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双侧肿瘤样糖尿病性乳腺病——5年随访期间疾病的进展与消退

Bilateral, tumorlike diabetic mastopathy-progression and regression of the disease during 5-year follow up.

作者信息

Bayer U, Horn L C, Schulz H G

机构信息

Department of Diagnostic Radiology, Leipzig University, Germany.

出版信息

Eur J Radiol. 1998 Feb;26(3):248-53. doi: 10.1016/s0720-048x(97)00029-6.

Abstract

Diabetic mastopathy is a recently described collection of radiographical and histological features found in dense fibrous masses of the breast in long standing Type I diabetes. We describe the first case of bilateral disease with the alternate progression and regression of the disease over a 5 year period. A 45-year-old woman has been affected of insulin dependent diabetes mellitus (IDDM) for 21 years. She developed palpable mass retromamillar of the right side, indistinguishable radiographically from cancer. The histology showed a diabetic mastopathy (DMP) with B-lymphocytic ductitis and lobulitis, a discrete monocellular vasculitis and a keloid-like fibrosis. After 22 months she developed a suspicious palpable mass contralateral on the left side. The FNAB presented an identical morphology on histology. Additionally 10 months later there were no palpable masses of both mammae. Mammographically no suspect alterations were observed. One year later the clinical and mammographical examination showed similar findings, mentioned before. The pathogenesis is still obscure and includes the hypothesis of extracellular accumulation, secondary to prolonged hyperglycemia in IDDM, production of alternated non-enzymatic glycosylated end products with neoantigen formation, B cell predominant inflammation with autoimmune response against neoantigens and cytokine release secondary to the autoimmune response.

摘要

糖尿病性乳腺病是一种最近才被描述的影像学和组织学特征的集合,见于长期患Ⅰ型糖尿病的女性乳房致密纤维肿块中。我们描述了第一例双侧病变病例,该疾病在5年期间交替进展和消退。一名45岁女性患胰岛素依赖型糖尿病(IDDM)21年。她右侧乳晕后出现可触及肿块,影像学表现与癌症难以区分。组织学显示为糖尿病性乳腺病(DMP),伴有B淋巴细胞性导管炎和小叶炎、离散的单细胞血管炎以及瘢痕疙瘩样纤维化。22个月后,她左侧出现可疑的可触及肿块。细针穿刺活检(FNAB)组织学表现相同。此外,10个月后双侧乳房均未触及肿块。乳腺X线摄影未观察到可疑改变。1年后,临床和乳腺X线检查显示出之前提到的类似表现。其发病机制仍不清楚,包括以下假说:IDDM长期高血糖继发细胞外积聚、产生具有新抗原形成的交替非酶糖基化终产物、以B细胞为主的炎症以及针对新抗原的自身免疫反应和自身免疫反应继发的细胞因子释放。

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