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胰岛素诱导的脂肪萎缩:免疫发病机制的证据。

Insulin-induced lipoatrophy: evidence for an immune pathogenesis.

作者信息

Reeves W G, Allen B R, Tattersall R B

出版信息

Br Med J. 1980 Jun 21;280(6230):1500-3. doi: 10.1136/bmj.280.6230.1500.

Abstract

Skin biopsy samples from 14 diabetic patients with lipoatrophy at injection sites and from five insulin-treated diabetic patients without such lipoatrophy (controls) were examined by immunofluorescence for the deposition of immunological components. Also sera from 13 of the patients with lipoatrophy and from all of the controls were assayed for insulin-binding capacity. Biopsy samples from the edge of lipoatrophic areas (eight cases) invariably showed abnormal deposition of immunological components in dermal vessel walls, whereas no such deposition was seen in the control samples. Mean serum insulin-binding capacity was 33.1 microgram/l in the patients with lipoatrophy compared with only 4.6 microgram/l in the controls. These findings suggest that insulin-induced lipoatrophy results from the local formation of immune complexes, complement fixation, and release of inflammatory mediators from the cellular infiltrate.

摘要

对14例注射部位出现脂肪萎缩的糖尿病患者以及5例接受胰岛素治疗但无此类脂肪萎缩的糖尿病患者(对照组)的皮肤活检样本进行免疫荧光检查,以检测免疫成分的沉积情况。此外,还对13例脂肪萎缩患者和所有对照组患者的血清进行了胰岛素结合能力检测。脂肪萎缩区域边缘的活检样本(8例)在真皮血管壁中均显示出免疫成分的异常沉积,而对照组样本中未观察到此类沉积。脂肪萎缩患者的平均血清胰岛素结合能力为33.1微克/升,而对照组仅为4.6微克/升。这些发现表明,胰岛素诱导的脂肪萎缩是由免疫复合物的局部形成、补体固定以及细胞浸润释放炎症介质所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c423/1601688/9cf91f54d6d9/brmedj00025-0023-a.jpg

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