一名醛固酮生成腺瘤患者的原发性醛固酮增多症和低钾血症引发的横纹肌溶解症:病例报告和文献综述。

IF 1 4区 医学 Q3 MEDICINE, GENERAL & INTERNAL
Internal Medicine Pub Date : 2025-03-15 Epub Date: 2024-08-10 DOI:10.2169/internalmedicine.3629-24
Nobumasa Ohara, Takashi Tani, Kenshi Terajima, Tetsutaro Ozawa, Yuichiro Yoneoka, Hiroki Shimada, Yasuhiro Nakamura, Go Hasegawa, Tsutomu Nishiyama
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引用次数: 0

摘要

有许多原发性醛固酮增多症(PA)患者因低钾血症诱发横纹肌溶解症而接受肾上腺切除术治疗醛固酮生成腺瘤(APA)的病例报道,但其免疫组织病理学和分子特征仍不清楚。我们在此报告了一例 28 岁女性 PA 患者,她因低钾血症诱发横纹肌溶解症而接受肾上腺切除术治疗单侧 APA。免疫组化分析显示,大多数腺瘤细胞的类固醇生成酶(包括 CYP11B2)呈阳性。基因分析显示,KCNJ5 存在体细胞突变。这些研究结果表明,患者的腺瘤具有很强的醛固酮生成能力,这可能与她严重的高醛固酮症以及由此导致的低钾血症引起的横纹肌溶解症有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Primary Aldosteronism and Hypokalemia-induced Rhabdomyolysis in a Patient with Aldosterone-producing Adenoma: A Case Report and Literature Review.

Many cases of primary aldosteronism (PA) in patients who developed hypokalemia-induced rhabdomyolysis and underwent adrenalectomy for aldosterone-producing adenoma (APA) have been reported; however, the immunohistopathological and molecular features remain unknown. We herein report the case of a 28-year-old woman with PA who presented with hypokalemia-induced rhabdomyolysis and underwent adrenalectomy for unilateral APA. An immunohistochemical analysis revealed that most adenoma cells were positive for steroidogenic enzymes, including CYP11B2. A genetic analysis revealed a somatic mutation in the KCNJ5. These findings suggest a strong aldosterone production capacity in our patient's adenoma, which was presumably related to her severe hyperaldosteronism and the resultant hypokalemia-induced rhabdomyolysis.

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来源期刊
Internal Medicine
Internal Medicine 医学-医学:内科
CiteScore
1.90
自引率
8.30%
发文量
0
审稿时长
2.2 months
期刊介绍: Internal Medicine is an open-access online only journal published monthly by the Japanese Society of Internal Medicine. Articles must be prepared in accordance with "The Uniform Requirements for Manuscripts Submitted to Biomedical Journals (see Annals of Internal Medicine 108: 258-265, 1988), must be contributed solely to the Internal Medicine, and become the property of the Japanese Society of Internal Medicine. Statements contained therein are the responsibility of the author(s). The Society reserves copyright and renewal on all published material and such material may not be reproduced in any form without the written permission of the Society.
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