腮腺腺病。分泌紊乱的超微结构、临床和实验结果[作者译]。

K Donath
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引用次数: 0

摘要

在唾液腺的分泌紊乱(“分泌障碍”)中,腮腺的唾液腺病是临床和形态学上确定的实体。典型的临床症状是双侧腮腺,经常复发,无痛性肿胀。其特征性病理表现为腺泡细胞肥大,无任何炎症征象。根据这一定义,唾液腺病必须与唾液腺疾病区分开来,这些疾病主要是由唾液腺组织的炎症引起的,继发分泌紊乱。从临床角度来看,根据与各种疾病的同向性可区分以下几种涎腺病:内分泌性涎腺病(见于糖尿病、性腺、垂体、甲状腺等功能障碍);营养不良代谢性唾液腺病(营养不良、维生素缺乏症、酗酒、慢性肝病等)和神经源性唾液腺病(植物神经系统功能障碍、药物损害,如降压药)。问题出现了,是否所有形式的唾液腺病有一个共同的病因和一个巧合的致病因素。下面的研究是为了进一步了解唾液腺病的病因和发病机制。该研究基于以下材料:a) 126例涎腺病患者的腮腺活检(汉堡大学病理研究所唾液腺疾病登记处,由Deutsche Forschungsgemeinschaft支持)。这些材料是从1965年到1973年收集的。b) 80例其他疾病(腮腺炎)患者的腮腺活检[4];腺泡细胞癌[4];其他腮腺和口腔肿瘤[72];进行比较。c) wistar大鼠腮腺涎腺的实验研究。对腮腺活检进行了组织学、形态学和超微结构的研究。研究集中在涎腺病的超微结构上。在解释涎腺病的病因和发病机制之前,首先有必要研究人类腮腺包括营养神经系统的正常超微结构。此外,有必要阐明分泌周期的功能形态学细节,并将这些发现整合到分泌紊乱的一般病理学概念中。我们的调查取得了以下结果:1。人腮腺正常超微结构:腺泡细胞的结构与其他动物相同(细胞质有基立核、粗内质网、高尔基体、分泌颗粒等)。进一步相同的成分是插层和纹状管、肌上皮细胞和营养神经系统(神经节后交感神经和副交感神经,但腮腺中没有神经节细胞)……
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Sialadenosis of the parotid gland. Ultrastructural, clinical and experimental findings in disturbances of secretion (author's transl)].

Among the secretory disturbances ("Dyschylien") of salivary glands the sialadenosis of the parotid gland is a clinic and a morphologic definited entity. The typical clinical symptom is a bilateral, often recurrent, and painless swelling of the parotid gland. The characteristic pathological findings consist in an acinar cell hypertrophy without any inflammatory signs. According to this definition, sialadenosis has to be separated from those diseases of salivary glands, which are primarily altered by inflammation of the salivary tissue with secondary secretory disturbances. From flinical point of view it is possible to distinguish the following kinds of sialadenosis according to the syntropy with various diseases: Endocrine sialadenosis (in diabetes mellitus, dysfunction of gonads, pituitary gland, thyroid gland etc.); dystrophic-metabolic sialadenosis (malnutrition, avitaminosis, alcohilsm, chronic liver diseases etc.), and neurogenic sialadenosis (dysfunction of the vegetative nervous system, drug damages e.g. antihypertensive agents). The question arises, whether all forms of sialadenosis have a common etiology and a coincidental pathogenic factor. The following studies were carried out with the aim to find further details concerning the etiology and pathogenesis of sialadenosis. The study is based on the following material: a) 126 Biopsies of parotid glands from patients with sialadenosis (Register of salivary gland diseases at the Institute of Pathology, University of Hamburg, supported by Deutsche Forschungsgemeinschaft). This material was collected from 1965 to 1973. b) 80 Biopsies of parotid glands from patients with other diseases (parotitis [4]; acinic cell carcinoma [4]; other parotid and oral tumors [72]; for comparison. c) Experimental studies on the parotid salivary glands of Wistar-rats. The biopsies of the parotid glands were studied histologically, morphometrically, and ultrastructurally. The investigations centered on the ultrastruct of sialadenosis. Before interpreting the ultrastructural findings in view of etiology and pathogenesis of sialadenosis, it was primarily necessary to study the normal ultrastructure of the human parotid gland including the vegetative nervous system. Furthermore it was necessary to elucidate details of a functional morphology of the secretory cycle and to integrade the findings into a concept of general pathology of secretory disturbances. The following results were achieved by our investigations: 1. Normal ultrastructure of human parotid gland: The architecture of the acinar cells is identical with these of other animal species (cytoplasm with a basal standing nucleus, rough endoplasmatic reticulum, Golgi-apparatus, secretory granules etc.). Further identical elements are intercalated and striated ducts, myoepithelial cells, and the vegetative nervous system (postganglionic sympathetic and parasympathetic neurites, however no ganglionic cells in the parotid gland)...

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