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Risk Assessment of Hepatocellular Carcinoma Using Transient Elastography Vs. Liver Biopsy in Chronic Hepatitis B Patients Receiving Antiviral Therapy

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ABSTRACT

Liver stiffness (LS) assessed using transient elastography (TE) can assess the risk of developing hepatocellular carcinoma (HCC). We evaluated whether TE, when compared with histological data as a reference standard, can predict the risk of HCC development in chronic hepatitis B (CHB) patients starting antiviral therapy.

Observational cohort database of 381 patients with CHB who underwent liver biopsy (LB) and TE were reviewed. All patients underwent surveillance for HCC development using ultrasonography and alpha-fetoprotein.

During the median follow-up period of 48.1 (interquartile range 30.3–69.3) months, HCC developed in 34 (8.9%) patients. In patients with HCC development, age, proportion of diabetes mellitus, histological fibrosis stage, and LS value were significantly higher than those in patients without (all P <0.05). The cumulative incidence rates of HCC increased significantly in association with elevated LS value in 3 stratified groups (LS value <8, 8–13, and >13 kPa; log-rank test, P <0.001), and with higher histological fibrosis stage in 3 stratified groups (F0–2, F3, and F4; log-rank test, P <0.001). On multivariate analysis, along with age, LS value was an independent predictor of HCC development (hazard ratio 1.041, P <0.001), whereas histological staging was not (P >0.05).

TE predicted HCC development independently in patients with CHB starting antiviral therapy. However, further investigation is needed to determine whether the current surveillance strategy can be optimized based on the LS value at the time of starting antiviral therapy.

No MeSH data available.


Related in: MedlinePlus

The cumulative incidence rates of HCC based on stratified LS values (<8, 8–13, and >13 kPa) and histological fibrosis stage (F0–2, F3, and F4) (A and B), and the cumulative incidence rates of LRE based on stratified LS values and histological fibrosis stage (C and D). The cumulative incidence rates of HCC and LRE increased significantly in association with higher LS value and with higher histological fibrosis stage (log-rank test, all P <0.001). HCC = hepatocellular carcinoma; LRE = liver-related event.
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Figure 2: The cumulative incidence rates of HCC based on stratified LS values (<8, 8–13, and >13 kPa) and histological fibrosis stage (F0–2, F3, and F4) (A and B), and the cumulative incidence rates of LRE based on stratified LS values and histological fibrosis stage (C and D). The cumulative incidence rates of HCC and LRE increased significantly in association with higher LS value and with higher histological fibrosis stage (log-rank test, all P <0.001). HCC = hepatocellular carcinoma; LRE = liver-related event.

Mentions: Considering the independent prognostic significance of LS values, we stratified our study population into 3 groups using the cutoff LS values of 8.0 and 13 kPa according to the stratifications used in several previous studies.15,17 The risk of HCC and the risk of LRE development increased in association with higher LS values among 3 stratified groups (log-rank test, all P <0.001) (Figure 2A and B). Although histological fibrosis stage was not a significant predictor of HCC and LRE development, when the patients were divided into 3 groups according to histological fibrosis stage (F0-2, F3, and F4), the risk of HCC and the risk of LRE development also increased in association with higher histological fibrosis stage (log-rank test, all P <0.001) (Figure 2C and D).


Risk Assessment of Hepatocellular Carcinoma Using Transient Elastography Vs. Liver Biopsy in Chronic Hepatitis B Patients Receiving Antiviral Therapy
The cumulative incidence rates of HCC based on stratified LS values (<8, 8–13, and >13 kPa) and histological fibrosis stage (F0–2, F3, and F4) (A and B), and the cumulative incidence rates of LRE based on stratified LS values and histological fibrosis stage (C and D). The cumulative incidence rates of HCC and LRE increased significantly in association with higher LS value and with higher histological fibrosis stage (log-rank test, all P <0.001). HCC = hepatocellular carcinoma; LRE = liver-related event.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998368&req=5

Figure 2: The cumulative incidence rates of HCC based on stratified LS values (<8, 8–13, and >13 kPa) and histological fibrosis stage (F0–2, F3, and F4) (A and B), and the cumulative incidence rates of LRE based on stratified LS values and histological fibrosis stage (C and D). The cumulative incidence rates of HCC and LRE increased significantly in association with higher LS value and with higher histological fibrosis stage (log-rank test, all P <0.001). HCC = hepatocellular carcinoma; LRE = liver-related event.
Mentions: Considering the independent prognostic significance of LS values, we stratified our study population into 3 groups using the cutoff LS values of 8.0 and 13 kPa according to the stratifications used in several previous studies.15,17 The risk of HCC and the risk of LRE development increased in association with higher LS values among 3 stratified groups (log-rank test, all P <0.001) (Figure 2A and B). Although histological fibrosis stage was not a significant predictor of HCC and LRE development, when the patients were divided into 3 groups according to histological fibrosis stage (F0-2, F3, and F4), the risk of HCC and the risk of LRE development also increased in association with higher histological fibrosis stage (log-rank test, all P <0.001) (Figure 2C and D).

View Article: PubMed Central - PubMed

ABSTRACT

Liver stiffness (LS) assessed using transient elastography (TE) can assess the risk of developing hepatocellular carcinoma (HCC). We evaluated whether TE, when compared with histological data as a reference standard, can predict the risk of HCC development in chronic hepatitis B (CHB) patients starting antiviral therapy.

Observational cohort database of 381 patients with CHB who underwent liver biopsy (LB) and TE were reviewed. All patients underwent surveillance for HCC development using ultrasonography and alpha-fetoprotein.

During the median follow-up period of 48.1 (interquartile range 30.3&ndash;69.3) months, HCC developed in 34 (8.9%) patients. In patients with HCC development, age, proportion of diabetes mellitus, histological fibrosis stage, and LS value were significantly higher than those in patients without (all P&#8202;&lt;0.05). The cumulative incidence rates of HCC increased significantly in association with elevated LS value in 3 stratified groups (LS value &lt;8, 8&ndash;13, and &gt;13 kPa; log-rank test, P&#8202;&lt;0.001), and with higher histological fibrosis stage in 3 stratified groups (F0&ndash;2, F3, and F4; log-rank test, P&#8202;&lt;0.001). On multivariate analysis, along with age, LS value was an independent predictor of HCC development (hazard ratio 1.041, P&#8202;&lt;0.001), whereas histological staging was not (P&#8202;&gt;0.05).

TE predicted HCC development independently in patients with CHB starting antiviral therapy. However, further investigation is needed to determine whether the current surveillance strategy can be optimized based on the LS value at the time of starting antiviral therapy.

No MeSH data available.


Related in: MedlinePlus