J Infect Dis. 2018 Jan 30. doi: 10.1093/infdis/jiy048. [Epub ahead of print]
Clinical predictors of liver fibrosis in patients with chronic hepatitis B virus infection from children to adults.Wu JF1, Song SH2,3, Lee CS4, Chen HL1,5, Ni YH1,5, Hsu HY1, Wu TC2,3, Chang MH1,5. Author information 1Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan.2National Yang Ming University School of Medicine, Taiwan.3Department of Pediatrics, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taipei, Taiwan.4Department of Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.5Department of Pediatrics, Taipei Veterans General Hospital, Taipei, Taiwan.
AbstractBackground: This study aimed to elucidate predictors of liver fibrosis in chronic hepatitis B virus (HBV)-infected subjects.
Methods: Transient elastography was performed to define liver fibrosis in 533 chronic HBV-infected patients at 30.72 ± 0.57 years of age. Protein array was performed on serum samples and lysates of Huh7 cells transfected with HBV mutants; the results were confirmed by ELISA. Single nucleotide polymorphisms in the interleukin-1β gene were examined chronic HBV-infected patients with and without liver fibrosis.
Results: Male gender, > 18 years old, and serum alpha-fetoprotein level > 3.6 ng/mL were independent predictors of a liver stiffness measurement of ≥ 7 kPa (P = 0.005, 0.019, and < 0.001, respectively). HBeAg-negative hepatitis is associated with increased liver stiffness (P<0.001). Elevation of serum interleukin-1β was demonstrated in subjects with liver fibrosis. Interleukin-1β was upregulated in Huh7 cells transfected with HBeAg-negative hepatitis-related mutants. The AA genotype at rs16944 and the CC genotype at rs1143627 of the interleukin-1β gene were associated with higher serum interleukin-1β levels and liver fibrosis.
Conclusions: Male gender, beyond childhood, elevated alpha-fetoprotein level, and HBeAg-negative hepatitis are risk factors for liver fibrosis. Interleukin-1β is involved in the progression of liver fibrosis in subjects with HBeAg-negative hepatitis.
KEYWORDS: Cytokines; Hepatitis B virus e antigen; Interleukin-1β; Liver fibrosis; Seroconversion