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坏死性淋巴结炎:临床病理、免疫组织化学及超微结构研究综述

Necrotizing lymphadenitis: a review of clinicopathological, immunohistochemical and ultrastructural studies.

作者信息

Asano S, Akaike Y, Jinnouchi H, Muramatsu T, Wakasa H

机构信息

Department of Pathology, Fukushima Medical College, Japan.

出版信息

Hematol Oncol. 1990 Sep-Oct;8(5):251-60. doi: 10.1002/hon.2900080503.

DOI:10.1002/hon.2900080503
PMID:2249796
Abstract

Necrotizing lymphadenitis (NEL) has been reported to be a reactive process described under differing terminology by Fujimoto et al. (1972), Kikuchi (1972), Wakasa et al. (1973) and other Japanese pathologists. Recently, this type of lymphadenitis has also been reported in America and Europe. In Japan, NEL is observed more frequently in the northern area, however, no characteristic seasonal occurrence has been noted. The disease affects young females more than males, particularly from the third and fourth decades onwards. Common cold-like symptoms, lymphadenopathy of the cervical region and leukopenia are characteristic clinical findings in the early stages. Morphological features of the involved lymph nodes include the presence of numerous immunoblasts, histiocytes and macrophages, the latter with phagocytized nuclear debris derived from degenerated lymphocytes. However, granulocytes are generally absent. Tubular inclusions are observed ultrastructurally. Immunohistochemical studies of peripheral blood using monoclonal antibodies have revealed that the helper/suppressor (Leu 3a/2a) ratio increases gradually with the clinical course because of a decrease in Leu 2a + cells. The pathogenesis of NEL is uncertain, but it has been speculated that there is cytolytic infection of lymphocytes by a virus or other organism, accompanied by secondary blastic transformation of suppressor T-lymphocytes.

摘要

坏死性淋巴结炎(NEL)据报道是一种反应性过程,Fujimoto等人(1972年)、菊池(1972年)、若狭等人(1973年)以及其他日本病理学家曾用不同术语描述过。最近,欧美也报道了这种类型的淋巴结炎。在日本,NEL在北部地区更为常见,但未发现有特征性的季节性发病情况。该病在年轻女性中比男性更常见,尤其是从三十多岁和四十多岁起。早期的典型临床表现为类似感冒的症状、颈部淋巴结病和白细胞减少。受累淋巴结的形态学特征包括存在大量免疫母细胞、组织细胞和巨噬细胞,后者吞噬有来源于退化淋巴细胞的核碎片。然而,通常没有粒细胞。超微结构观察可见管状包涵体。使用单克隆抗体对外周血进行免疫组织化学研究显示,由于Leu 2a +细胞减少,辅助/抑制(Leu 3a/2a)比值随临床病程逐渐升高。NEL的发病机制尚不确定,但据推测存在病毒或其他生物体对淋巴细胞的溶细胞感染,并伴有抑制性T淋巴细胞的继发性母细胞转化。

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