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肾衰竭中丙氧芬诱发的低血糖症。

Propoxyphene-induced hypoglycemia in renal failure.

作者信息

Shah Pankaj, Aniszweski Jarek, Service F John

机构信息

Division of Endocrinology, Diabetes, Metabolism, & Nutrition, Mayo Clinic Rochester, Rochester, Minnesota 55905, USA.

出版信息

Endocr Pract. 2006 Mar-Apr;12(2):170-3. doi: 10.4158/EP.12.2.170.

Abstract

OBJECTIVE

To present a case of symptomatic hypoglycemia induced by propoxyphene.

METHODS

The historical features, results of laboratory evaluations, and clinical course of a man with end-stage renal disease in whom hypoglycemia developed during treatment with propoxyphene are described.

RESULTS

A 54-year-old man with chronic renal failure had recurrent episodes of hypoglycemia (plasma glucose level, 40 mg/dL). While he continued treatment with propoxyphene, 58 hours into a 72-hour fast the plasma glucose concentration was 38 mg/dL, in conjunction with a beta-hydroxybutyric acid level of 0.9 mmol/L and inappropriately elevated plasma insulin, serum C-peptide, and proinsulin levels. A plasma drug screen was negative for sulfonylureas. A selective arterial calcium stimulation test yielded negative results. A 72-hour fast after discontinuation of propoxyphene therapy resulted in no hypoglycemia, and he experienced no hypoglycemic episodes for at least 2 years after withdrawal of the propoxyphene treatment.

CONCLUSION

The importance of obtaining a thorough medication history in a patient with renal failure and hypoglycemic episodes is highlighted by this case of propoxyphene-induced hypoglycemia. The mechanism of this effect is not known, although non-micro receptor agonism or noncompetitive N-methyl-D-aspartate receptor antagonism may have a role in causing hypoglycemia.

摘要

目的

报告一例由丙氧芬诱发的症状性低血糖病例。

方法

描述一名终末期肾病男性患者在接受丙氧芬治疗期间发生低血糖的病史特点、实验室检查结果及临床病程。

结果

一名54岁慢性肾衰竭男性反复出现低血糖发作(血浆葡萄糖水平为40mg/dL)。在他继续使用丙氧芬治疗期间,禁食72小时至58小时时,血浆葡萄糖浓度为38mg/dL,同时β-羟基丁酸水平为0.9mmol/L,血浆胰岛素、血清C肽和胰岛素原水平异常升高。血浆药物筛查磺脲类药物呈阴性。选择性动脉钙刺激试验结果为阴性。停用丙氧芬治疗后进行的72小时禁食未出现低血糖,停用丙氧芬治疗后至少2年他未再经历低血糖发作。

结论

该例丙氧芬诱发的低血糖病例突出了在肾衰竭合并低血糖发作患者中获取详尽用药史的重要性。尽管非微受体激动或非竞争性N-甲基-D-天冬氨酸受体拮抗作用可能在导致低血糖中起作用,但这种效应的机制尚不清楚。

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