrosis in patients with CHC and the variation of these markers after therapy with interferon. Patients and methods: In 72 patients with hepatitis C, AST/ALT ratio, GGT levels, platelet count, the APRI index (calculated as the ratio of AST to platelets) and

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“…5,[11][12][13][14][15][16][17] During the fibroproliferative stage, treatment of the underlying cause of liver disease results in the best prognostic outcome with disease reversal occurring in many patients. [18][19][20][21] Matrix metalloproteinase (MMP)-mediated degradation of fibrillar collagens is a well-established aspect of recovery from liver fibrosis in both experimental models and human disease, with a majority of the MMPs being synthesized by HSCs. 7,[22][23][24] The tissue inhibitor of metalloproteinase (TIMP) family of endogenous inhibitors is involved in regulating the activity of MMPs and collectively, MMP and TIMP activity contribute to regulation of HSC activity during fibrogenesis and recovery.…”

mentioning

confidence: 99%

Versican: a novel modulator of hepatic fibrosis

Bukong

Maurice

Chahal

et al. 2016

Laboratory Investigation

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Little is known about the deposition and turnover of proteoglycans in liver fibrosis, despite their abundance in the extracellular matrix. Versican plays diverse roles in modulating cell behavior in other fibroproliferative diseases, but remains poorly described in the liver. Hepatic fibrosis was induced by carbon tetrachloride treatment of C57BL/6 mice over 4 weeks followed by recovery over a 28-day period. Primary mouse hepatic stellate cells (HSCs) were activated in culture and versican was transiently knocked down in human (LX2) and mouse HSCs. Expression of versican, A Disintegrinlike and Metalloproteinase with Thrombospondin-1 motifs (ADAMTS)-1, -4, -5, -8, -9, -15, and -20, and markers of fibrogenesis were studied using immunohistochemistry, real-time quantitative PCR, and western blotting. Immunohistochemistry showed increased expression of versican in cirrhotic human livers and the mouse model of fibrosis. Carbon tetrachloride treatment led to significant increases in versican expression and the proteoglycanases ADAMTS-5, -9, -15, and -20, alongside TNF-α, α-smooth muscle actin (α-SMA), collagen-1, and TGF-β expression. During recovery, expression of many of these genes returned to control levels. However, expression of ADAMTS-5, -8, -9, and -15 showed delayed increases in expression at 28 days of recovery, which corresponded with decreases in versican V0 and V1 cleavage products (G1-DPEAAE 1401 and G1-DPEAAE 441 ). Activation of primary HSCs in vitro significantly increased versican, α-SMA, and collagen-1 expression. Transient knockdown of versican in HSCs led to decreases in markers of fibrogenesis and reduced cell proliferation, without inducing apoptosis. Versican expression increases during HSC activation and liver fibrosis, and proteolytic processing occurs during the resolution of fibrosis. Knockdown studies in vitro suggest a possible role of versican in modulating hepatic fibrogenesis.

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Direct and indirect evidence for the reversibility of cirrhosis

Cited by 97 publications

References 47 publications

Reversing Advanced Hepatic Fibrosis in NASH: Clearly Possible, but Widely at Hand?

Reversing Advanced Hepatic Fibrosis in NASH: Clearly Possible, but Widely at Hand?

Valor preditivo de marcadores séricos de fibrose hepática em pacientes portadores de hepatite crônica viral C

Versican: a novel modulator of hepatic fibrosis

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