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Abstract：
Although lymphoma is the most frequent malignancy in common variable immunodeficiency (CVID), solid tumors, especially affected by oncogenic viruses, are not considered. Furthermore, in vitro genetic studies and cell cultures are not adequate for immune system and HBV interaction. We adopted a previously introduced clinical model of host-virus interaction (i.e., infectious process in immunodeficiency) for analysis of B cells and the specific IgG role (an observational study of a CVID patient who received intravenous immunoglobulin (IVIG). Suddenly, the patient deteriorated and a positive results of for HBs and HBV-DNA (369 × 106 copies) were detected. Despite lamivudine therapy and IVIG escalation (from 0.3 to 0.4 g/kg), CT showed an 11 cm intrahepatic tumor (hepatocellular carcinoma). Anti-HBs were positive in time-lapse analysis (range 111-220 IU/mL). Replacement therapy intensification was complicated by an immune complex disease with renal failure. Fulminant HCC in CVID and the development of a tumor as the first sign is of interest. Unfortunately, treatment with hepatitis B immune globulins (HBIG) plays a major role in posttransplant maintenance therapy. Anti-HB substitution has not been proven to be effective, oncoprotective, nor safe. Therefore, immunosuppression in HBV-infected recipients should be carefully minimized, and patient selection more precise with the exclusion of HBV-positive donors. Our clinical model showed an HCC pathway with important humoral host factors, contrary to epidemiological/cohort studies highlighting risk factors only (e.g., chronic hepatitis). The lack of cell cooperation as well as B cell deficiency observed in CVID play a crucial role in high HBV replication, especially in carcinogenesis.
摘要：
尽管淋巴瘤是常见可变免疫缺陷（CVID）中最常见的恶性肿瘤，实体瘤,尤其是受致癌病毒的影响，不考虑。此外，体外遗传研究和细胞培养对于免疫系统和HBV相互作用是不够的。我们采用了先前引入的宿主病毒相互作用的临床模型(即，免疫缺陷中的感染过程），用于分析B细胞和特异性IgG作用（对接受静脉注射免疫球蛋白（IVIG）的CVID患者的观察性研究。突然,患者恶化,检测到HBs和HBV-DNA阳性结果(369×106个拷贝).尽管拉米夫定治疗和IVIG升级（从0.3到0.4g/kg），CT显示11厘米肝内肿瘤（肝细胞癌）。抗HBs在延时分析中呈阳性（范围111-220IU/mL）。强化替代疗法因合并肾功能衰竭的免疫复合物疾病而复杂化。CVID中的暴发性HCC和肿瘤的发展作为第一个迹象是感兴趣的。不幸的是,乙型肝炎免疫球蛋白（HBIG）治疗在移植后维持治疗中起着重要作用。抗HB替代尚未被证明是有效的，肿瘤保护,也不安全。因此,HBV感染受者的免疫抑制应谨慎最小化，和患者选择更精确，排除HBV阳性供体。我们的临床模型显示具有重要体液宿主因子的HCC通路，与仅强调风险因素的流行病学/队列研究相反(例如，慢性肝炎）。在CVID中观察到的缺乏细胞合作以及B细胞缺乏在高HBV复制中起关键作用，尤其是在癌变过程中。
