کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5590559 | 1570149 | 2017 | 5 صفحه PDF | دانلود رایگان |

Occult Hepatitis B Infection (OBI) is a form of chronic HBV infection characterized by low level HBV DNA, without detectable HBV surface antigen (HBsAg). OBI is frequently associated with the presence of anti-HBc and in some cases also with anti-HBs. Patients, who formerly received non-inactivated factor concentrates, can potentially be considered at high risk for OBI, especially since these patients usually are HIV or HCV co-infected. This study aimed to assess the prevalence of occult HBV infection in Greek patients with hereditary bleeding disorders. The study sample comprised of 114 patients from a single haemophilia center. All patients were screened for HBV serum markers and individually tested for HBV DNA using a qualitative PCR. Presence of HBV DNA was further confirmed by quantification of viral load with an ultrasensitive in-house real time PCR. 88 and 21 patients with haemophilia A and B, respectively, 4 patients with von Willebrand Disease and 1 patient with severe factor VII deficiency were screened for the presence of OBI. Anti-HBc were detected in 53 (46.5%) subjects; 18 of them were anti-HBs(â) and 35 anti-HBs(+). Anti-HBe were present in 26 subjects. Two out of 114 patients were HBsAg(+). Of the remaining 112 HBsAg(â) patients tested, two (1.8%) were found HBsAg(â), HBV DNA(+), anti-HBc(+) and anti-HBs(â) and were identified as potential OBI cases. Both cases exhibited very low DNA levels; 38.2Â IU/mL in patient A and 14.2Â IU/mL in patient B. Both patients were HBeAg(â), but patient A had HBe antibodies. Patient B was also HIV/HCV co-infected. In conclusion, two cases of OBI with low HBV viraemia were identified among patients with congenital bleeding disorders. Although the incidence in our sample is moderately low (1.8%), close monitoring of these infections is of great clinical significance, especially in patients with co-infections and concomitant immunosuppression.
Journal: Infection, Genetics and Evolution - Volume 54, October 2017, Pages 397-401