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获得性免疫缺陷综合征患者中喷他脒诱导的糖尿病的胰腺病理学

Pancreatic pathology in pentamidine-induced diabetes in acquired immunodeficiency syndrome patients.

作者信息

Hauser L, Sheehan P, Simpkins H

机构信息

Department of Pathology, SUNY (Downstate), Brooklyn 11203.

出版信息

Hum Pathol. 1991 Sep;22(9):926-9. doi: 10.1016/0046-8177(91)90185-r.

Abstract

An acquired immunodeficiency syndrome patient who was treated with pentamidine for a pneumocystis infection developed hypoglycemia followed by diabetes mellitus. The pathologic findings in the pancreas consisted of a significant decrease in the number of insulin-positive cells as measured by immunoperoxidase techniques when compared with comparable tissue from an age- and sex-matched control. There was also a decrease in the staining intensity of the insulin-positive cells, an absolute increase in the glucagon-positive cells, and no significant change in the number of somatostatin-positive cells. Routinely stained histologic sections showed morphologic changes in the islets with features different from those described in insulin-dependent diabetes mellitus or those caused by the toxin Vacor. The islets had increased vascular spaces, no islet cell necrosis, no fibrosis, and no lymphocytic infiltrates when compared with an age-matched control.

摘要

一名获得性免疫缺陷综合征患者因肺孢子菌感染接受喷他脒治疗后出现低血糖,随后发展为糖尿病。与年龄和性别匹配的对照者的可比组织相比,通过免疫过氧化物酶技术测量,胰腺的病理发现为胰岛素阳性细胞数量显著减少。胰岛素阳性细胞的染色强度也降低,胰高血糖素阳性细胞绝对增加,生长抑素阳性细胞数量无显著变化。常规染色的组织学切片显示胰岛的形态学改变,其特征不同于胰岛素依赖型糖尿病或毒素灭鼠优所致的改变。与年龄匹配的对照相比,胰岛的血管间隙增加,没有胰岛细胞坏死、纤维化和淋巴细胞浸润。

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Survival from pentamidine induced pancreatitis and diabetes mellitus.
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Pentamidine-induced pancreatic beta-cell dysfunction.喷他脒诱发的胰腺β细胞功能障碍。
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