Hepatitis C viremia interferes with serum hepatitis B virus surface antigen and DNA levels in hepatitis B uremics

被引:11
|
作者
Huang, Chung-Feng [1 ,2 ,3 ,4 ,5 ]
Yeh, Ming-Lun [1 ,2 ]
Lee, Jia-Jung [5 ,6 ]
Chen, Mei-Chin [7 ]
Dai, Chia-Yen [1 ,2 ,5 ,7 ]
Huang, Jee-Fu [1 ,2 ,5 ,8 ]
Chang, Jer-Ming [6 ,8 ,9 ]
Chen, Hung-Chun [6 ,9 ]
Hwang, Shang-Jyh [6 ,9 ]
Chuang, Wan-Long [1 ,2 ,5 ]
Yu, Ming-Lung [1 ,2 ,5 ]
机构
[1] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Internal Med, Hepatobiliary Div, Kaohsiung 807, Taiwan
[2] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Hepatitis Ctr, Kaohsiung 807, Taiwan
[3] Kaohsiung Med Univ, Coll Med, Inst Clin Med, Kaohsiung 807, Taiwan
[4] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Occupat Med, Kaohsiung Municipal Ta Tung Hosp, Kaohsiung 807, Taiwan
[5] Kaohsiung Med Univ, Coll Med, Fac Internal Med, Sch Med, Kaohsiung 807, Taiwan
[6] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Internal Med, Div Nephrol, Kaohsiung 807, Taiwan
[7] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Prevent Med, Kaohsiung 807, Taiwan
[8] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Internal Med, Kaohsiung Municipal Hsiao Kang Hosp, Kaohsiung 807, Taiwan
[9] Kaohsiung Med Univ, Fac Renal Care, Coll Med, Kaohsiung Municipal Hsiao Kang Hosp, Kaohsiung 807, Taiwan
关键词
HBV; HCV; HBsAg; Uremia; Dual infection; INTERLEUKIN-28B GENETIC-VARIANTS; NATURAL-HISTORY; HEMODIALYSIS-PATIENTS; RENAL-DISEASE; GENOTYPE; INFECTION; IMPACT; HOST; POLYMORPHISMS; COINFECTION;
D O I
10.1007/s12072-014-9527-7
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Hepatitis B virus (HBV) and HCV might cause reciprocal interference. We aimed to elucidate the influence of HCV and interleukin-28B (IL-28B) genetic variants in the HBV DNA and HBsAg levels in uremic HBV carriers. Assessment of HCV and HBV viral loads, HBsAg levels and IL-28B genotype were performed in 229 HBsAg-positive patients from a cohort of 1,681 uremics. Patients with HCV viremia had significantly lower HBV DNA (2.58 +/- A 0.80 vs. 3.16 +/- A 1.48 log IU/mL, p = 0.005) and HBsAg levels (1.33 +/- A 1.35 vs. 2.23 +/- A 1.31 log IU/mL, p = 0.002) compared with those without. IL-28B rs8099917 genotype had no impact on HBsAg and HBV DNA levels. In multivariate regression analysis, HCV RNA levels had a more significant negative correlation with HBsAg levels [beta -0.905; 95 % confidence interval (CI) -1.477, -0.334; p = 0.002] than with HBV DNA levels (beta -0.586; 95 % CI -1.206, 0.034; p = 0.06). The serum HBV DNA and HBsAg levels had a positive correlation (r = 0.43, p < 0.001) among the 215 HBeAg-negative patients. However, the correlation was not observed in patients with HCV viremia (r = 0.23, p = 0.29). Linear regression analysis revealed that age (beta -0.286; 95 % CI -0.043, -0.014; p < 0.001) and the HBV DNA level (beta 0.373; 95 % CI 0.239, 0.549; p < 0.001) correlated independently with the HBsAg level among HBeAg-negative patients without HCV viremia, but not among those with concomitant HCV viremia. HCV viremia suppressed both HBsAg and HBV DNA levels. The HBsAg levels correlated with the HBV DNA levels only in patients without concomitant HCV viremia.
引用
收藏
页码:224 / 232
页数:9
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