新英格兰医学杂志：乙肝病毒感染药物治疗学

g the apparent immune-tolerant period in some patients11,12 or the presence of necroinflammatory quiescence during the immune-clearance phase later in the course of chronic HBV infection.

The HBeAg status distinguishes two additional categories of chronic HBV infection. HBeAg-reactive chronic HBV infection is accompanied by high-level HBV replication, and spontaneous seroconversion from HBeAg-positive to antibody (anti-HBe)–positive infection coincides with a reduction in HBV replication and clinical improvement.13,14,15 HBeAg-negative chronic HBV infection, in which precore or core-promoter gene mutations preclude or reduce the synthesis of HBeAg, accounts for an increasing proportion of cases.16 Patients with HBeAg-negative chronic HBV infection tend to have progressive liver injury, fluctuating alanine aminotransferase (ALT) activity, and lower levels of HBV DNA than patients with HBeAg-reactive HBV infection; however, they cannot have treatment-induced HBeAg seroconversion, a durable response that may permit the discontinuation of antiviral therapy.

Eight HBV genotypes - and differences in clinical outcome according to genotype - are recognized.17,18,19 For example, patients with genotype A are more likely to undergo interferon-induced HBeAg seroconversion20; HBeAg seroconversion and slower disease progression are more frequent in patients with genotype B than in patients with genotype C.19 These differences, however, are not sufficiently established to guide management.

The progression of liver disease in HBV infection is fostered by active virus replication, reflected by the presence in serum of an HBV DNA level above a threshold of approximately 1000 to 10,000 IU per milliliter. Persons with a serum HBV DNA level below 1000 IU per milliliter and a normal ALT level consistently are considered to be inactive carriers with a low risk of clinical progression,21 although, rarely, reactivation can occur spontaneously or with immunosuppression.2

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