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[慢性涎腺扩张性腮腺炎作为肌上皮涎腺炎病变(干燥综合征)前驱病变的组织病理学发病机制]

[Histopathogenesis of chronic sialectatic parotitis as precursor of myoepithelial sialadenitis lesion (Sjögren syndrome)].

作者信息

Ussmüller J, Donath K

机构信息

Univ. Hals-Nasen-Ohren-Klinik Hamburg-Eppendorf.

出版信息

Laryngorhinootologie. 1998 Dec;77(12):723-7. doi: 10.1055/s-2007-997231.

Abstract

BACKGROUND

Chronic sialectatic parotitis (CSP) is classified as a characteristic form of chronic recurrent parotitis the etiology and pathogenesis of which still remains unclear. The multiplicity of different therapeutic advices, especially the permanent failure of antibiotic treatment, underlines the lack of an appropriate causal therapy.

CASE REPORT

Detailed histopathological investigations of an 41-year old woman were possible over a seven-year period. These follow-up observations enabled clarification of the histopathogenesis of CSP by means of immunohistochemistry.

RESULTS

During the course and development of CSP different stages can be observed: The initial phase is characterised by mild infiltration of B-lymphocytes (CD20, CD45 R) and plasma cells in the environment of ectatic ducts. Progredient stages show neogenetic lymph follicles periductular as well as metaplasia of the ductal epithelium. Terminal phases of CSP are characterised by near-total lymphatic transformation of parenchyma, follicular lymphatic hyperplasia (KiM4) and myoepithelial proliferation. In this phase myoepithelial sialadenitis (MESA, i.e. benign lymphoepithelial lesion, possibly part of Sjögren's syndrome) develops. Beyond it low grade non-Hodgkin's lymphoma of the MALT-Type of the submandibular gland occurred finally.

CONCLUSIONS

CSP presents as a precursor of MESA. Immunohistological detection of follicular dentritic network (KiM4) within extensive lymphatic hyperplasia periductular demonstrates overshooting humoral immune reaction of B-lymphocytes. Hence, CSP should be classified with regard to pathogenesis as an immunopathological disorder of the MALT system.

摘要

背景

慢性涎腺扩张性腮腺炎(CSP)被归类为慢性复发性腮腺炎的一种特征形式,其病因和发病机制仍不清楚。不同治疗建议的多样性,尤其是抗生素治疗的持续失败,凸显了缺乏适当的病因治疗方法。

病例报告

对一名41岁女性进行了为期七年的详细组织病理学研究。这些随访观察通过免疫组织化学方法明确了CSP的组织发病机制。

结果

在CSP的病程和发展过程中,可以观察到不同阶段:初始阶段的特征是扩张导管周围有轻度B淋巴细胞(CD20、CD45R)和浆细胞浸润。进展阶段表现为导管周围新生淋巴滤泡以及导管上皮化生。CSP的终末期特征是实质几乎完全淋巴转化、滤泡性淋巴增生(KiM4)和肌上皮增殖。在此阶段发生了肌上皮涎腺炎(MESA,即良性淋巴上皮病变,可能是干燥综合征的一部分)。除此之外,最终在下颌下腺发生了低度MALT型非霍奇金淋巴瘤。

结论

CSP表现为MESA的前驱病变。导管周围广泛淋巴增生内滤泡树突状网络(KiM4)的免疫组织学检测显示B淋巴细胞过度的体液免疫反应。因此,就发病机制而言,CSP应归类为MALT系统的免疫病理紊乱。

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