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尸检系列中肩胛区的亚临床弹力纤维瘤

Subclinical elastofibromas in the scapular region in an autopsy series.

作者信息

Järvi O H, Länsimies P H

出版信息

Acta Pathol Microbiol Scand A. 1975 Jan;83(1):87-108. doi: 10.1111/j.1699-0463.1975.tb01361.x.

Abstract

In a series of 235 autopsies, changes in the subcapscular thoracic fascia similar to elastofibroma dorsi (Järvi & Saxen 1959, -et al. 1969) were found in 39 cases, all at least 58 years old. In people over 55 years, the frequency was 24.4 per cent in females and 11.2 per cent in males. In addition to hypertrophy and secondary degeneration of elastic fibres, necrosis of collagenous-, adipose-, muscular-, and nervous tissue, as well as formation of clefts, cysts and bursae was found in 85 per cent of cases presenting elastic changes--both in connection with them and outside the degenerated areas--as well as in 39 per cent of cases where no elastic degeneration occurred. Other changes included extensive scarring of the tissue, followed by reduction of fat and, more seldom, oedema and inflammatory infiltration. Breaks in the elastic cage, necrosis and fibrosis of arterial walls were found in 44 per cent of cases of elastic degeneration and in 14 per cent of cases without degeneration. In veins, more extensive wall fibrosis occurred, leading to necrosis; in cases of elastic degeneration the adventitial elastic network was also involved. Venous changes were found in 90 per cent of the cases of elastic degeneration and in 30 per cent of cases without degeneration. Direct mechanical stress on elastic tissue may be an important cause of hypertrophy and secondary degeneration of elastic fibres, and also of diffuse increase of collagenous tissue. On the other hand, nutritional deficiency due to failing resistance of the vascular system against friction of the scapula and streching movements of the upper extremities may play a main part in necrotic tissue changes.

摘要

在235例尸检中,39例发现肩胛下胸筋膜有类似于背部弹力纤维瘤(耶尔维与萨克森,1959年;等人,1969年)的变化,所有病例年龄均至少58岁。在55岁以上人群中,女性发生率为24.4%,男性为11.2%。除弹性纤维肥大和继发性变性外,在出现弹性变化的病例中有85%发现胶原组织、脂肪组织、肌肉组织和神经组织坏死,以及裂隙、囊肿和黏液囊形成,这些变化既与弹性变化有关,也出现在退变区域之外;在未发生弹性退变的病例中,这一比例为39%。其他变化包括组织广泛瘢痕形成,随后脂肪减少,较少见的还有水肿和炎症浸润。在44%的弹性退变病例和14%的无退变病例中发现弹性纤维网断裂、动脉壁坏死和纤维化。在静脉中,出现更广泛的壁纤维化,导致坏死;在弹性退变病例中,外膜弹性网络也受累。在90%的弹性退变病例和30%的无退变病例中发现静脉变化。弹性组织上的直接机械应力可能是弹性纤维肥大和继发性变性以及胶原组织弥漫性增加的重要原因。另一方面,由于血管系统抵抗肩胛骨摩擦和上肢伸展运动的能力下降导致的营养缺乏,可能在坏死组织变化中起主要作用。

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