In:
JAIDS Journal of Acquired Immune Deficiency Syndromes, Ovid Technologies (Wolters Kluwer Health), Vol. 82, No. 2 ( 2019-10-1), p. 175-180
Kurzfassung:
HIV-1 infection impairs cellular immunity, causing a detrimental effect on the natural course of hepatitis B virus (HBV) infection. HBV vaccination is less effective in HIV-1–infected patients. This study aimed to gain insight into HIV-1 infection with persistence of hepatitis B surface antigen (HBsAg) defining chronic hepatitis B infection (CBI) after a primary infection and the possible associated factors. Setting: Division of Infectious Diseases, San Raffaele Hospital, Italy. Methods: This retrospective study analyzed HIV-1–infected patients diagnosed with acute hepatitis B infection (AHB) based on clinical or laboratory records. CBI was defined as a positive HBsAg result recorded 〉 6 months after an AHB diagnosis. Multivariate logistic regression was applied to assess factors (evaluated at AHB diagnosis) that were associated with CBI. Results: Of 63 HIV-1–infected patients with AHB, 23 (36.5%) developed CBI. On multivariate analysis, CBI risk was less likely in patients with HIV-RNA of 〉 50 copies/mL (adjusted odds ratio = 0.03, 95% confidence interval: 0.001 to 0.58, P = 0.021). Dually acting antiretroviral treatment, including one or more drugs active against HIV/HBV (lamivudine, emtricitabine, and tenofovir), seemed to be protective in terms of the clinical outcome of CBI (adjusted odds ratio = 0.07, 95% confidence interval: 0.01 to 1.02, P = 0.050). Among the 23 patients with CBI, 15 (65.2%) lost the hepatitis B e-antigen, while 11 (47.8%) had HBsAg seroclearance during follow-up. Conclusions: In HIV-1–infected subjects with AHB, the persistence of HBsAg seemed to occur frequently. Factors associated with a lower CBI risk were detectable HIV load and the use of dually acting antiretroviral treatment during AHB.
Materialart:
Online-Ressource
ISSN:
1525-4135
DOI:
10.1097/QAI.0000000000002106
Sprache:
Englisch
Verlag:
Ovid Technologies (Wolters Kluwer Health)
Publikationsdatum:
2019
ZDB Id:
2038673-4
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