Cytomegalovirus neuropathy in acquired immunodeficiency syndrome: A clinical and pathological study

Cytomegalovirus neuropathy in acquired immunodeficiency syndrome: A clinical and pathological study
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获得性免疫缺陷综合征中的巨细胞病毒神经病:临床和病理学研究

DOI:
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发表时间:
1991
影响因子:
11.2
通讯作者:
J. Vildé
J. Vildé
中科院分区:
医学1区
文献类型:
--
作者:
G. Said;C. Lacroix;P. Chemouilli;C. Goulon‐Goeau;E. Roullet;D. Penaud;T. Broucker;G. Meduri;D. Vincent;M. Torchet;D. Vittcoq;C. Leport;J. Vildé

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我们已经观察到典型的巨细胞病毒细胞病理学与周围神经的多灶性炎症和坏死性病变活检标本从4例谁开发了一个快速进行性,多灶性神经病变晚期的过程中的人类免疫缺陷病毒感染。炎性浸润,其中含有大量的多形性胶质细胞,与混合,轴突,和神经纤维脱髓鞘病变。其中1例患者在接受DHPG(9-[2-羟基-1(羟甲基)乙氧基甲基]鸟嘌呤)治疗后改善,18个月后保持稳定。另外3例在神经病变发作后不久死亡。在另一名患有获得性免疫缺陷综合征的患者中,该患者发生了严重的下肢运动神经病,神经活检未发现巨细胞病毒夹杂物,但神经功能缺损在DHPG治疗后得到改善。2个月后患者死于恶病质;尸检时在脊髓中发现大量巨细胞病毒病变。我们描述的多灶性坏死性神经内膜神经病变伴多形核细胞浸润可能有助于鉴别活检标本中不存在特征性包涵体的巨细胞病毒性神经病。
We have observed typical cytomegalovirus cytopathology associated with multifocal inflammatory and necrotic lesions of peripheral nerve in biopsy specimens from 4 patients who developed a rapidly progressive, multifocal neuropathy late in the course of human immunodeficiency virus infection. The inflammatory infiltrates, which contained numerous polymorphonuclear cells, were associated with mixed, axonal, and demyelinative lesions of nerve fibers. One of these patients improved on treatment with DHPG (9‐[2‐hydroxy‐1(hydroxymethyl) ethoxymethyl] guanine) and remains stable after 18 months. The other 3 died soon after the onset of the neuropathy. In another patient with acquired immunodeficiency syndrome, who developed a severe, predominantly motor neuropathy of the lower limbs, the nerve biopsy did not reveal cytomegalovirus inclusions, but the neurological deficit improved on treatment with DHPG. The patient died from cachexia 2 months later; numerous cytomegalovirus lesions were found in the spinal cord at the time of postmortem examination. The multifocal necrotic endoneurial nerve lesions with polymorphonuclear cell infiltration we describe may help identify cytomegalovirus neuropathy when characteristic inclusions are not present in the biopsy specimen.
弗雷明汉心脏研究中存在一种导致低收缩压的罕见基因的证据。
DOI: 10.1159/000153936
发表时间: 1990
期刊: Human heredity
影响因子: 1.8
作者:
Carter,CL;Kannel,WB
通讯作者: Kannel,WB