Curing hepatitis C
infection moderately reduces portal hypertension, but has less impact in people
with more severe liver stiffness due to fibrosis, Spanish researchers reported
at the 2016 AASLD Liver Meeting last week in Boston.
hypertension – high blood pressure in the portal vein supplying the liver – is
caused by scarring of the liver due to hepatitis C, which restricts the flow of
blood in the portal vein and into the liver. If portal hypertension persists,
blood vessels may form to relieve the pressure, leading to the development of
varices and subsequent risk of gastrointestinal bleeding. Portal hypertension is
a major risk factor for decompensation in people with cirrhosis.
is managed through the use of beta-blockers as therapy and by use of endoscopy
to prevent the recurrence of bleeding. Many people find both medication and regular endoscopy difficult to tolerate.
A protein made in the liver, needed to maintain a balance of the fluids in the body. In a blood test, lower than normal levels of albumin and total protein may indicate liver damage or disease. If there is not enough albumin, fluid may accumulate in the abdomen (ascites).
Stretched veins which may burst and cause severe bleeding; a complication of cirrhosis.
Although direct-acting antivirals (DAAs) eradicate
hepatitis C virus (HCV) in the vast majority of people, it is unclear if a successful response to
treatment results in a reduction in portal hypertension and in the risk of
decompensation in people with advanced liver disease.
German research found that people with Child-Pugh stage B cirrhosis or
higher portal blood pressure were less likely to experience substantial
reductions in portal blood pressure or normalisation of portal pressure.
investigate this question, Spanish researchers carried out a prospective
multicentre study of the evolution of portal pressure and haemodynamics after DAA treatment in people who achieved sustained virologic
response (SVR12) on an interferon-free regimen.
The study population
comprised 198 people with HCV-related liver cirrhosis and clinically
significant portal hypertension (CSPH, hepatic venous pressure gradient [HVPG] > 10mmHg). All were
treated with all-oral direct-acting agent regimens. Patients had assessments of
HVPG, right-heart catheterisation and liver stiff measurements at baseline and
at 24-weeks after completion of therapy.
cent of participants were male, with an average age of 60 and a median body
mass index of 28. Most people (70%) had oesophageal varices and 31% had one or
more previous episode of decompensated liver disease. Eighty per cent had Child-Pugh A cirrhosis, 20% had Child-Pugh B cirrhosis.
decreased significantly after attainment of SVR. The mean baseline HVPG was
15.8 mmHg and the mean reduction was -2 mmHg. After treatment the proportion of
people with HVPG > 10mmHg fell from 100% to 83%; the proportion with
HVPG > 12mmHg fell from 80% to 66% and the proportion with HVPG >
16 mmHg fell from 43% to 27%.
relevant decrease in portal hypertension of at least 10% was observed in 54% of
people, with 34% having a decrease of 20% or more. After controlling for
potential confounders, the only factors associated with a decrease of at least
10% were serum albumin < 3.5g/dL.(p = 0.05) and baseline liver stiffness
measurement (p = 0.04). Among those with HVPG >10mmHg 48% of those with
baseline liver stiffness < 13.6 kPA had clinical significant portal
hypertension 24 weeks after treatment initiation, compared to 92% of those with
baseline liver stiffness > 21 kPA.
Decrease in mean
HVPG did not differ according to use of beta-blockers. However, due to higher
CSPH at baseline, CSPH persisted in 95% of people taking beta-blockers
compared to 77% of people not taking this type of treatment (p< 0.01).
catheterisation measures were available for 82 individuals and showed a
significant rise in MAP, which the investigators attributed to increased
systemic vascular resistance (+1.4 and +25%; p < 0.05) with stable cardiac
output. Moreover, other important measures, including mPAP and pulmonary
vascular resistance also increased after therapy (+1.5% and +21%; p < 0.05).
Pulmonary arterial hypertension (mPAP of 25mmHG or above) developed in nine
people and worsened in four, but only two individuals developed increased
pulmonary vascular resistance.