Effect of adenine arabinoside on cytomegalovirus infections.
Effect of adenine arabinoside on cytomegalovirus infections.
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腺嘌呤阿拉伯糖苷对巨细胞病毒感染的影响。
DOI：
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发表时间：
1974
影响因子：
6.4
通讯作者：
C. Alford
中科院分区：
文献类型：
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作者：
L. Ch'ien;N. J. Cannon;R. Whitley;A. Diethelm;W. Dismukes;C. W. Scott;R. Buchanan;C. Alford
17例巨细胞病毒感染患者中的12例（2例单核细胞增多症，5例弥散性感染和免疫抑制，5例先天性感染婴儿）接受5- 20mg /kg腺嘌呤阿拉伯糖苷（ara-A）静脉滴注治疗6 - 18天。婴儿和单核细胞增多症患者治疗前尿巨细胞病毒滴度较高，治疗后尿病毒抑制时间较免疫抑制患者延长。然而，在所有患者中，数量较少的病毒在一至三周后复发。在免疫抑制患者治疗期间，尿巨细胞病毒排泄仅轻微减少，并伴有持续的病毒血症。临床2例婴儿和2例单核细胞增多症患者病情好转；免疫抑制患者无改善。在接受治疗的患者中，没有出现明显的临床肝、肾或骨髓毒性。一组未经治疗的三名免疫抑制患者和两名单核细胞增多症患者有持续的病毒血症和病毒血症。结果提示亚毒性剂量的ara-A可抑制人巨细胞病毒尿排泄。免疫抑制患者的不良反应可能是由于免疫抑制的严重程度、ara-A代谢的个体差异、并发感染的存在，或者可能是巨细胞病毒株的特异性。巨细胞病毒（CMV）引起许多疾病综合征，包括先天性感染、单核细胞增多症和免疫抑制宿主[1]的播散性感染。先天性巨细胞病毒感染的致残性神经系统并发症已经促使各种治疗尝试，包括使用干扰素诱导剂和抗病毒化疗药物[2-7]。在免疫抑制的宿主中，播散性巨细胞病毒感染可能很严重。目前
Twelve of 17 patients with cytomegalovirus infections (two with mononucleosis, five with disseminated infection and immunosuppression, and five congenitally infected infants) were treated with 5-20 mg of adenine arabinoside (ara-A)/kg intravenously for six to 18 days. Infants and patients with mononucleosis had higher titers of cytomegalovirus in urine before treatment and more prolonged urinary viral suppression after treatment than immunosuppressed patients. However, a quantitatively lesser viruria returned after one to three weeks in all patients. During therapy in immunosuppressed patients, urinary excretion of cytomegalovirus was only slightly reduced, with persistent viremia. Clinically, two infants and two patients with mononucleosis improved; no immunosuppressed patient improved. No significant clinical toxicity to the liver, kidney, or bone marrow occurred in treated patients. An untreated group of three immunosuppressed patients and two with mononucleosis had persistent viremia and viruria. The results suggest that a subtoxic dosage of ara-A suppresses urinary excretion of cytomegalovirus in man. The poor response in immunosuppressed patients may be due to the severity of immunosuppression, individual variation in metabolism of ara-A, the presence of concurrent infections, or, possibly, specificity of cytomegalovirus strains. Cytomegalovirus (CMV) causes many disease syndromes including congenital infection, mononucleosis, and disseminated infection in immunosuppressed hosts [1]. The disabling neurologic complications often associated with congenital CMV infections have already prompted various therapeutic attempts, including the use of interferon inducers and antiviral chemotherapeutic agents [2-7]. In immunosuppressed hosts disseminated CMV infections may be severe. At present