Aplastic anemia and viral hepatitis. Non-A, Non-B, Non-C?
Aplastic anemia and viral hepatitis. Non-A, Non-B, Non-C?
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DOI：
10.1001/jama.1992.03480150057037
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发表时间：
1992-04
期刊：
影响因子：
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通讯作者：
J. Hibbs;N. Frickhofen;S. Rosenfeld;S. Feinstone;S. Kojima;A. Bacigalupo;A. Locasciulli;A. Tzakis;H. Alter;N. Young
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文献类型：
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作者：
J. Hibbs;N. Frickhofen;S. Rosenfeld;S. Feinstone;S. Kojima;A. Bacigalupo;A. Locasciulli;A. Tzakis;H. Alter;N. Young
目的验证罕见且往往致命的肝炎相关性发育不全综合征与丙型肝炎病毒感染有关的假设。设计案例系列。背景：美国、日本、意大利和德国的三级转诊中心。28例患者因黄疸就诊后90天内出现再生障碍性贫血，或血清转氨酶水平高于正常值150%（肝炎相关性再生障碍性贫血患者），3例患者因非甲、非乙型肝炎肝移植后出现再生障碍性贫血。聚合酶链反应检测血清、骨髓和肝脏样本中是否存在丙型肝炎；抗体检测;免疫分型测定活化的外周细胞毒性T淋巴细胞百分比。结果10例（36%）肝炎相关性发育不全患者血清中检出肝炎核糖核酸。然而，丙型肝炎病毒血症与发育不全发病后接受的输血有关：在血清取样时接受21单位或更多血液制品的12例肝炎相关发育不全患者中有7例（58%）是病毒血症，而16例接受20单位或更少血液制品的肝炎相关发育不全患者中只有3例（19%）是病毒血症（P < 0.05）。在诊断时，三名美国国立卫生研究院病例患者的血液和骨髓样本中未发现丙型肝炎病毒。3例肝移植后发生再生障碍性贫血的非甲、非乙型肝炎患者的肝脏均不含丙型肝炎病毒核糖核酸。活化的CD8+ T淋巴细胞在肝炎相关性发育不全早期升高3 - 20倍。结论：我们的研究结果表明，在肝炎相关性发育不全和暴发性肝炎中存在一种新的、非a、非b和非c型药物。
OBJECTIVE To test the hypothesis that the rare, often fatal, syndrome of hepatitis-associated aplasia is associated with hepatitis C virus infection. DESIGN Case series. SETTING Tertiary referral centers in the United States, Japan, Italy, and Germany. PATIENTS Twenty-eight patients with onset of aplastic anemia within 90 days after seeking medical attention for jaundice, or having serum transaminase levels 150% or more of normal (hepatitis-associated aplasia patients) and three patients who developed aplastic anemia following liver transplantation for non-A, non-B hepatitis. OUTCOME MEASURES Presence of hepatitis C in serum, bone marrow, and liver samples, detected by the polymerase chain reaction; antibody testing; and percentage of activated peripheral cytotoxic T lymphocytes determined by immunophenotyping. RESULTS Hepatitis ribonucleic acid was present in the serum samples of 10 (36%) patients with hepatitis-associated aplasia. However, hepatitis C virus viremia was associated with transfusions received after the onset of aplasia: seven (58%) of 12 patients with hepatitis-associated aplasia who had received 21 or more units of blood products at the time of serum sampling were viremic, compared with only three (19%) of 16 patients with hepatitis-associated aplasia who had received 20 or less units of blood products (P less than .05). Hepatitis C virus was not found in blood and bone marrow samples of three National Institutes of Health case patients tested at the time of diagnosis. None of three livers from non-A, non-B hepatitis patients who developed aplastic anemia after liver transplantation contained hepatitis C virus ribonucleic acid. Activated CD8+ T lymphocytes were elevated three- to 20-fold early in the course of hepatitis-associated aplasia. CONCLUSIONS Our results implicate a novel, non-A, non-B, and non-C agent in both hepatitis-associated aplasia and fulminant hepatitis.