METABOLIC SYNDROME IS ASSOCIATED WITH LACK OF
FIBROSIS REGRESSION DURING CHRONIC HEPATITIS B
TREATMENT: A 3-YEAR LONGITUDINAL STUDY WITH PAIRED
TRANSIENT ELASTOGRAPHIES
Wai-Kay Seto1, Lung Yi Mak1, James Fung1, Ching Lung Lai2
and Man Fung Yuen1, (1)Medicine, The University of Hong
Kong, (2)The University of Hong Kong, Hong Kong
Background: Fibrosis regression during long-term
nucleoside analogue for chronic hepatitis B virus (HBV)
infection is not universally guaranteed Metabolic factors
may play a role in HBV-related fibrogenesis, but their impact
on fibrosis regression during HBV treatment has not been
prospectively evaluated Methods: Nucleoside analoguetreated
patients with a baseline transient elastography
(TE) (Fibroscan, Echosens), anthropometry and virological
assessment between January 2015 to April 2016 and at
least severe liver fibrosis noted on TE were invited for a
second assessment after 3 years. Severe liver fibrosis (F3)
was defined as liver stiffness >9.0kPa with normal alanine
aminotransferase (ALT) level, or >12.0kPa with ALT one to
five times above the upper limit of normal (ULN). Cirrhosis
(F4) was defined as liver stiffness >12kPa with normal ALT,
or >13.4kPa in patients with ALT 1-5 above ULN. Remaining
measurements are categorized as F≤2. Fibrosis regression
was defined as a down-staging of liver fibrosis from F4 to
F≤3 or F3 to F≤2. Liver steatosis was quantified via controlled
attenuation parameter measurements Metabolic syndrome
was defined following the International Diabetes Federation
consensus Results: 160 patients (mean age 59 2±9 3 years,
73 1% male) with a median nucleoside analogue treatment
duration of 6.1 (IQR 3.3-8.5) years were recruited. Median
liver stiffness significantly decreased from 12.4 (IQR 10.6-
19.6) kPa at baseline to 11.9 (IQR 8.4-17.3) kPa at year 3
(p=0.004). 60 patients (37.5%) developed fibrosis regression,
with 12 (20%) and 48 (80%) down-staged to F3 and F≤2 at
year 3 respectively By multivariate analysis, the presence of
metabolic syndrome was independently associated with the
lack of fibrosis regression (p=0.005, OR 3.1, 95% CI 1.4-6.7).
Median reduction in liver stiffness in patients with (n=76) and
without metabolic syndrome (n=84) were 1 2 kPa and 3 3 kPa
respectively (p=0 003) Low platelet count was also associated
with lack of fibrosis regression (p=0.018, OR 1.009, 95%
1 001-1 016) Other clinical, virological and metabolic factors
demonstrated no associations Conclusion: Metabolic
syndrome negates the beneficial effect of chronic hepatitis B
treatment with reduced rates of fibrosis regression. Control of
metabolic factors may be needed to achieve better long-term
outcomes in chronic HBV infection.作者: StephenW 时间: 2019-10-31 17:31