导致 CA 19-9 明显升高的一个非常罕见的原因：胰高血糖素样肽-1 受体激动剂

IF 4.6 2区医学 Q1 ENDOCRINOLOGY & METABOLISM

Diabetes & metabolism Pub Date : 2024-09-11 DOI:10.1016/j.diabet.2024.101578

Rongyue Liang , Zhifang Fu , Long Chen , Shuang Zhou , Hongmei Jiao

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引用次数: 0

摘要

目的胰高血糖素样肽-1（GLP-1）受体激动剂（GLP1-RAs）常用于治疗 2 型糖尿病（T2DM）。各种不良反应已逐渐见诸报端。本病例介绍了一种罕见的现象，即 GLP1-RA 导致碳水化合物抗原 19-9（CA 19-9）明显升高，但无肿瘤证据。方法采用混合方法，结合从定期门诊和随访中获得的病史，以及从实验室检查和影像学检查中获得的辅助检查。结论 GLP1-RA在治疗T2DM期间可能导致肿瘤标志物水平升高，因此有必要在治疗期间进行监测。应根据个人情况调整抗糖尿病治疗方案。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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A very rare cause of markedly elevated CA 19–9: Glucagon-like peptide-1 receptor agonists

Aim

Glucagon-like peptide-1 (GLP-1) receptor agonists (GLP1-RAs) are commonly used to treat type 2 diabetes mellitus (T2DM). Various adverse reactions have been gradually reported. This case presents a rare phenomenon in which a GLP1-RA caused a marked elevation in carbohydrate antigen 19–9(CA 19–9) without evidence of a tumor.

Methods

A mixed-methods approach was utilized, incorporating medical history obtained from regular outpatient consultations and follow-up visits, along with ancillary examinations derived from laboratory tests and imaging.

Results

The use of a GLP1-RA for treating T2DM resulted in an increase in CA 19–9 without evidence of a tumor, which gradually normalized after discontinuation of the drug.

Conclusion

GLP1-RAs may lead to elevated levels of tumor markers during the treatment of T2DM, necessitating monitoring during therapy. Antidiabetic management should be adjusted on an individual basis as needed.

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来源期刊

Diabetes & metabolism 医学-内分泌学与代谢

CiteScore

12.00

自引率

4.20%

发文量

审稿时长

13 days

期刊介绍： A high quality scientific journal with an international readership Official publication of the SFD, Diabetes & Metabolism, publishes high-quality papers by leading teams, forming a close link between hospital and research units. Diabetes & Metabolism is published in English language and is indexed in all major databases with its impact factor constantly progressing. Diabetes & Metabolism contains original articles, short reports and comprehensive reviews.