Cirrhosis reversal: a duel between dogma and myth

Desmet, Valeer; Roskams, Tania

doi:10.1016/j.jhep.2004.03.007

Cited by 222 publications

(168 citation statements)

References 61 publications

Supporting

Mentioning

149

Contrasting

Unclassified

Order By: Relevance

“…It has been said that cirrhosis can be considered a vascular disease of the liver 38 and that the hemodynamic parameters, splanchnic and renal, can describe severity. In this study we have shown that HVPG is a hemodynamic marker 6 that can be used as a marker of fibrosis progression before cirrhosis, and, together with TJB, can be performed with an adequate technique to yield adequate samples.…”

Section: Discussionmentioning

confidence: 99%

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

et al. 2007

View full text Add to dashboard Cite

Progression of fibrosis following recurrent hepatitis C virus (HCV) infection is frequent after liver transplantation (LT).Histology remains the gold standard to assess fibrosis, but the value of hepatic venous pressure gradient (HVPG) is being explored. We evaluated patients with recurrent HCV infection after LT to assess whether HVPG correlates with liver histology, particularly fibrosis. A total of 90 consecutive patients underwent 170 HVPG measurements concomitant with transjugular liver biopsy (TJB), with 31.5 (range, 6-156) months of follow up. Median biopsy length was 22 mm and total portal tract count was 12 (complete 6, partial 6). Median HVPG was 4 mmHg: 38% of patients Ն6 mmHg (portal hypertension, PHT), 13% Ն10 mmHg. HVPG correlated with Ishak stage (r ϭ 0.73, P Ͻ 0.001) for mild (0-3) and severe fibrosis (4-6), and grade score (r ϭ 0.47, P Ͻ 0.001), but neither correlated with interval from LT nor biopsy length. HVPG was Ն10 mmHg in 15 patients: 12 had stage 5 or 6, and 3 severe portal expansion. HVPG was repeated in 49, between 7 and 60 months with weak correlation to fibrosis score (r ϭ 0.30, P ϭ 0.045). A total of 12 patients with HVPG Ն6 mmHg had fibrosis score Յ3, while 8 patients had normal HVPG but fibrosis stage Ն4. These discrepancies were mostly associated with specific histological features such as perisinusoidal fibrosis rather than errors in measuring HVPG. In 29 with HVPG Ͻ6 mmHg at 1 yr, none decompensated compared to 4 of 13 (31%) with PHT. In conclusion, HVPG correlates with fibrosis and its progression, due to recurrent HCV infection, assessed in TJB. Liver Transpl 13:1305Transpl 13: -1311Transpl 13: , 2007 The severity of portal hypertension (PHT) correlates with the severity of liver disease and cirrhosis, both functionally and histologically 1 and also with the Model for End-Stage Liver Disease, 2 such that it has independent prognostic value separate from clinical and laboratory assessment. 2,3 Hepatic vein catheterisation 4 was modified by Groszmann et al. 5 using a balloon catheter. The measurement of hepatic venous pressure gradient (HVPG) (the difference between wedge hepatic venous pressure [WHVP] Ϫ free hepatic venous pressure) is reproducible 6 and is the preferred technique for evaluating PHT, correlating 1:1 with the direct measurement of portal vein pressure in patients with sinusoidal and postsinusoidal causes of cirrhosis, 7,8 particularly alcoholic and viral-related cirrhosis. Normally HVPG ranges from 1 to 5 mmHg; pressures Ն6 mmHg indicate PHT. 6 WHVP increases with progression of chronic hepatitis and PHT, before histologically detectable cirrhosis. 9 A gradient Ͼ5 mmHg was always associated with significant changes in liver biopsy in 1 study, although a normal gradient did not completely rule out cirrhosis, 10 suggesting that WHVP could provide supplementary information to liver biopsy, with a higher predictive value for assessing stage and activity of chronic liver disease, than routine biochemical tests. 10 Other studies have correlated HVPG both with severit...

show abstract

Section: Discussionmentioning

confidence: 99%

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

et al. 2007

View full text Add to dashboard Cite

show abstract

“…However, as pointed out by different Authors [6,11,15], no incontrovertible evidence has been reported for complete reversal of advanced cirrhosis since a careful analysis of these studies may lead to prudently state that just a variable degree of fibrosis reversion in human patients is described. As discussed by Pinzani and his colleagues [6], this may also be related to a substantial lack of a common language and worldwide consensus on definitions available to unequivocally distinguish conditions of pre-cirrhosis or compensated cirrhosis from true or decompensated cirrhosis, the former being able to show reversal, sometimes significant, the latter being mostly unable to do so.…”

Section: Liver Fibrosis As a Potentially Reversible Processmentioning

confidence: 99%

Cellular and molecular mechanisms in liver fibrogenesis

Novo

Cannito

Paternostro

et al. 2014

Archives of Biochemistry and Biophysics

178

194

View full text Add to dashboard Cite

“…Furthermore, in any system, it is notoriously difficult to write professor-proof and error-proof definitions of the lesions to be scored. Regrettably, this caused occasionally illfounded clinical conclusions about reversal of cirrhosis, 72 ignoring its macronodular and incomplete septal forms, 73 and hence eliciting my firm protest, 74,75 although I do agree that in selected circumstances cirrhosis may reverse. 76 This keeps in mind the old adage: "⌸␣ ␣ ⑀ ,…”

Section: Chronic Hepatitismentioning

confidence: 99%

The amazing universe of hepatic microstructure

Desmet

2009

Hepatology

View full text Add to dashboard Cite

An informal review is presented by the author of his 50 years of involvement in practice and research in hepatopathology. Some background for the author's attitude and meandering pathway into his professional career serves as introduction to a short discussion of the main topics of his interest and expertise. Histogenesis of liver cancer was the theme of early work for a Ph.D. thesis, the results of which were lost into oblivion due to local rules and circumstances, but were rescued three decades later. His conclusions about the cells of origin of liver cancer remain concordant with the newer concepts in the field after nearly half a century. Studies in the field of chronic hepatitis became a long saga, involving the first classification of this syndrome by "the Gnomes" in 1968, histochemical investigations of viral antigens, lymphocyte subsets and adhesion molecules, and a quarter century later, the creation of a new classification presently in use. Cholestasis was a broadening field in diagnostic entities and involved the study of liver lesions, comprising pathways of bile regurgitation (including reversed secretory polarity of hepatocytes) and so-called ductular reaction. The latter topic has a high importance for the various roles it plays in modulating liver tissue of chronic cholestasis into biliary cirrhosis, and as the territory of hepatic progenitor cells, crucial for liver regeneration in adverse conditions and in development of liver cancer. Study of the embryology of intrahepatic bile ducts helped to clarify the strange appearance of the ducts in "ductal plate configuration" in several conditions, including some forms of biliary atresia with poor prognosis and all varieties of fibrocystic bile duct diseases with "ductal plate malformation" as the basic morphologic lesion. (HEPATOLOGY 2009;50: 333-344.)

show abstract

Cirrhosis reversal: a duel between dogma and myth

Cited by 222 publications

References 61 publications

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

Cellular and molecular mechanisms in liver fibrogenesis

The amazing universe of hepatic microstructure

Contact Info

Product

Resources

About