Hepatic venous pressure measurement: An old test as a new prognostic marker in cirrhosis?

Armonis, A

doi:10.1053/jhep.1997.v25.ajhep0250245

Cited by 67 publications

(108 citation statements)

References 14 publications

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“…HVPG measurement can give additional information to the liver biopsy 39 after LT for HCV cirrhosis, which may also be useful in the nontransplantation situation. 2,3,7,[15][16][17]40 …”

Section: Discussionmentioning

confidence: 99%

“…2) (expressed as difference between the last and first measurement) had a weak correlation with changes in fibrosis score (r ϭ 0.30, P ϭ 0.045). However, no significant correlation was found between change in grade and HVPG (P ϭ 0.042) and median HVPG did not change (5 mmHg; range, [1][2][3][4][5][6][7][8][9][10][11][12][13][14]. Regarding the whole paired group, the mean of the first evaluations for HVPG was 5.31 Ϯ 2.9 vs. 6.29 Ϯ 4.5 for the last (P ϭ 0.82); when evaluating those with PHT at first measurement, a better correlation was found, with mean first HVPG at 8.4 Ϯ 2.3 vs. 10 Ϯ 5 for the last HVPG (P ϭ 0.076).…”

Section: Total Cohortmentioning

confidence: 93%

“…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.…”

Section: Progression Of Fibrosis Following Recurrent Hepatitis C Virumentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

“…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 severity and etiology of cirrhosis, 3,7,11 with only 1 study documenting a difference between HCV and alcoholic cirrhosis. 12 A significant correlation has been shown between antiviral response and HVPG changes in HCV chronic hepatitis, 13,14 and between HVPG and histological features of cirrhosis.…”

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confidence: 99%

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

et al. 2007

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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...

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“…HVPG measurement can give additional information to the liver biopsy 39 after LT for HCV cirrhosis, which may also be useful in the nontransplantation situation. 2,3,7,[15][16][17]40 …”

Section: Discussionmentioning

confidence: 99%

Section: Total Cohortmentioning

confidence: 93%

Section: Progression Of Fibrosis Following Recurrent Hepatitis C Virumentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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

et al. 2007

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Hydrostatic pressure induces profibrotic properties in hepatic stellate cells via the RhoA/ROCK signaling pathway

Huang

Khalifa

et al. 2022

FEBS Open Bio

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Elevated interstitial fluid hydrostatic pressure is commonly observed in diseased livers. We herein examined the hypothesis that hydrostatic pressure induces hepatic stellate cells to acquire profibrotic properties under pathological conditions. Human hepatic stellate cells were exposed to 50 mmHg pressure for 24 h. Although we observed few changes of cell growth and morphology, PCR array data on the expression of fibrosis‐associated genes suggested the acquisition of profibrotic properties. The exposure of hepatic stellate cells to 50 mmHg pressure for 24 h also significantly enhanced the expression of RhoA, ROCK1, α‐SMA, TGF‐β1, p‐MLC, and p‐Smad2, and this was effectively attenuated by the ROCK inhibitor Y‐27632. Our ex vivo experimental data suggest that elevated interstitial fluid hydrostatic pressure under pathological conditions may promote liver fibrosis by inducing acquisition of profibrotic properties of hepatic stellate cells through the RhoA/ROCK signaling pathway.

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Analysis of Pax7 expressing myogenic cells in zebrafish muscle development, injury, and models of disease

Seger

Hargrave

Wang

et al. 2011

Developmental Dynamics

117

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*The transcription factor Pax7 is a marker and regulator of muscle progenitors and satellite cells that contribute to the embryonic development and postembryonic growth of skeletal muscle in vertebrates, as well as to its repair and regeneration. Here, we identify Pax7 1ve myogenic cells in the zebrafish and characterize their behavior in postembryonic stages. Mononucleate Pax7 1ve cells can first be found associated with myofibers at 72 hours post fertilization (hpf). To follow the behavior of muscle progenitor cells in vivo, we generated transgenic lines expressing fluorescent proteins under the control of the pax7a or pax3a promoters. We established an injury model using cardiotoxin injection and monitored cell proliferation and myogenic regulatory factor expression in myogenic precursors cells and muscle fibers after injury using proliferation markers and the transgenic lines. We also analyzed Pax7 1ve cells in animals with dystrophic phenotypes and found an increased number compared with wild-type. Developmental Dynamics 240:2440-2451,

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Hepatic venous pressure measurement: An old test as a new prognostic marker in cirrhosis?

Cited by 67 publications

References 14 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

Hydrostatic pressure induces profibrotic properties in hepatic stellate cells via the RhoA/ROCK signaling pathway

Analysis of Pax7 expressing myogenic cells in zebrafish muscle development, injury, and models of disease

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